Messenger RNA (mRNA) SARS Coronavirus ‘Vaccines’ and their Potential Autoimmunity Part 2

Messenger RNA (mRNA) SARS Coronavirus ‘Vaccines’ and their Potential Autoimmunity Part 2

Febuary 24, 2021

Messenger RNA (mRNA) SARS Coronavirus ‘Vaccines’ and their Potential Autoimmunity Part 2

James Odell, OMD, ND, L.Ac.

Reference Commentary – The material published in this commentary is intended to foster scholarly inquiry and a rich discussion of the controversial topic of bioethics and health policy. The views expressed in this article are solely the authors and do not represent the policy or position of the Bioregulatory Medicine Institute (BRMI), nor any of its Board Advisors or contributors. The views expressed are not intended to malign any religious or ethnic group, organization, company, individual, or any other. Every effort has been made to attribute the sources of this article to the rightful authors listed in references.The content of this article is presented in summary form, is general, and is provided for informational purposes only: it is not advice, nor should it be treated as such. If you have any healthcare-related concerns, please call, or see your physician or other qualified healthcare providers. Never disregard medical advice or delay seeking it because of something you have read in this article.


In my last article entitled COVID 19 mRNA Vaccines, published in the 24th BRMI E-Journal, I reviewed many of the safety concerns about the experimental messenger RNA SARS coronavirus ‘vaccines’ not being discussed in the medical media. Because no long-term safety studies have had time to be performed to ensure that any of these products do not cause cancer, seizures, paralysis, heart disease, or autoimmune diseases, it is of paramount importance for the public to become informed as to any potential risk. Unfortunately, the medical media and pharmaceutical manufacturers have not provided adequate or complete information on the potential adverse effects these experimental mRNA ‘vaccines’ may cause. Partly, because much of this research is being gathered in real-time. In short, there is a gross lack of informed consent as much is still not known about their efficacy and safety. This commentary is an attempt to disclose pertinent information that potential recipients should know to make a truly informed decision as to whether to receive the injection.


After the last article, I received many inquiries about details of vaccine immunity in relation to this new mRNA platform. Many readers requested that information be simplified on vaccine immunology, whereas others asked that for more details about the technical aspects of vaccine immunity and their potential for autoimmunity. So, this part-two reference commentary is an attempt to compromise and further evaluate both how vaccines affect immunity and their potential for causing autoimmunity.


Emergency Use Authorization


The Pfizer-BioNTech and Moderna COVID-19 ‘vaccines’ have not been approved or licensed by the U.S. Food and Drug Administration (FDA), but instead have received authorized for emergency use by the FDA under an Emergency Use Authorization (EUA) for use in individuals 16 years of age and older. Thus, both products are experimental in that they have not been approved by the FDA for a biological license and were approved under EUA without long term safety data. The FDA has not fully evaluated the data and still has not decided if the potential risks outweigh the benefits of receiving it. Human trial data is not complete and published yet, and this is partly why it is considered ‘experimental’ and still unlicensed by the FDA as a biological drug.


According to the FDA website, medical products that may be considered for a EUA are those that “may be effective” to prevent, diagnose, or treat serious or life-threatening diseases or conditions that can be caused by a CBRN agent(s) (chemical, biological, radiological, and nuclear) identified in the HHS Secretary’s declaration of emergency or threat of emergency under section 564(b). The “maybe effective” standard for EUAs provides for a lower level of evidence than the “effectiveness” standard that the FDA uses for product approvals.


The World Health Organization announced on January 8th that Pfizer’s COVID-19 vaccine was not recommended for pregnant women unless they are at particularly high risk for the virus or a health care worker. They followed that recommendation with another on February 2nd advising against pregnant women taking the Moderna coronavirus vaccine unless they are health care workers or have preexisting conditions. Pregnant and lactating women were excluded from Pfizer/BioNTech and Moderna’s COVID-19 vaccine clinical trials, and they are not included in any ongoing trials for vaccines manufactured by other companies. That means there is no safety data available to know for sure whether these ‘vaccines’ are safe for people who are pregnant or breastfeeding. It is not known if or how these experimental drugs will affect fertility in the short or long term. What is known is that there have been several reports to Vaccine Adverse Event Reporting System (VAERS) of miscarriages following the shot.


Viral Messenger RNA as a Synthetic Pathogen of Unknown Risk


The central dogma of biology states that DNA makes RNA and RNA make proteins.However, there are many different types of RNAs, and only one of them, the messenger RNA (mRNA), gives rise to proteins. Messenger ribonucleic acids (mRNAs) transfer the information from DNA to the cell machinery that makes proteins. Specifically, mRNA delivers the information encoded in one or more genes from the DNA to the ribosome, a specialized cellular structure, or organelle, where that information is decoded into a protein. Ribosomes read the mRNA and translate the message into functional proteins in a process called ‘translation’. Depending on the newly synthesized protein’s structure and function, it will be further modified by the cell, exported to the extracellular space, or will remain inside the cell. The primary function of mRNA is to act as an intermediary between the genetic information in DNA and the amino acid sequence of proteins. Thus, messenger RNA is an intermediary between the gene, and the product, the protein.


In vaccines, it is the protein that ultimately elicits the immune response, not the RNA. Historically, vaccines are proteins, either viral, or bacterial, and it is the vaccine’s protein that, if all goes well, develops an immune response to elicit neutralizing antibodies. Vaccine-mediated immunity is often multifactorial, and the best protection is likely to be elicited by the combination of strong humoral and cell-mediated immune responses.


So, by definition, an mRNA ‘vaccine’ is not a true vaccine. First, because it is not a protein that directly elicits an immune response. It first must be decoded into protein, and it is then that protein that in turn creates the desired immune response. Secondly, by FDA definition, since it is a component used as a treatment to affect a body’s function, it is by legal definition a ‘medical device’ or a physical ‘device’ that comes in a molecular-sized package. Thus, strictly speaking, this messenger RNA device is a synthetic pathogen utilizing a genetic engineering process as a biological response modifier, not at all like a classical vaccine. In principle, biological response modifiers are biologically active agents including antibodies, small peptides, and/or other (small) molecules of mRNA, DNA, that can influence the immune response. Most importantly, this synthetic viral pathogen device is a new and different molecular platform, one that has never been injected into the public’s arm.


With these mRNA synthetic pathogens, what is injected into the body is not a weakened virus or even selected antigens, but rather protein-coding instructions that tell your body’s cells how to make the antigens on their own. Again, that process is called “translation.”


Erroneously referring to this intervention as a ‘vaccine’ exploits the public’s ingrained trust in previous vaccination programs. It keeps us in the illusion of vaccine safety in place of taking the necessary measures to investigate the impact of this new experimental device on our health. In studies of vaccination decision-making, risk perception is often intricately linked with ideas of trust in health professionals, in government, or public health institutions and the interplay between these actors. When medical professionals or institutions no longer fulfill their obligation of information transparency and disclosure of potential risks, this is a harmful violation of trust. Many people do not understand what FDA Emergency Use Authorization entails. It means it is still experimental and carries risk yet unknown. The public becomes the experiment.


Another wrinkle in information disclosure is the manufacturer’s complete lack of liability. As I described in the previous article, the Public Readiness and Emergency Preparedness Act of 2005 has now allowed vaccine manufacturers unlimited freedom to create, develop, and market COVID-19 vaccines without any liability whatsoever. All liability is protected by the PREP Act, which means if anyone has an adverse event or death caused by this vaccine there really is no recourse. This was put into the Federal Register in March of 2020 and does not expire till the end of 2024. So, anything that is developed over the next four years that has to do with a biological agent, such as a vaccine or drug or biotechnology, no matter how nefarious, is protected from liability under the umbrella of COVID-19.


Messenger RNA


This mRNA experimental synthetic pathogen carries mRNA genetic material from SARS-CoV-2 coronavirus into cells where that cellular machinery with the synthetic pathogen produces a protein to which the body mounts an immune response. In the case of COVID-19, inert spike (S) antigen proteins are produced. This then enables SARS-CoV-2 coronavirus particles to enter host cells and triggers humoral (antibody-mediated) acquired immunity. So, what could possibly go wrong with bodily cells that are artificially programmed to produce foreign viral proteins to which the immune system is going mount an immune response? Well, that biochemical reaction could create an autoimmune reaction. As this mRNA platform has never been used in humans before, the potential for this to go wrong and elicit widespread autoimmune diseases and deaths is enormous.


Pfizer, Moderna, Dr. Anthony Fauci, and Dr. Soumya Swaminathan, the WHO’s chief scientist, have now made it abundantly clear that the novel mRNA strand entering the cell is not intended to stop transmission but rather as a treatment. However, America’s Frontline Doctors and numerous other doctors have been censored from public discourse on the profoundly viable and formerly ubiquitous treatments such as hydroxychloroquine, ivermectin, zinc, vitamin C, and vitamin D3. If these effective treatments had not been denied us, both in access and scientific data, but disseminated to the global community, we might not have needed an ‘emergency use’ technology at all. Bear in mind for FDA to issue an emergency use authorization, there must be no adequate, approved, and available alternative to the candidate product for diagnosing, preventing, or treating the disease or condition. Could this be why these available and effective alternative products are constantly censored in the media and social media?


Antibodies and Vaccines


To understand how vaccines create immune responses it is necessary to briefly clarify and review the function of antibodies and both the adaptive and innate immune system. Antibodies, also known as immunoglobulins (Ig), are specialized proteins that bind to a uniquely shaped object – called an antigen – that is found on the surface of a pathogen. These pathogens can be things such as bacteria or viruses. Antibodies are produced by B lymphocytes, known as B cells, which are specialized white blood cells of the immune system. B cells have antibodies on their cell surface that allow them to recognize anything foreign. When they encounter a pathogen such as a virus, the B cells transform into plasma cells, which start producing antibodies that are designed to bind to an antigen that is specific to that pathogen.


B-plasma cells release large amounts of antibodies into the body’s circulation. This protects us in two main ways. First, antibodies can bind to antigens on the outside of the pathogen to stop it from entering our cells. This is particularly important for viruses, which enter human cells to replicate. Second, by binding to antigens on the pathogen, antibodies also signal other white blood cells known as phagocytic cells, which engulf and destroy the pathogen. So, in short, antibodies can both neutralize a virus and mark it for destruction.


Antibodies form part of our adaptive immune response, which is a refined, targeted response to a specific antigen. The first time we encounter a virus, some of our B cells become plasma cells, but others transform into memory B cells. The second time you are exposed to the same pathogen, these memory cells quickly transform into plasma cells that produce large amounts of antigen-specific antibodies to fight the infection.


There are many types of antibodies, each with different purposes, which are created in response to chemical signals. Different B cells in the body will produce multiple different antibodies that bind to different sites, but only binding to some of these sites will inactivate the virus. For a vaccine to work, it must produce a binding or neutralizing antibody. It is never certain that a vaccine will produce neutralizing antibodies. One important difference in antibodies produced from vaccines and antibodies from natural infections is that the immune system does not form as many different types of antibodies from a vaccination as it would in the course of a natural infection. Thus, natural infection often protects the individual for life, whereas artificial infection from a vaccine usually requires repeated boosters to maintain antibody levels.


However, in some circumstances, the binding of an antibody might worsen an infection. For example, antibodies might bind to a virus in such a way that helps the virus enter cells more easily. This might mean that a person re-infected after an initial mild infection might then have a more severe disease. Or it might mean that a person could have a worse response to a potential infection (like with COVID-19) if they have previously been vaccinated for the disease. This scenario has been called “antibody-dependent enhancement” (ADE) and will be discussed later in this article.


Three main types of antibodies are produced in response to infection: IgA, IgG, and IgM. IgM rises soonest and typically declines after infection. IgG and IgA persist and usually reflect longer-term immune responses. The detection of IgM antibodies is sometimes used as a test for recent infection. For example, an IgM antibody is commonly used to check for recent coronavirus infection. A particularly important type is IgG antibodies, which tend to be more long-lived than IgM antibodies. This subtype of antibodies is critical not just for controlling the initial disease but for preventing future disease if you are later re-exposed. It is observed that IgM levels increased during the first week after SARS-CoV-2 infection, peak 2 weeks later, and then they are reduced to near-background levels in most patients. IgG has been detectable after 1 week and may be maintained at a high level for a long period.


Some people make many high-quality antibodies that are good at recognizing the relevant antigen and binding to it. If this happens, the virus is rapidly bound by antibodies and eliminated before it can even cause an infection. Other people make antibodies, but they are not as effective at binding the pathogen. In this situation, the antibodies only provide partial protection at best. Then there are also those people who either produce little or no antibodies or poor-quality antibodies. Generally, many elderly fall into this category. In this case, vaccine immunity is not so effective, so they may experience a prolonged infection with more severe symptoms. They are also likely to be re-infected at a later point in time. This is part of the reason vaccines do not always confer immunity or confer only partial immunity for a limited period.


The adaptive immune system involves more than just B cells, plasma cells, and antibodies – it also includes T cells. T cells are another population of white blood cells that can develop into memory cells, just as B cells can. They can also differentiate into specialized cells that kill virus-infected cells. The functions of T cells and B cells are different. B cells develop into plasma cells that produce antibodies (T cells do not); T cells directly kill virus-infected cells (B cells do not). Sometimes individuals with a very vigorous T cell immune response will be protected from a pathogen even though they produce low amounts of antibody. The T cell immune response is much more difficult to measure than the antibody response and is usually only evaluated in a specialized laboratory or research setting. Our adaptive immune response is important because once developed, it is highly specific for the pathogen and provides us with immunologic memory.


We also have another type of immune system known as the innate immune system. The innate immune system is our frontline defense, the first system to respond to a new infection. This includes cells such as neutrophils, macrophages, and dendritic cells. Unlike the adaptive immune system, which includes antigen-specific antibodies that take time to develop, the innate immune system responds to antigens very quickly but in a non-specific way. It attacks anything that “looks” foreign to the body, like components of a bacterial cell wall, or viral RNA and DNA. Quite often, the innate immune response will take care of an infection before the adaptive immune system even has a chance to start manufacturing antibodies.


SARS-CoV-2 Antibody Blood Test


Many people are now taking the COVID-19 antibody blood test. This immune response test detects the immune proteins or antibodies that the body produces in response to the virus. It does not detect the virus itself; thus, an antibody test does not determine whether you are currently infected with the COVID-19 virus. Antibody testing is best undertaken at least two weeks after the onset of symptoms. Because SARS-CoV-2 belongs to a large family of coronaviruses, the test may inadvertently detect the antibody of related coronavirus strains (such as the HKU1, NL63, OC43, or 229E strains) and trigger a false-positive reading. False-negatives are even more common with SARS-CoV-2 antibody tests, due in part to the variable sensitivities of the tests. The sensitivity and specificity of antibody tests vary over time and results should be interpreted in the context of clinical history. Compared to venous blood tests, rapid finger-stick tests tend to be less reliable and more likely to return a false-negative result. In short, the evidence is currently insufficient to know whether individuals with SARS-CoV-2 antibodies have protective immunity.


Current SARS-CoV-2 ‘Vaccines’


At the time of this writing, there are 2 experimental mRNA SARS-CoV-2vaccines’ publicly available, one by Pfizer/BioNTech the other from Moderna, and one viral vector vaccine by Johnson and Johnson. As previously mentioned, mRNA-based ‘vaccines’ have never before been used on humans and these two are still not FDA licensed for human use, though they have been made publicly available through Emergency Use Authorization. These mRNA formulas contain a synthetic sequence of messenger RNA that is concealed within a patented lipid nanoparticle delivery system. After entering cellular ribosomes (that house the transcription machinery of the cells) of the muscle cells into which the synthetic pathogenic mRNA is injected, it then instructs cells to produce a copy of the spike protein of the virus. In essence, it means that the human body becomes the vaccine factory of the protein. This process is genetic engineering. Even more concerning, is that these synthetic pathogen devices place a novel molecule, spike protein, in/on the surface of host cells. This spike protein then becomes a potential receptor for another possibly novel pathogenic infectious agent.


Recently the Janssen Vaccines, a subsidiary of Johnson and Johnson has also received FDA Emergency Use Authorization for the company’s single-shot COVID-19 vaccine for adults 18 and older. Thus, it is now the third vaccine available in the U.S. This vaccine is based on an adenovirus vector Ad26 (not a mRNA vaccine like Pfizer or Moderna). Ad26.COV2.S expresses the full-length spike protein, stabilized by furin cleavage site mutations and two consecutive proline stabilizing mutations in the hinge region. It contains the wild-type signal peptide. The science behind recombinant adenoviral vector vaccines has been around for a long time, but the only commercially available adenovirus-based vaccine is a rabies vaccine for animals. Viral vector vaccines are more of a conventional vaccine platform, unlike mRNA vaccines. Viral vector vaccine work by carrying a DNA express or antigen(s) into host cells, thereby eliciting cell-mediated immunity in addition to the humoral immune responses. Adenovirus-based vaccines may also pose some problems in that the adenovirus is so common that the vaccine may not be as effective once booster doses are given, or that some people may already have immunity to the virus used in the vaccine. Additionally, incorporating a spike protein into the viral vector vaccine potentially creates this protein receptor to attract another novel pathogenic infectious agent.


Another frontrunner is the non-replicating viral vector vaccine by the AstraZeneca/Oxford University group. This also employs a genetically modified (non-replicating) chimpanzee viral vector vaccine, now designated AZD1222. The AstraZeneca/Oxford’s vaccine instead of utilizing a human adenovirus in its vaccine uses a genetically modified chimpanzee-derived adenovirus that encodes the spike protein of Middle East respiratory syndrome coronavirus (MERS-CoV).


According to the recent World Health Organization’s Draft landscape of COVID-19 candidate vaccines, there are currently 64 candidate vaccines in clinical development with a further 173 in pre-clinical development, these relying on 8 different vaccine platforms in addition to the two already relied on by the 3 frontrunners. Most (31%) rely on the more conventional protein subunit platform that has been widely used for seasonal influenza vaccines.


This article will continue to focus on mRNA vaccines, not viral vector vaccines.


SARS-CoV-2 Autoimmunity and Inflammatory Cytokines


Autoimmune disease occurs when the body’s immune system cannot discern the difference between its cells and foreign cells, and in turn, this causes the body to attack its normal cells. Simply speaking, in autoimmunity the patient’s immune system is activated against the body’s proteins. Molecular mimicry is an antigenic similarity between molecules found on some disease- causing microorganisms and specific previously healthy body cells or tissues. In short, molecular mimicry occurs when a pathogen expresses a protein that is remarkably similar in sequence or shape to a protein in the host. It has been suggested that molecular mimicry may contribute to a potential adverse reaction to the SARS-CoV-2 mRNA shot. Thus, antibodies to SARS-CoV-2 cross-reacting with structurally similar host protein sequences and raising an acute autoimmune response against them.


Cytokines are the hormonal messengers responsible for many of the biological effects in the immune system, such as cell-mediated immunity and allergic-type responses. Although they are numerous, cytokines can be functionally divided into two groups: those that are proinflammatory and those that are essentially anti-inflammatory but that promote allergic responses. As previously discussed, T cell lymphocytes play a central role in the adaptive immune response. T lymphocytes are also a major source of cytokines. These cells bear antigen-specific receptors on their cell surface to allow recognition of foreign pathogens. They can also recognize normal tissue during episodes of autoimmune diseases. There are two main subsets of T lymphocytes, distinguished by the presence of cell surface molecules known as CD4 and CD8. T lymphocytes expressing CD4 are also known as helper T cells, and these are regarded as being the most prolific cytokine producers. This subset can be further subdivided into Th1 and Th2, and the cytokines they produce are known as Th1-type cytokines and Th2-type cytokines.


Th1 or Th2 differ in a few important ways. The most apparent difference is that Th1 cytokines are produced by Th1 helper cells, as opposed to Th2 helper cells. Whether an attacking virus or bacteria invades inside or outside of cells is also important, as intracellular invaders tend to trigger Th1 cytokine responses, while outside agents call upon Th2 cytokine responses. As such, Th1 cytokines activate white blood cells called macrophages inside of tissues. In contrast, Th2 cytokines activate antibodies in what is known as a humoral immune response, and this type of response will most likely occur when the concentration of an invading substance (virus) is high.


Th1-type cytokines tend to produce the pro-inflammatory responses responsible for killing microorganisms and for perpetuating autoimmune responses. Interferon-gamma is the main Th1 cytokine. Excessive pro-inflammatory responses can lead to uncontrolled tissue damage, so there needs to be a mechanism to counteract this. The Th2-type cytokines include interleukins 4, 5, and 13, which are associated with the promotion of IgE and eosinophilic responses. Over-expression of IL-5 significantly increases eosinophil numbers and antibody levels. It has been proposed that IL-5 be used as a biomarker for antibody-dependent enhancement or pathogenic priming.


Regulatory T-cells (formerly called suppressor T cells) are a component of the immune system that suppresses the immune responses of other cells. Th1 assists in the activation of these regulatory T-cells which are meant to slow down B-cells and cytotoxic T-cells. If the regulatory T-cells are malfunctioning or deficient due to a decrease in Th1, the cytotoxic T-cells may take over and start killing healthy cells (autoimmune). This leads to increased immune stimulation, followed by an inflammatory cytokine storm and potential for autoimmune disorders. It is observed that some people find themselves with an autoimmune condition after a traumatic event or stressful event (e.g., a parent or sibling passing away). The physiological stress response caused Th1 to decrease, which lead to Th2 dominance.


Additionally, excess Th2 responses will counteract the Th1 mediated microbicidal action. The optimal scenario would therefore seem to be that humans should produce a well-balanced Th1 and Th2 response, suited to the immune challenge. Unfortunately, vaccines being an artificial induced immune response, historically have been implicated in creating an imbalance in this Th1 and Th2 response, resulting in pro-inflammatory Th2-type cytokines.


In chronic inflammatory autoimmune diseases, white cells such as neutrophils and other leukocytes are constitutively recruited by these proinflammatory cytokines and chemokines, resulting in tissue damage. This inflammatory reaction is called a ‘cytokine storm’. It is an overreaction of the immune system, in which an excess of certain proinflammatory cytokines trigger an onslaught of white blood cells that attack an area or organ of the body resulting in tissue damage, and in extreme cases, organ failure. An example of a cytokine storm in the lungs of a COVID-19 patient can draw inflammatory causing white blood cells into the spaces between air sacs, blocking oxygen from reaching the blood, which can prove fatal. Both genetic and environmental factors are thought to contribute both to the severity of viral infections and in determining who potentially develops an autoimmune condition.


Thus, it is observed that severe/fatal cases of COVID-19 are associated with immune hyperactivation and excessive cytokine release, leading to multiorgan failure. A broad range of mechanisms appears to be involved. However, it has been suggested that ‘molecular mimicry’ may contribute to this problem, with antibodies to SARS-CoV-2 spike glycoproteins cross-reacting with structurally similar host heptapeptide protein sequences (for example, in interleukin-7 and alveolar surfactant proteins), and raising an acute autoimmune response against them.1 Auto-inflammatory dysregulation in genetically susceptible individuals might also contribute to acute but also chronic autoimmunity during and after COVID-19.2


Though the exact etiology of many autoimmune diseases remain unknown, various factors are believed to contribute to the emergence of autoimmune disease in people including the genetic predisposition, corruption of the internal milieu resulting in microbe triggers such as bacterial, viral, fungal, and parasitic infections, including imbalances of the gut microbiota (dysbiosis of the intestinal microbiome), as well as numerous toxicological environmental agents, hormonal factors, and the host’s immune system dysregulation. All these factors interplay was coined by Shoenfeld et al., many years ago in “The Mosaic of Autoimmunity.”3


Certain viruses have long been implicated in the initiation of chronic inflammatory or autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, Sjogren’s syndrome, multiple sclerosis, polymyositis, uveitis, Henoch–Schönlein purpura, systemic juvenile idiopathic arthritis, and others.4 In May 2020 a German study entitled “COVID-19-induced acute respiratory failure: an exacerbation of organ-specific autoimmunity?”, examined a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological, and histomorphology similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease-induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ-specific autoimmunity in predisposed patients.5 In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease-related autoantibodies.6


Autopsies of Chinese citizens who have died from COVID-19 following SARS-CoV-19 infection show evidence of lung interstitial changes, suggesting the development of pulmonary fibrosis. This suggests, at least partly, an autoimmunology basis of the pathogenesis of COVID-19.


Vaccine Autoimmunity


In the past few decades, the study of autoimmune biology, the failure to recognize self-antigens as “self”, has grown immensely. One in five Americans has an autoimmune condition. Vaccines, particularly viral vaccines, have been observed playing a role in inducing autoimmune disease for a long time. Autoimmune reactions are among the most serious adverse events observed in vaccines. An example is Guillain-Barré syndrome (GBS), an autoimmune polyneuropathy. GBS has been attributed to certain vaccinations, particularly, with monovalent or combination measles, mumps, and rubella vaccines, influenza vaccine, oral polio vaccine, diphtheria, and tetanus toxoids. GBS has also been associated with the 1976 swine-influenza vaccine. 7, 8, 9, 10, 11, 12, 13, 14, 15, 16 Some studies have shown an increased risk of GBS following receipt of seasonal H1N1 monovalent influenza vaccines.17,18 Bear in mind GBS is not the only autoimmune disease that has been documented as an adverse reaction to vaccination.


Vaccine autoimmunity reactions occur from several causes. One explanation is that they may be induced via “molecular mimicry”, and often, in specific families who happen to have a genomic mutation that makes one of their proteins more like the protein in the vaccine. It appears that in addition to molecular mimicry there are other mechanisms by which this SARS-CoV-2 mRNA “vaccine” could induce a hyperinflammatory autoimmune syndrome. One of the most documented is ‘pathogenic priming’ or ‘disease enhancement’, euphemistically called in literature ‘antibody-dependent enhancement or ADE’.


Pathogenic priming or disease enhancement occurs after vaccination or when an infection a person can experience more serious, enhanced disease when later being exposed to the pathogen against which that the vaccine was intended to protect. When the enhancement is specifically related to a vaccine, it is sometimes called vaccine-associated hypersensitivity (VAH). Pathogenic priming or disease enhancement has been demonstrated in SARS-CoV infection years ago, mediated by antibodies directed to the envelope spike proteins.19 Thus, a simple definition of pathogenic priming or ADE is increasing specific antibodies that do not protect, but instead, make a viral infection even worse. This unwanted antibody reaction has long been a thorn in the side of vaccine manufacturers. There are “neutralizing” antibodies as opposed to non-neutralizing ones – a neutralizing antibody, as the name implies, binds to its target in a way that shuts its function down. That is generally done by blocking the receptor of a given protein target or smothering the binding surface that it would need to function. For the coronavirus, a straightforward example of a neutralizing antibody would be one that binds to the tip of the spike protein, the receptor-binding domain that is the part that recognizes and binds to the human ACE2 protein on a cell surface. Block that thoroughly enough, and it would follow that you have blocked the virus’s ability to infect your cells.


More technically, in antibody-mediated viral neutralization, neutralizing antibodies binding to the receptor-binding domain of the viral spike protein, as well as other domains, prevent the virus from docking onto its entry receptor, ACE2. In antibody-dependent enhancement, low quality, low quantity, non-neutralizing antibodies bind to virus particles through the antigen-binding fragment or Fab domains. Fc receptors (FcRs) expressed on monocytes or macrophages bind to Fc domains of antibodies and facilitate viral entry and infection. (An Fc receptor is a protein found on the surface of certain cells – including, among others, B lymphocytes, follicular dendritic cells, natural killer cells, macrophages, neutrophils, eosinophils, basophils, human platelets, and mast cells – that contribute to the protective functions of the immune system.) Upon engagement by the Fc domains on antibodies, activating FcRs with ITAMs initiate signaling to upregulate pro-inflammatory cytokines and downregulate anti-inflammatory cytokines. This causes what is commonly described as a cytokine storm. Immune complexes and viral RNA in the endosomes can signal through Toll-like receptor 3 (TLR3), TLR7, and/or TLR8 to activate host cells, resulting in immunopathology.


(ITAM is an immunoreceptor tyrosine-based activation motif. A conserved sequence of four amino acids repeated twice in the cytoplasmic tails of non-catalytic tyrosine-phosphorylated receptors, cell-surface proteins found mainly on immune cells. Its major role is being an integral component for the initiation of a variety of signaling pathways and subsequently the activation of immune cells, although different functions have been described, for example, an osteoclast maturation.)


Thus, the concern about disease enhancement or ADE arises from the possibility that antibodies present at the time of infection may increase the severity of an illness. Uptake of SARS-CoV through ADE in macrophages led to elevated production of TNF and IL-6.20


In mice infected with SARS-CoV, ADE was associated with decreased levels of the anti-inflammatory cytokines IL-10 and TGFβ and increased levels of the pro-inflammatory chemokines CCL2 and CCL3. 21


Furthermore, immunization of non-human primates with a modified vaccinia Ankara (MVA) virus encoding the full-length S protein of SARS-CoV promoted activation of alveolar macrophages, leading to acute lung injury.22


The enhancement of disease by ADE or pathogenic priming has been described clinically in several studies such as children given formalin-inactivated respiratory syncytial virus (RSV) or measles vaccines in the 1960s, and in dengue hemorrhagic fever due to secondary infection with a heterologous dengue serotype.23, 24, 25, 26


ADE is a primary reason why vaccines for SARS-1 and MERS, were not previously manufactured commercially. Early researchers concluded coronavirus vaccines were too dangerous to proceed to human studies, as demonstrated in animal studies and were no longer necessary because SARS and MERS had waned naturally.


For example, previous vaccine studies in mice, with several whole-inactivated SARS-CoV candidates (with and without aluminum adjuvants) reduced lung viral titer and/or mortality upon viral challenge, but at the same time induced increased lung immunopathology in the form of eosinophilic infiltration (i.e., unusual presence of eosinophilic cells in the lung tissue) upon infection.27, 28, 29 Importantly, one study showed that in older mice, protection was lower and eosinophilic immune infiltration was exacerbated as compared to younger mice.30 Similarly, an inactivated MERS-CoV vaccine in aluminum adjuvant resulted in the production of neutralizing antibody and reduced lung viral titers (upon viral challenge), but induced increased eosinophil infiltration upon homologous coronavirus challenge, despite reducing lung viral titer and/or mortality.31


There has been expressed by many doctors a genuine concern over the risk of pathogenic priming or ADE with these new experimental viral mRNA synthetic pathogen platforms. The results from the fast-tracked human trials and subsequent emergency authorization are not sufficient to rigorously evaluate their true potential risk. The fact that only hundreds (not tens of thousands) of people for each vaccine who have been vaccinated have also been exposed to wild SARS-CoV-2 is not adequate to know if sub-groups of people could be susceptible to disease enhancement following exposure to the virus.


These concerns are sufficient enough for Drs Anne Arvin, Herbert Virgin, and colleagues from Vir Biotechnology in San Francisco and Stanford, writing in one of the world’s most prestigious journals, Nature, to have stated in July 2020 that ADE is “…a general concern for the development of vaccines and antibody therapies because the mechanisms that underlie antibody protection against any virus have a theoretical potential to amplify the infection or trigger harmful immunopathology. This possibility requires careful consideration at this critical point in the pandemic of coronavirus disease 2019”.32


Another concerned voice is, J. Patrick Whelan, MD, PhD, a pediatric rheumatologist, who has warned the FDA about the potential for mRNA vaccines designed to create immunity to the SARS-CoV-2 spike protein to instead cause injuries. Whelan’s training (at Harvard, Texas Children’s Hospital and Baylor College of Medicine) includes degrees in biochemistry, medicine, and rheumatology. For 20 years, he worked as a pediatric rheumatologist. Whelan warned that a recently infected patient who is subject to covid-19 vaccination is likely to suffer from autoimmune attacks along the ACE-2 receptors present in the heart, and in the microvasculature of the brain, liver, and kidney. The risk is doubled because two shots are required.


It is a well-documented fact that SARS-CoV-2 readily targets humans through the vascular endothelium. The virus is known to enter endothelial cells through the ACE-2 receptor on the endothelium. Because of this unique gain-of-function, one of the medical emergencies that may occur in covid-19 patients is thromboembolic complications (formation of a blood clot inside a blood vessel). If viral antigens are present in the endothelial lining of blood vessels, then the vaccine will cause an antigen-specific immune response that attacks those precious tissues, potentially causing cardiovascular events. Research warns that the vaccine may damage the vascular endothelium, especially in the elderly. Dr. Whelan claims that vaccine-induced endothelial inflammation is “certain to cause blood clot formation with the potential for major thromboembolic complications in a subset of such patients. The potential to cause microvascular injury (inflammation and small blood clots called microthrombi) to the brain, heart, liver and kidney … were not assessed in the safety trials.”


An essential stage in any vaccine licensing process should involve a careful analysis for potential of ADE/pathogenic priming, yet in the political and socioeconomic rush towards mass ‘vaccination’ this has been skipped as no longer-term safety testing has been conducted. At a minimum laboratory assessment of interleukin-5 should have been conducted in the human test trials to determine any evidence of eosinophilia autoimmune responses or pathogenic priming.


Current Adverse Reactions


Worldwide there have now been hundreds of deaths and thousands of serious adverse reactions reported after receiving the viral mRNA injection. The Vaccine Adverse Event Reporting System (VAERS), a co-managed program by the CDC and FDA, has accumulated an extensive list of these adverse reactions here in the U.S.


As of Feb. 12th, 929 deaths, 616 life-threatening adverse events, 316 cases of permanent disability, and more than 5,000 hospitalizations and emergency room visits after COVID vaccinations were reported to VAERS. 33 Fifty-three percent of those who died were male, forty-four percent were female, the remaining death reports did not include the gender of the deceased. The average age of those who died was 77, the youngest was a 23-year-old. The Pfizer shot was taken by 58% of those who died, while the Moderna shot was taken by 41%. As of February 4th, there had been 163 cases of Bell’s Palsy reported and 775 reports of anaphylaxis.34


According to the CDC VAERS website, “VAERS reports alone cannot be used to determine if a vaccine caused or contributed to an adverse event or illness.” Rather, it is considered to be a tool for detecting “signals” or patterns of significant problems with vaccines. While the VAERS database numbers are sobering, according to a U.S. Department of Health and Human Services study,35 the actual number of adverse events is likely significantly higher. VAERS is a passive surveillance system that relies on the willingness of individuals and professionals to submit reports voluntarily. Thus, we really do not know the full extent of adverse reactions to these products. Globally there are reports of hundreds of nursing home residents dying immediately of a day or two after the shot.


The medical establishment and its controlled media networks are downplaying the numerous severe adverse events caused by these mRNA products, either calling them coincidental, blaming them on a new viral variant, or claiming their “rare” occurrence is from the toxic additive known as polyethylene glycol (PEG). Though PEG reaction is real and widespread, the experimental mRNA synthetic pathogen technology will probably prove to be the real culprit.


Both the Moderna and Pfizer-BioNTech mRNA product contains polyethylene glycol. To be clear, we know that PEG is harmful and should not be injected into humans. It has never been used in other vaccines to date. Growing evidence suggests that a large percentage of people can generate allergic immune responses to PEG-modified therapeutics. The presence of anti-PEG antibodies has been associated with anaphylactic or hypersensitivity reactions after the administration of PEG- containing formulation.36, 37, 38.


A 2016 study reported an astonishing 72% of specimens possessed anti-PEG antibodies with 8% of those being extremely elevated more than 500 ng/mL. The authors concluded that the widespread prevalence of pre-existing anti-PEG antibodies underscores the importance of screening patients for anti-PEG Ab levels before the administration of PEG-containing products.39


In contrast to the popular assumption that PEG is biologically inert, PEG is both immunogenic and antigenic. While PEGylation of therapeutic agents have shown and will continue to show, a great value in medicine to address toxicity, immunogenicity, and rapid clearance of an unconjugated drug while maintaining efficacy in the treatment of many diseases, it is possible that a subset of patients with anti-PEG may not benefit from treatment with PEG-conjugated agents.


The PEG delivery system allows the mRNA spike protein to be expressed by any cell not just the cells with entry receptors like the wild-type viral sequence. Afterward the cell goes through programmed cell death. One question is what happens when cells like dopaminergic neurons go through this process and die? Instant Parkinson’s?




Currently, Pfizer/BioNTech and Moderna mRNA products have been approved by the FDA under an Emergency Use Authorization (EUA) but are still FDA unlicensed biologicals. This mRNA technology is being labeled as ‘vaccines’, when by legal definition they are viral mRNA synthetic-pathogen devices. These experimental products are presently being distributed to millions and eventually potentially billions of people worldwide. Both products were expedited or “fast-tracked” through human trials and have not had adequate evaluation or surveillance for any long-term side effects. The historic timeline for taking a vaccine from concept to licensed product is estimated at 10–15 years, though some licensed vaccines have taken up to 30 years.40


This extended timeline is due largely to the stringent pre-clinical and clinical testing that is required of human vaccine candidates. The extremely short duration human trials of these experimental products are unprecedented, and their performance and safety profiles are still largely unknown. The profit-motivated rush to deploy mRNA vaccines for treatment of the Wuhan coronavirus has caused regulators and researchers to skip (or accelerate) many critical steps in quality control and clinical trials.


Remembering that previous efforts to develop vaccines against human coronaviruses have faced challenges, with several preclinical studies demonstrating disease enhancement and death in vaccinated animals after viral challenge. This was characterized by eosinophilic infiltrates resulting in immunopathology, after the induction of a T helper cell type 2 (Th2)-biased response, or a weak neutralizing antibody response that might contribute to antibody-dependent enhancement of infection.41


Analyzing the induction of immune responses after vaccination is driven, in part, by concerns about enhanced disease from potentially immunopathologic Th2 responses, as seen in animal studies of vaccines against other coronaviruses.42, 43, 44, 45


Hence, one of the side effects of giving a mass vaccine could be an emergence of an epidemic of autoimmune diseases, especially in individuals who are genetically prone to autoimmunity. After many years, and considerable attention, the understanding of pathogenic priming or ADE of disease after vaccination is insufficient to confidently predict that a given immune intervention for a viral infection will not have certain negative and grave outcomes in humans.


The remaining elephant in the room is that of the greatest unknown, of tampering with the human genome. The possibility that synthetic viral mRNA fragments might, through some currently unknown process, permanently alter the genome of the host. mRNA ‘vaccine’ manufacturers currently claim this is impossible, but the history of medicine is full of examples of arrogant scientists making catastrophic assumptions about the human body that turned out to be overly optimistic. Using viral mRNA to create proteins has unknown long-term consequences. There is much we have yet to comprehend of the complexity of the human body and immune system. RNA expresses proteins but it has many other functions, specifically as an epigenetic modifier. RNA can modify genetics without being reverse transcribed into DNA.46 RNA has multiple mechanisms of modifying DNA expression including modifying DNA promoter regions.47 In short, the viral pathogen mRNA technology being used has many unknown long-term effects on the human genome.


If this human experiment does prove to cause adverse problems in time, it will already have been administered to millions worldwide and will be too late. This synthetic pathogenic genetic engineering cannot be removed, and it cannot be turned off. It will have been irretrievably unleashed into the cellular system of humankind.


There are many other potential adverse events that can be induced by the experimental mRNA based ‘vaccines’ against COVID-19 undisclosed here. These synthetic pathogen devices place a novel molecule to create a spike protein, in/on the surface of host cells. This spike protein can become a potential receptor for another possibly novel pathogenic infectious agent. Data is not publicly available to provide information on how long the mRNA is translated in the vaccine recipient and how long after translation the spike protein will be present in the recipient’s cells. Forever? What is done here genetically cannot be undone. Genetic diversity protects species from mass casualties caused by infectious agents. One individual may be killed by a virus while another may have no ill effects from the same virus. By placing the identical receptor, the spike protein, on cells of everyone in a population, the genetic diversity for at least one potential receptor disappears. Everyone in the population now becomes potentially susceptible to binding with the same infectious agent.


Research into mRNA vaccines is still in its infancy, even though various biotech pioneers have been working on ways to achieve mRNA vaccines for around two decades. Yet more decades of research will likely be required to achieve acceptable levels of safety and efficacy. Unfortunately, we have become the test animal.


For manufacturers mRNA “vaccines” offer economic advantages over traditional vaccines. They are cheaper and faster to manufacture. They typically require no adjuvants or other toxic additives to work as intended (aside from the potentially antigenic and toxic lipids that envelope the naked mRNA). Furthermore, they can direct the body to manufacture almost any protein imaginable. That is how it works in theory, of course.


But they also present enormous risks of which the results could be catastrophic and irreparable. mRNA “vaccines” could inadvertently trick the human body into attacking its critical functions such as fertility, neurological function, cell repair, and other indispensable processes. Additionally, mRNA “vaccines” could be maliciously exploited to weaponize vaccines to target essential physiological functions in humans. This is similar in effect to “RNA interference” technology which is a gene suppressing innovation that has been studied for use as an insect-killing pesticide technology in crops. Although the mechanisms of mRNA vaccines and RNA interference technology are vastly different, they can achieve many of the same outcomes such as induced infertility or death in targeted organisms, which could include humans. Technically, this could also be exploited to target specific genetic subgroups of humans – the elderly.


Any COVID ‘vaccine(s)’ approved for emergency use should be voluntary, since the ‘vaccine(s)’ are considered investigational and are held to a much lower standard for both efficacy and safety. For example, compared to the non-emergency approval process to get full licensure, an emergency approval allows for a vaccine that “may” be effective, compared to the non-emergency approval process where a vaccine must demonstrate “substantial” effectiveness. Emergency Use Authorization (EUA) law is clear: States are barred from mandating a vaccine approved for emergency usage. (See Section VI. Preemption.) It also should be illegal for private businesses, airlines, or your employer to mandate a vaccination while it is approved under a EUA.


Lastly, the manufacturers have been exempted from any liability that they may inflict on the public. In February, Health and Human Services Secretary Alex Azar invoked the Public Readiness and Emergency Preparedness Act. The 2005 law empowers the HHS secretary to provide legal protection to companies making or distributing critical medical supplies, such as vaccines and treatments unless there’s “willful misconduct” by the company. The protection lasts until 2024. That means that for the next four years, these companies “cannot be sued for money damages in court” over injuries related to the administration or use of products to treat or protect against SARS-CoV. Thus, there is not a manufacturer nor government in the world that will be held financially accountable when people succumb to grave harm.


1. Ehrenfeld M, Tincani A, Andreoli L, et al. Covid-19 and autoimmunity. Autoimmun Rev 2020;19:102597.

2. Caso F, Costa L, Ruscitti P. Could Sars-coronavirus-2 trigger autoimmune and / or autoinflammatory mechanisms in genetically predisposed subjects? Autoimmune Rev 2020;19:102524.

3. Shoenfeld, Yehuda, and David A. Isenberg. “The mosaic of autoimmunity.” Immunology today 10, no. 4 (1989): 123-126.

4. COHEN, ARNON DOV, and YEHUDA SHOENFELD. “The viral-autoimmunity relationship.” Viral immunology 8, no. 1 (1995): 1-9.

5. Gagiannis, Daniel, Julie Steinestel, Carsten Hackenbroch, Michael Hannemann, Vincent G. Umathum, Niklas Gebauer, Marcel Stahl, Hanno M. Witte, and Konrad Steinestel. “COVID-19-induced acute respiratory failure: an exacerbation of organ-specific autoimmunity?.” medRxiv (2020).

6. Zhou, Yaqing, Tao Han, Jiaxin Chen, Can Hou, Lei Hua, Shu He, Yi Guo et al. “Clinical and Autoimmune Characteristics of Severe and Critical Cases of COVID‐19.” Clinical and Translational Science (2020).

7. Grose, Charles, and Ilya Spigland. “Guillain-Barré syndrome following administration of live measles vaccine.” The American journal of medicine 60, no. 3 (1976): 441-443.

8. Schonberger, Lawrence B., Dennis J. Bregman, John Z. Sullivan-Bolyai, Richard A. Keenlyside, Donald W. Ziegler, Henry F. Retailliau, Donald L. Eddins, and John A. Bryan. “Guillain-Barré syndrome following vaccination in the national influenza immunization program, United States, 1976–1977.” American journal of epidemiology 110, no. 2 (1979): 105-123.

9. Haber, Penina, Frank DeStefano, Fredrick J. Angulo, John Iskander, Sean V. Shadomy, Eric Weintraub, and Robert T. Chen. “Guillain-Barré syndrome following influenza vaccination.” Jama 292, no. 20 (2004): 2478-2481.

10. Baxter, Roger, Ned Lewis, Nandini Bakshi, Claudia Vellozzi, Nicola P. Klein, and CISA Network. “Recurrent Guillain-Barre syndrome following vaccination.” Clinical infectious diseases 54, no. 6 (2012): 800-804.

11. Vellozzi, Claudia, Shahed Iqbal, and Karen Broder. “Guillain-Barre syndrome, influenza, and influenza vaccination: the epidemiologic evidence.” Clinical infectious diseases 58, no. 8 (2014): 1149-1155.

12. Haber, Penina, James Sejvar, Yann Mikaeloff, and Frank DeStefano. “Vaccines and guillain-barre syndrome.” Drug Safety 32, no. 4 (2009): 309-323.

13. Chen, Yong, Jinlin Zhang, Xuhua Chu, Yuanling Xu, and Fubao Ma. “Vaccines and the risk of Guillain-Barré syndrome.” European journal of epidemiology 35, no. 4 (2020): 363-370.

14. Evans, David, Simon Cauchemez, and Frederick G. Hayden. ““Prepandemic” immunization for novel influenza viruses,“swine flu” vaccine, Guillain-Barre syndrome, and the detection of rare severe adverse events.” Journal of Infectious Diseases 200, no. 3 (2009): 321-328.

15. Lehmann, Helmar C., Hans-Peter Hartung, Bernd C. Kieseier, and Richard AC Hughes. “Guillain-Barré syndrome after exposure to influenza virus.” The Lancet infectious diseases 10, no. 9 (2010): 643-651.

16. Schonberger, Lawrence B., Dennis J. Bregman, John Z. Sullivan-Bolyai, Richard A. Keenlyside, Donald W. Ziegler, Henry F. Retailliau, Donald L. Eddins, and John A. Bryan. “Guillain-Barré syndrome following vaccination in the national influenza immunization program, United States, 1976–1977.” American journal of epidemiology 110, no. 2 (1979): 105-123.

17. Vellozzi, Claudia, Karen R. Broder, Penina Haber, Alice Guh, Michael Nguyen, Maria Cano, Paige Lewis et al. “Adverse events following influenza A (H1N1) 2009 monovalent vaccines reported to the Vaccine Adverse Event Reporting System, United States, October 1, 2009–January 31, 2010.” Vaccine 28, no. 45 (2010): 7248-7255.

18. Greene, Sharon K., Melisa Rett, Eric S. Weintraub, Lingling Li, Ruihua Yin, Anthony A. Amato, Doreen T. Ho et al. “Risk of confirmed Guillain-Barré syndrome following receipt of monovalent inactivated influenza A (H1N1) and seasonal influenza vaccines in the Vaccine Safety Datalink Project, 2009–2010.” American journal of epidemiology 175, no. 11 (2012): 1100-1109.

19. Wang, Sheng-Fan, Sung-Pin Tseng, Chia-Hung Yen, Jyh-Yuan Yang, Ching-Han Tsao, Chun-Wei Shen, Kuan-Hsuan Chen et al. “Antibody-dependent SARS coronavirus infection is mediated by antibodies against spike proteins.” Biochemical and biophysical research communications 451, no. 2 (2014): 208-214.

20. Wang, Sheng-Fan, Sung-Pin Tseng, Chia-Hung Yen, Jyh-Yuan Yang, Ching-Han Tsao, Chun-Wei Shen, Kuan-Hsuan Chen et al. “Antibody-dependent SARS coronavirus infection is mediated by antibodies against spike proteins.” Biochemical and biophysical research communications 451, no. 2 (2014): 208-214.

21. Yasui, Fumihiko, Chieko Kai, Masahiro Kitabatake, Shingo Inoue, Misako Yoneda, Shoji Yokochi, Ryoichi Kase et al. “Prior immunization with severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) nucleocapsid protein causes severe pneumonia in mice infected with SARS-CoV.” The Journal of Immunology 181, no. 9 (2008): 6337-6348.

22. Liu, Li, Qiang Wei, Qingqing Lin, Jun Fang, Haibo Wang, Hauyee Kwok, Hangying Tang et al. “Anti–spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection.” JCI insight 4, no. 4 (2019).

23. Kim, Hyun Wha, JOSE G. CANCHOLA, CARL D. BRANDT, GLORIA PYLES, ROBERT M. CHANOCK, KEITH JENSEN, and ROBERT H. PARROTT. “Respiratory syncytial virus disease in infants despite prior administration of antigenic inactivated vaccine.” American journal of epidemiology 89, no. 4 (1969): 422-434.

24. Polack, Fernando P., Scott J. Hoffman, Gonzalo Crujeiras, and Diane E. Griffin. “A role for nonprotective complement-fixing antibodies with low avidity for measles virus in atypical measles.” Nature medicine 9, no. 9 (2003): 1209-1213.

25. Katzelnick, Leah C., Lionel Gresh, M. Elizabeth Halloran, Juan Carlos Mercado, Guillermina Kuan, Aubree Gordon, Angel Balmaseda, and Eva Harris. “Antibody-dependent enhancement of severe dengue disease in humans.” Science 358, no. 6365 (2017): 929-932.

26. Guzman, Maria G., Mayling Alvarez, and Scott B. Halstead. “Secondary infection as a risk factor for dengue hemorrhagic fever/dengue shock syndrome: an historical perspective and role of antibody-dependent enhancement of infection.” Archives of virology 158, no. 7 (2013): 1445-1459.

27. Iwasaki, Akiko, and Yexin Yang. “The potential danger of suboptimal antibody responses in COVID-19.” Nature Reviews Immunology 20, no. 6 (2020): 339-341.

28. Honda-Okubo, Yoshikazu, Dale Barnard, Chun Hao Ong, Bi-Hung Peng, Chien-Te Kent Tseng, and Nikolai Petrovsky. “Severe acute respiratory syndrome-associated coronavirus vaccines formulated with delta inulin adjuvants provide enhanced protection while ameliorating lung eosinophilic immunopathology.” Journal of virology 89, no. 6 (2015): 2995-3007.

29. Tseng, Chien-Te, Elena Sbrana, Naoko Iwata-Yoshikawa, Patrick C. Newman, Tania Garron, Robert L. Atmar, Clarence J. Peters, and Robert B. Couch. “Immunization with SARS coronavirus vaccines leads to pulmonary immunopathology on challenge with the SARS virus.” PloS one 7, no. 4 (2012): e35421.

30. Iwata-Yoshikawa, Naoko, Akihiko Uda, Tadaki Suzuki, Yasuko Tsunetsugu-Yokota, Yuko Sato, Shigeru Morikawa, Masato Tashiro, Tetsutaro Sata, Hideki Hasegawa, and Noriyo Nagata. “Effects of Toll-like receptor stimulation on eosinophilic infiltration in lungs of BALB/c mice immunized with UV-inactivated severe acute respiratory syndrome-related coronavirus vaccine.” Journal of virology 88, no. 15 (2014): 8597-8614

31. Bolles, Meagan, Damon Deming, Kristin Long, Sudhakar Agnihothram, Alan Whitmore, Martin Ferris, William Funkhouser et al. “A double-inactivated severe acute respiratory syndrome coronavirus vaccine provides incomplete protection in mice and induces increased eosinophilic proinflammatory pulmonary response upon challenge.” Journal of virology 85, no. 23 (2011): 12201-12215.

32. Arvin, Ann M., Katja Fink, Michael A. Schmid, Andrea Cathcart, Roberto Spreafico, Colin Havenar-Daughton, Antonio Lanzavecchia, Davide Corti, and Herbert W. Virgin. “A perspective on potential antibody-dependent enhancement of SARS-CoV-2.” Nature 584, no. 7821 (2020): 353-363.

33. Electronic Support for Public Health–Vaccine Adverse Event Reporting System (ESP:VAERS) (



36. Hershfield, Michael S., Nancy J. Ganson, Susan J. Kelly, Edna L. Scarlett, Denise A. Jaggers, and John S. Sundy. “Induced and pre-existing anti-polyethylene glycol antibody in a trial of every 3-week dosing of pegloticase for refractory gout, including in organ transplant recipients.” Arthritis research & therapy 16, no. 2 (2014): 1-11.

37. Armstrong, Jonathan K., Georg Hempel, Susanne Koling, Linda S. Chan, Timothy Fisher, Herbert J. Meiselman, and George Garratty. “Antibody against poly (ethylene glycol) adversely affects PEG‐asparaginase therapy in acute lymphoblastic leukemia patients.” Cancer 110, no. 1 (2007): 103-111.

38. Garay, Ricardo P., Raafat El-Gewely, Jonathan K. Armstrong, George Garratty, and Pascal Richette. “Antibodies against polyethylene glycol in healthy subjects and in patients treated with PEG-conjugated agents.” Expert opinion on drug delivery 9, no. 11 (2012): 1319-1323.

39. Yang, Qi, Timothy M. Jacobs, Justin D. McCallen, Dominic T. Moore, Justin T. Huckaby, Jasmine N. Edelstein, and Samuel K. Lai. “Analysis of pre-existing IgG and IgM antibodies against polyethylene glycol (PEG) in the general population.” Analytical chemistry 88, no. 23 (2016): 11804-11812.

40. Douglas, R. Gordon, and Vijay B. Samant. “The vaccine industry.” Plotkin’s Vaccines (2018): 41.

41. Lambert, Paul-Henri, Donna M. Ambrosino, Svein R. Andersen, Ralph S. Baric, Steven B. Black, Robert T. Chen, Cornelia L. Dekker et al. “Consensus summary report for CEPI/BC March 12–13, 2020 meeting: assessment of risk of disease enhancement with COVID-19 vaccines.” Vaccine 38, no. 31 (2020): 4783-4791.

42. Jackson, Lisa A., Evan J. Anderson, Nadine G. Rouphael, Paul C. Roberts, Mamodikoe Makhene, Rhea N. Coler, Michele P. McCullough et al. “An mRNA vaccine against SARS-CoV-2—preliminary report.” New England Journal of Medicine (2020).

43. Sahin, U. et al. Concurrent human antibody and TH1 type T-cell responses elicited by a COVID-19 RNA vaccine. Preprint at (2020).

44. Sadoff, J. et al. Safety and immunogenicity of the Ad26.COV2.S COVID-19 vaccine candidate: interim results of a phase 1/2a, double-blind, randomized, placebo-controlled trial. (2020)

45. Zhu, Feng-Cai, Yu-Hua Li, Xu-Hua Guan, Li-Hua Hou, Wen-Juan Wang, Jing-Xin Li, Shi-Po Wu et al. “Safety, tolerability, and immunogenicity of a recombinant adenovirus type-5 vectored COVID-19 vaccine: a dose-escalation, open-label, non-randomised, first-in-human trial.” The Lancet 395, no. 10240 (2020): 1845-1854.

46. Marnef, Aline, and Gaëlle Legube. “m 6 A RNA modification as a new player in R-loop regulation.” Nature genetics 52, no. 1 (2020): 27-28.

47. Wei, Jian-Wei, Kai Huang, Chao Yang, and Chun-Sheng Kang. “Non-coding RNAs as regulators in epigenetics.” Oncology reports 37, no. 1 (2017): 3-9.

Recent Posts

COVID-19 mRNA Vaccines

COVID-19 mRNA Vaccines

December 28, 2020

COVID-19 mRNA Vaccines

James Odell, OMD, ND, L.Ac.

Editorial – The material published in this editorial is intended to foster scholarly inquiry and a rich discussion of the controversial topic of bioethics and health policy. The views expressed in this article are solely the authors and do not represent the policy or position of the Bioregulatory Medicine Institute (BRMI), nor any of its Board Advisors or contributors. The views expressed are not intended to malign any religious or ethnic group, organization, company, individual, or any other. Every effort has been made to attribute the sources of this article to the rightful authors listed in references.

With the recent licensing and roll out of COVID-19 vaccines in the U.K., Canada, the U.S. (Pfizer/ BioNTech and Moderna), and Russia (Sputnik) there are several serious safety concerns that have not been addressed or even mentioned in the medical media. In short, it is beyond reckless and totally unnecessary to administer these experimental vaccines to millions of people when there is only limited short term safety data. Absolutely no long-term safety studies have been done to ensure that any of these vaccines do not cause cancer, seizures, heart disease, allergies, and autoimmune diseases, as seen with other vaccines and observed in earlier coronavirus vaccine animal studies. Because animal studies were bypassed for these vaccines due to ‘fast-tracking’, millions of humans are now the primary test animal. Additionally, these vaccines were developed using a completely new mRNA technology that has never been licensed for human use. In essence, we have absolutely no knowledge of what to expect from these new mRNA vaccines. Since viruses mutate frequently, the chance of any vaccine working for more than a year is unlikely. That is why the influenza (flu) vaccine changes every year. This editorial comprehensively discloses current COVID-19 vaccine development, administration, and safety concerns in detail.


Ribonucleic acid (RNA) is a nucleic acid present in all living cells. Its principal role is to act as a messenger carrying instructions from DNA for controlling the synthesis of proteins. Although in some viruses’ RNA rather than DNA carries the genetic information. In each cell of a living organism, DNA is the molecule that contains the genetic information of the organism. It is composed of a series of four building blocks, whose sequence gives the instructions to fabricate proteins. This process requires a transient intermediary called messenger RNA that carries the genetic information to the cell machinery responsible for protein synthesis. RNA is the only molecule known to recapitulate all biochemical functions of life: definition, control, and transmission of genetic information, creation of defined three-dimensional structures, enzymatic activities, and storage of energy.


RNA became the focus of intense research in molecular medicine at the beginning of the millennium. Messenger viral RNA (mRNA) is now developed as a vaccine and this technology poses many questions and serious health concerns that have been left unanswered by the vaccine manufacturers. Unlike previous vaccines an mRNA vaccine is a new type of vaccine that inserts fragments of viral mRNA into human cells, which are reprogrammed to produce pathogen antigens, which then if all goes well, stimulate an adaptive immune response against the targeted pathogen. That seems straightforward, but what else is in the vaccines, and is this new technology truly proven safe and effective?


History of Coronavirus Vaccine Animal Studies and

Antibody Dependent Enhancement (ADE)


Researchers have been trying to develop a coronavirus vaccine since the Severe Acute Respiratory Syndrome (SARS-1) outbreak in 2002. Thus, over a span of 18 years there have been numerous coronavirus vaccine animal studies conducted, which unfortunately demonstrated significant and serious side-effects. Either the animals were not completely protected, became severely ill with accelerated autoimmune conditions, or died.1, 2, 3, 4, 5, 6, 7


Animal side effects and deaths were primarily attributed to what is called Antibody-Dependent Enhancement (ADE). In the 1960s, immunologists discovered ADE and since then have extensively researched and identified its mechanism. Virus ADE is a biochemical mechanism in which virus-specific antibodies (usually from a vaccine) promote the entry and/or the replication of another virus into white cells such as monocytes/macrophages and granulocytic cells. This then modulates an overly strong immune response (abnormally enhances it) and induces chronic inflammation, lymphopenia, and/or a ‘cytokine storm’, one or more of which have been reported to cause severe illness and even death. Essentially, ADE is a disease dissemination cycle causing individuals with secondary infection to be more immunologically upregulated than during their first infection (or prior vaccination) by a different strain. ADE of disease is always a concern for the development of vaccines and antibody therapies because the mechanisms that underlie antibody protection against any virus has a theoretical potential to amplify the infection or trigger harmful immunopathology.8, 9, 10 ADE of the viral entry has been observed and its mechanism described for many viruses including coronaviruses.11, 12, 13 Basically, it was shown that antibodies target one serotype of viruses but only sub neutralize another, leading to ADE of the latter exposed viruses. Thus, ADA of viral entry has been a major concern and stumbling block for vaccine development and antibody-based drug therapy. For example, it has been shown that when patients are infected by one serotype of dengue virus (i.e., primary infection), they produce neutralizing antibodies targeting the same serotype of the virus. However, if they are later infected by another serotype of dengue virus (i.e., secondary infection), the preexisting antibodies cannot fully neutralize the virus. Instead, the antibodies first bind to the virus and then bind to the IgG Fc receptors on immune cells and mediate viral entry into these cells.14 A similar mechanism has been observed for HIV, Ebola, and influenza viruses. Thus, sub neutralizing antibodies (or non-neutralizing antibodies in some cases) are responsible for ADE of these viruses.15, 16, 17, 18, 19, 20


Generally, the conclusion of some of those studies was that great caution needs to be exercised when moving forward to human trials primarily because of the potential of accelerated autoimmunity reaction. Because ADE has been demonstrated in animals21, coronavirus vaccine research never progressed to human trials, at least not till the recent SARS coronavirus-2 fast-track campaign.


More technical Understanding of SARS-CoV-2 ADE Mechanisms


As a forementioned, a potential barrier to the development of safe and efficacious COVID-19 vaccines is the risk that insufficient titers of neutralizing antibodies might trigger ADE of disease. Previous research in SARS-CoV infection demonstrated ADE is mediated by the engagement of Fc receptors (FcRs) expressed on different immune cells, including monocytes, macrophages and B cells.22, 23, 24 A Fc receptor is a protein found on the surface of certain cells – including, among others, B lymphocytes, follicular dendritic cells, natural killer cells, macrophages, neutrophils, eosinophils, basophils, human platelets, and mast cells – that contribute to the protective functions of the immune system.


Akiko Iwasaki and colleagues describe this coronavirus ADE mechanism in more detail in their 2020 research published in Nature Reviews Immunology.25 They confirm that pre-existing SARS-CoV-specific antibodies may thus promote viral entry into FcR-expressing cells. This process is independent of ACE2 expression and endosomal pH and proteases, suggesting distinct cellular pathways of ACE2-mediated and FcR-mediated viral entry.

In short, previous experience with veterinary coronavirus vaccines and animal models of SARS-CoV and MERS-CoV infection has raised safety concerns about the potential for ADE and/or vaccine-associated enhanced respiratory disease. These events were associated either with macrophage-tropic coronaviruses susceptible to antibody-dependent enhancement of replication or with vaccine antigens that induced antibodies with poor neutralizing activity and Th2-biased responses.


After two decades of failed animal trials, the question is posed as to why fast-tracking coronavirus vaccine will now result in a different outcome? Given that many of these fast-track trials have bypassed animal studies, are only performed on healthy volunteers and children (not the elderly or those with pre-morbidities), and that trials are conducted without an inert double-blind placebo-controlled environment, and are not given sufficient time to observe effects on the human trials, there is a serious safety concern. Many, many virologists, and epidemiologists feel this fast-track policy is a recipe for mass disaster. Microbiologist Dr. Sucharit Bhakdi and Dr. Karina Reiss in their new book Corona, False Alarm? give clarity to many of the issues surrounding the pandemic, especially the current coronavirus vaccines.26


Traditional vs. mRNA Vaccines


Historically, the manufacturing process for creating vaccines involves many trade secrets and numerous other ingredients as adjuvants and preservatives.27, 28 ‘Traditional or classical vaccines’ may contain attenuated or inactivated viruses and bacteria or proteins, as well as adjuvants, such as aluminum, to stimulate an immune response that produces artificial immunity, as well as a host of other ingredients called “excipients”. For example, older viral vaccines for smallpox and measles vaccine contain live attenuated viruses; injectable influenza vaccines contain inactivated viruses; the recombinant hepatitis B virus vaccine is a protein subunit vaccine, while the newer human papillomavirus (HPV) virus vaccine contains virus-like particles.


To date, there are several different types of potential vaccines for COVID-19 in development, including:

  • Inactivated or weakened virus vaccines, which use a form of the virus that has been inactivated or weakened, but still generates an artificial immune response.

  • Protein-based vaccines, which use fragments of proteins or protein shells that mimic the COVID-19 virus to generate an artificial immune response.

  • Viral vector vaccines, which use a virus that has been genetically engineered to generate an artificial immune response.

  • RNA and DNA vaccines, that uses genetically engineered RNA or DNA to generate a protein that itself prompts an artificial immune response.

For the past two decades, researchers have been experimenting with new technology platforms, notably ones that introduce foreign DNA and RNA into cells of the body, to develop experimental vaccines for SARS, MERS, HIV, and other diseases but, historically none have been proven effective and safe for humans.


Thus, for a traditional vaccine, the antigen is introduced in the body to produce an immune response. However, in the case of DNA- or RNA-based vaccines, no antigen is introduced, only the RNA or DNA containing the genetic information to produce the antigen. That is, for this specific class of vaccines, the introduction of DNA and RNA provides the instructions to the body to produce the antigen itself.29


mRNA vaccines differ greatly in their design and biochemical mechanisms from traditional vaccines. Traditional vaccines stimulate an antibody response by injecting a human with antigens (proteins or peptides), or an attenuated virus, or a recombinant antigen-encoding viral vector. These ingredients are prepared and grown outside of the human body, which takes time, and even when they are injected into the bloodstream, they do not enter the human cell.30


In contrast, mRNA vaccines insert a synthetically created fragment or snip of the virus RNA sequence directly into the human cells (known as transfection). This snip of viral RNA material then activates an enzyme called reverse transcriptase which replicates that RNA snip repeatedly. This then reprograms the cells to produce their own viral antigens, which, if all goes as planned, stimulates an adaptive immune response, resulting in the production of new antibodies that bind to the antigen and activate T-cells.31, 32, 33


Simply speaking, the new mRNA vaccines inject (transfects) molecules of synthetic genetic material from non-human sources (viral sequences) into our cells. Once in the cells, the genetic material interacts with our transfer RNA (tRNA) to make a foreign protein that supposedly teaches the body to destroy the virus being coded for. These created proteins are not regulated by our own DNA and are thus completely foreign to our cells. What they are fully capable of doing is completely unknown.


Till now, messenger-RNA vaccines have never been licensed for public use. In the last two decades, there has been deep-pocket funding for the development of mRNA vaccines against infectious diseases, particularly with the currently declared pandemic and vaccine fast track campaign. Historically, their application has until recently been restricted by the instability and inefficient in vivo delivery of mRNA. New technological advancements in RNA biology, chemistry, stability, and delivery systems have now accelerated the development of fully synthetic mRNA vaccines. The consensus is that mRNA vaccines are faster and cheaper to produce than traditional vaccines and for vaccine manufacturers, more cost-effectiveness translates to greater profits. Certainly, there are unique and unknown risks to messenger RNA vaccines, including local and systemic (ADE) inflammatory responses that could lead to autoimmune conditions.


mRNA Vaccines Mechanisms


mRNA vaccines have strands of genetic material called mRNA inside a special coating. That coating protects the mRNA from enzymes in the body that would otherwise break it down. It also helps the mRNA enter the muscle cells near the vaccination site. mRNA vaccines use a different approach that takes advantage of the process that cells use to make proteins: cells use DNA as the template to make messenger RNA (mRNA) molecules, which are then translated to build proteins. An RNA vaccine consists of an mRNA strand that codes for a disease-specific antigen. Once the mRNA is in the cell, human biology takes over. Ribosomes read the code and build the protein, and the cells express the protein in the body. Thus, cells use the genetic information to produce the disease-specific antigen. This antigen is then displayed on the cell surface, where it is recognized by the immune system.34


mRNA vaccines have been studied before for influenza, Zika, rabies, and cytomegalovirus. The concept for the development of an mRNA vaccine is rather straightforward. Once the antigen of choice from the pathogen target is identified, the gene is sequenced, synthesized, and cloned into the DNA template plasmid. mRNA is then transcribed in vitro, and the vaccine is delivered to the subject. The mRNA vaccine utilizes the host cell machinery for in vivo translation of mRNA into the corresponding antigen, thereby mimicking a viral infection to elicit potent humoral and cellular immune responses. The final cellular location of the antigen is determined by the signal peptide and transmembrane domain. This can be intrinsic to the natural protein sequence or engineered to direct the protein to the desired cellular compartment.35, 36


Once the viral mRNA is injected into the body, it faces immune responses that are programmed to destroy it. Our cells have evolved elaborate defense mechanisms intended to destroy foreign, unprotected, or “naked” RNA. However, the susceptibility of mRNA to degradation can be reduced by modifying the RNA during synthesis. One modification is to add in ‘nucleoside analogs’ that resemble the normal nucleosides found within RNA (A, U, C and G,) but have minor structural changes that make the RNA more resistant to enzyme degradation by the body’s ribonucleases. (Nucleosides are the structural subunit of nucleic acids such as DNA and RNA.)


Additional structural modifications and the inclusion of regulatory sequences can also improve the stability of mRNA.37 For example,the vaccine viral mRNA is delivered in the form of a complex with lipid nanoparticles, to stabilize the mRNA, making it easier to penetrate the cell, and increases the amount of antigen produced per cell.38 Lipid nanoparticle formulations also elicit a stronger immune response compared to naked mRNA.39This is where it gets tricky and potentially dangerous because some of the lipid nanoparticles developed for these mRNA vaccines can be strongly immunologically reactive and elicit an unwanted autoimmune reaction.


PEGylated Lipid Nanoparticles


Thus, mRNA is threatened by rapid degradation by ubiquitous extracellular ribonucleases before being taken up by cells.40 The mRNA molecule is also vulnerable to destruction from temperature changes as well as our immune system. Thus, the efficacy of mRNA vaccines requires ‘complexing agents’ which protect RNA from degradation. Complexation may also enhance uptake by cells and/or improve delivery to the translation machinery in the cytoplasm. To this end, mRNA is often complexed with either lipids or polymers. These mRNA vaccines are coated with PEGylated lipid nanoparticles (polyethylene glycol). This coating hides the mRNA from our immune system which ordinarily would attack and destroy kill any foreign material injected into the body. PEGylated lipid nanoparticles have been used in several different drugs for years. Unfortunately, PEGylated lipid nanoparticles have been shown to imbalance certain immune responses and can induce allergies and even autoimmune diseases.41, 42, 43, 44, 45, 46


A 2016 study in Analytical Chemistry reported detectable and sometimes high levels of anti-PEG antibodies (including first line-of-defense IgM antibodies and later stage IgG antibodies) in approximately 72% of contemporary human samples and about 56% of historical specimens from the 1970s through the 1990s. Of the 72% with PEG IgG antibodies, 8% had anti-PEG IgG antibodies > 500ng/ml., which is considered extremely elevated.47 Extrapolated to the U.S. population of 330 million who may receive this vaccine, 16.6 million may have anti-PEG antibody levels associated with adverse effects.The researchers confessed that the results were entirely unexpected. The authors concluded that:


“…sensitive detection and precise quantitation of anti-PEG Ab levels in a clinical setting will be essential to ensuring the safe use of PEGylated drugs in all target patient populations going forward.”


Multiple previous studies regarding the prevalence of anti-PEG antibodies in the population have stated that pre-screening should be done prior to any administration of a PEG-containing medication. Screening is likely to be even more important in the case of a vaccine intended for parenteral administration to as many people as possible that contains a substance to which a majority of the population unknowingly has anti-PEG antibodies.


Production of mRNA vaccines


To further understand PEGylated lipid nanoparticles and their role in vaccine delivery, it is helpful to understand a little more about how an mRNA vaccine is manufactured. A major manufacturing advantage of mRNA vaccines is that RNA can be produced in the laboratory from a DNA template using readily available materials, again less expensively and faster than conventional vaccine production, which utilize a variety of cell types such as chicken eggs or other mammalian cells such a fetal material.48 This all comes down to economics. It is faster and cheaper to make.


Traditional vaccines normally contain a strong adjuvant (often aluminum) supplying an enhanced signal for the initiation of the adaptive immune response. However, it is thought that mRNA vaccines sort of have their own adjuvant effect by themselves, partly by virtue of being foreign nucleic acids. It has not been disclosed if any of these candidates (from any company) have an adjuvant added to them. (More information on adjuvants later in this article.)


Moreover, according to Arcturus, the company manufacturing the Pfizer/BioNTech lipid delivery system, this involves a multi-component delivery system called LUNAR® (Lipid-enabled and Unlocked Nucleomonomer Agent modified RNA). “This system has access to over 150 proprietary lipids that have been utilized for mRNA-based COVID-19 vaccines.”49 Basically, all we know is this involves proprietary PEGylated lipid nanoparticles.


Current mRNA Vaccines and Potential Side-Effects


According to the WHO and the Milken Institute, as of August 2020, there were 202 companies and universities worldwide working on a coronavirus vaccine. The vaccine types vary from traditionally established vaccines (e.g., inactivated, and live attenuated) to vaccines that have only recently gained clinical approval (e.g., subunit) to those that have never been licensed for human use, till now (e.g., mRNA, DNA, non replicating viral vector, replicating viral vector). A striking feature of the vaccine development landscape for SARS coronavirus-2 is the range of technology platforms being evaluated, including nucleic acid (DNA and RNA), virus-like particle, peptide, viral vector (replicating and non-replicating), recombinant protein, live attenuated virus and inactivated virus approaches. Since November 9th, Moderna, the pharma giant Pfizer and its German collaborator BioNTech, and a Russian Institute have all offered “preliminary evidence that their mRNA spike-based vaccines can achieve greater than 90% protective efficacy.”


The vaccine pharmaceutical industry contends that an mRNA-based vaccine is “safer for the patient” than classical vaccines. But is that verified true? The manufacturer’s rationale is that mRNA is a non-infectious, non-integrating platform, there is no potential risk of infection or insertional mutagenesis. Since mRNA vaccines have never been licensed and have not undergone long-term testing, we cannot know this for certain. Additionally, there is also concern that these vaccine mRNA may have long-standing dire consequences on the body’s immunity, fertility, and DNA integrity.


According to researchers at the University of Pennsylvania and Duke University50, mRNA vaccines have these potential safety issues:

  • Local and systemic inflammation.

  • The biodistribution and persistence of expressed immunogen.

  • Stimulation of auto-reactive antibodies.

  • Induction of a potent type 1 interferon response, which has been associated with inflammation and potential autoimmunity. Thus, identification of individuals at an increased risk of autoimmune reactions before mRNA vaccination should be undertaken.

  • Presence of extracellular RNA, which may contribute to edema and pathogenic thrombus formation (blood clots). Extracellular naked RNA has been shown to increase the permeability of tightly packed endothelial cells and may thus contribute to edema.51 Another study showed that extracellular RNA promoted blood coagulation and pathological thrombus formation.52

  • Potential toxic effects of any non-native nucleotides and delivery system components (particularly those that have not been disclosed by manufacturers).

There is also concern about potential mRNA modifications to the genetics of the body. Once injected into the body mRNA vaccines take the RNA from the virus into the cell where it may create unwanted detrimental genetic modifications. Over the last five years, there has been an enormous increase in the amount of research into RNA modifications; this field is called epitranscriptomics. The role of DNA modification in gene regulation is well established, but much less is known about how mRNA modification influences the way genes are expressed. In fact, numerous studies have shown viral mRNAs to be implicated as a driver in some forms of cancer and autoimmune diseases.53, 54, 55, 56


Thus, long-term safety evaluation is essential and should precede the licensing of different mRNA modalities and delivery systems. Normally, vaccine development is a lengthy and complicated process, often lasting 10-15 years and involving a combination of public and private involvement. Unfortunately, the rapid worldwide competition between pharmaceutical companies to develop a COVID-19 vaccine has bypassed multiple safety controls, rendering the result both dubious and potentially dangerous for the public. Financial interests have taken precedence over the health and safety of the public. Hasty development of vaccines is always risky, and only thorough research employing all the safety precautions will lead to a safe and effective vaccine.


The current licensed COVID-19 vaccine is not being offered to pregnant women. This is because researchers do not know enough about how COVID-19 vaccination can affect children, pregnant women, or their babies. There is also no data on the safety of COVID-19 vaccines for breastfeeding women. The Pfizer/BioNTech vaccine is not available to children under age 16.


Moderna and Pfizer Vaccine Ingredients and Dosage


As unbelievable as it sounds, neither Pfizer/BioNTech nor Moderna have ‘completely’ disclosed everything in their vaccines. Apparently, to be licensed by the FDA they do not have to disclose to the public the entire composition of their vaccine. This is what we do know. Both Moderna and Pfizer/ BioNTech vaccines are mRNA vaccines and they are different in composition, delivery, and storage. They have different nucleoside analogs, and each has unique ways to essentially attenuate the capacity of messenger RNA to induce innate immunity. They each have a different complex liquid delivery system, and this is one reason why one is much more amenable to shipping and storing at minus 20º whereas the other requires shipping and storing at minus 70º.


Moderna’s vaccine uses 100 micrograms of RNA per dose, while Pfizer-BioNTech’s uses only 30 micrograms. In both the Moderna and Pfizer-BioNTech vaccines the mRNA is encapsulated in lipid nanoparticles (LPN). These microscopic droplets of oily liquid — about 0.1 micron in diameter — enclose and protect the mRNA as they are manufactured, transported, and injected into people.As previously mentioned, the composition of the lipid nanoparticles is different in the two vaccines.


Pfizer/BioNTech obtains their nanoparticles from Acuitas, a specialist Canadian company, while Moderna has developed its own lipid technology.


Listed ingredients of the Pfizer/BioNTech COVID-19 vaccine include:

  • 30 mcg of a nucleoside-modified messenger RNA (modRNA) encoding the viral spike (S) glycoprotein of SARS-CoV-2

  • lipids (0.43 mg (4-hydroxybutyl)azanediyl)bis (hexane-6,1-diyl) bis (2-hexyldecanoic)

  • .05 mg 2[polyethylene glycol)-2000]-N,N-ditetradecylacetamide

  • .09 mg 1,2-distearoyl-sn-glycero-3-phosphocholine, and 0.2 mg cholesterol)

  • .01 potassium chloride

  • .01 mg monobasic potassium phosphate

  • .36 mg sodium chloride

  • .07 mg dibasic sodium phosphate dehydrate

  • 6 mg sucrose

  • the diluent (.09 percent Sodium Chloride Injection) contributes an additional 2.16 mg sodium chloride per dose

So far as revealed in the public domain Moderna’s vaccine (mRNA-1273) specifically contains lipid nanoparticle dispersion containing an mRNA that encodes for the prefusion stabilized spike protein 2019-nCoV. mRNA-1273 consists of an mRNA drug substance that is manufactured into LNPs composed of the proprietary ionizable lipid, SM-102, and 3 commercially available lipids, cholesterol, DSPC (1,2-distearoyl-sn-glycero-3-phosphocholine is a phosphatidylcholine with alkyl chain comprising 18 carbons), and PEG2000 DMG (1,2-dimyristoyl-rac-glycero-3-methoxypolyethylene glycol-2000). Adjuvants and other biotechnology if added have not been publicly disclosed. This vaccine requires two injections given 28 days apart.


For more information on clinical trials of all corona vaccines in development visit the Regulatory Affairs Professionals Society (RAPS).58


mRNA Vaccine Viral Shedding and Viral Vaccine Interference


Vaccine shedding is a term used for the release of virus following administration of a live-virus vaccine. This has been particularly observed in the administration of live polio vaccines. Neither of the vaccines in distribution or in development use the live virus that causes COVID-19. Thus, current consensus among vaccine developers is that vaccine viral shedding is not expected with mRNA vaccines. However, bear in mind mRNA viral vaccines is a new platform, and this issue is in unknown territory.

Viral interference describes the situation whereby infection or vaccine inoculation with one virus limits infection and replication of a second virus. For example, epidemiological studies show that following infection with influenza virus, there is a short period during which a host experiences a lower susceptibility to infection with other similar viruses. This viral interference appears to be independent of any antigenic similarities between the viruses. It certainly is possible that the mRNA vaccine may elicit vaccine viral interference and causes people to be more susceptible to other viruses, such as influenza.


SARS-CoV-2 Spike Protein Shares Sequence with a Human Protein Syncytin-1


Syncytin-1 is a protein that functions for placental development and therefore is essential for fertility. Fifteen years ago, it was proposed that a synthetic Syncytin-1 vaccine could be developed as a contraceptive that would work to produce antibodies against human Syncytin-1.59


It is proposed by some doctors that the Pfizer COVID vaccine may elicit an antibody response against Syncythin-1 and cause infertility because of a similar or shared amino acid sequence in the spike protein of SARS-CoV-2 and the Syncythin-1 placental protein. Pharmaceutically sponsored fact-checkers, and Pfizer employed virologists were quick to discount such an idea as “unlikely”. They claim that this amino acid sequence is too short for the immune system to meaningfully confuse it with this important placental protein. However unlikely, if this later proves true for some susceptible women, then that could cause infertility of an unspecified duration. Consider that scientific consensus is not 100 percent sure these similar amino acid sequences will cause Syncythin-1 antibodies to be produced. The role of retroviral proteins, especially syncytins, in the trophoblastic fusion process and placental morphogenesis were only identified and hypothesized about 20years ago.60 There is still much to learn, and much we still do not know about similar amino acid sequences and their effect on human physiology. Thus, this issue warrants further research, and until then we should proceed with caution and assume that it may possibly cause public harm.




Adjuvants are immunostimulatory molecules administered together with the vaccine to help boost immune responses mainly by activating additional molecular receptors that predominantly recognize pathogens or danger signals. These pathways function primarily within the innate immune system, and each adjuvant generally has a different range of stimulation of these pathogen or danger receptors. While the vaccine goal is to stimulate recognition and response by lymphocytes, not innate cells, the activation of the innate immune cells is required to activate the lymphocytes to obtain both B and T-cell responses. Many adjuvants have previously failed in the clinic due to toxicity issues. These chemicals can have a wide range of compositions, including lipids, proteins, nucleic acids, and even inorganic material, such as aluminum salts. What they all have in common is that they hyper-stimulate receptors in immune cells and most do this through their cellular toxicity.


Pfizer/BioNTech and Moderna do not explicitly state the use of an adjuvant within their vaccines, but RNA already contains immunostimulatory properties and signals through pathogen recognition receptors. It remains to be seen whether the immunostimulation from RNA is strong enough to confer full protection against SARS-CoV-2. There is also a possibility that the lipid nanoparticle carriers they utilize confer adjuvant properties themselves. Or for that matter, elicit an abnormal autoimmune reaction.


It is unknown if any future licensed COVID-19 mRNA vaccines will contain aluminum or something else as an adjuvant, as commonly used in other viral vaccines. Despite almost 90 years of widespread use of aluminum adjuvants, medical science’s understanding of their mechanisms of action is still remarkably poor. There is also a concerning scarcity of data on toxicology and pharmacokinetics of these compounds. Despite this, the false notion that aluminium in vaccines is safe appears to be widely accepted. Experimental research clearly shows that aluminum adjuvants have a potential to induce serious immunological disorders in humans. Aluminum in adjuvant form carries a risk for autoimmunity, long-term brain inflammation, and associated neurological complications and may thus have profound and widespread adverse health consequences.61


Stability and Storage


These mRNA vaccines require cold storage to maintain the nanoparticles and to stop the mRNA from degrading. The Pfizer/BioNTech vaccine (BNT162b2) is to be stored at a temperature of -94 degrees Fahrenheit (-70 Celsius) and will last for only 24 hours at refrigerated temps between 35.6° and 46.4° Fahrenheit. It will be shipped on dry-ice (–80°C). The Moderna vaccine (mRNA-1273), must be stored at -4° Fahrenheit (-20 C) and shipped at this –20°C temperature using gel packs.62

Thus, preserving this constant cold temperature is a major hurdle for the implementation of its vaccine marketing campaign, particularly the Pfizer/BioNTech vaccine. Given those constraints, analysts argued that Pfizer’s vaccine could only be used at certain hospitals and clinics with the proper equipment, and would require intensive one-day vaccination events at such sites that would cover a fraction of the healthy population. Not only do most vaccination sites lack the freezing requirements needed, but also shipping companies are currently unable to ship mass quantities of ultracold vaccines. Pfizer has partnered with UPS to develop ultracold shipping containers that can hold the vaccine at the required temperature. The packages utilize cold-resistant glass vials to hold the vaccine and dry ice to maintain cold temperatures. Although this may seem like a sustainable solution, the US presently has a shortage of both dry-ice (due to a shortage in CO2) and cold-resistant glass.63 Mass shipping using these containers would cause a huge strain on the supply chain and likely would require investments of billions of dollars.64




Pfizer-BioNTech has said that they will be able to supply 50 million doses by the end of this year and around 1.3 billion by the end of 2021. If licensed, Moderna has said it intends to provide the US government with 20 million doses by the end of this year, and manufacture between 500 million and one billion doses globally throughout 2021. There are currently more than 320 Covid-19 vaccine candidates in development. Several of them, including the Oxford/AstraZeneca vaccine, are emerging from phase III trials, so we can expect more announcements like this soon.


No Liability Due to the PREP Act

With the upcoming SARS coronavirus-2 vaccines the vaccine industry is completely liability-free (not legally liable). The governmental nonliability guarantee for vaccine the manufacturers of current mRNA vaccines being implemented, or any future vaccines chosen to fast-track, comes out of the Emergency Use Authorization Authority (EUA Authority) that originated out of Project Bioshield. The Project Bioshield Act was an act passed by the United States Congress in 2004 calling for $5 billion for purchasing vaccines that would be used in the event of a bioterrorist attack. This was further defined by the PREP Act of 2005, the Public Readiness and Emergency Preparedness Act, which further granted the non-liability of vaccine manufacturers previously outlined in the 1986 Injury Compensation Program for childhood vaccines. On March 10, 2020, the Secretary invoked the PREP Act and determined that COVID-19 constitutes a public health emergency. Therefore, the HHS declaration authorizes PREP Act immunity for the “manufacture, testing, development, distribution, administration, and use” of covered countermeasures. An amendment to the PREP Act, which was updated in April65, stipulates that companies “cannot be sued for money damages in court” over injuries caused by medical countermeasures for Covid-19. Such countermeasures include vaccines, therapeutics, and respiratory devices. The only exception to this immunity is if death or serious physical injury is caused by “willful misconduct.” And even then, the people who are harmed will have to meet heightened standards for “willful misconduct” that are favorable to defendants.66


While people harmed by vaccines for other diseases are able to file claims with the National Vaccine Injury Compensation Program, which was established in 1986, the PREP Act now bars anyone who feels they were harmed by a vaccine for the coronavirus from using that program.


The PREP Act has allowed vaccine manufacturers unlimited freedom to create, develop, and market vaccines without any liability whatsoever. Manufacturers have been allowed to bypass animal studies and go directly to human trials. They also can add anything they deem important to the vaccine formula they choose – whether it be a known toxin or carcinogen. All liability is protected by the PREP Act, which means if anyone has an adverse event, or death caused by this vaccine there really is no recourse. This was put into the Federal Register in March of 2020 and does not expire till the end of 2024. So, anything that is developed over the next four years that has to do with a biological agent, such as a vaccine or drug or biotechnology, no matter how nefarious, is protected from liability under the umbrella of COVID-19.




The world, pushed by the pharmaceutical owned media, is clamoring for a safe, effective COVID-19 vaccine. Many laboratories and companies have scrambled to rapidly develop these vaccines, resulting in more than 200 vaccine candidates. Without proceeding with animal studies, many of these companies have entered human phase I, II and III clinical trials within a short period of 6 months. Pfizer/BioNTech and Moderna ‘vaccines’ moved quickly through human testing, without giving time for proper evaluation of earlier phases. They have not been approved or licensed by the U.S. Food and Drug Administration (FDA) ,but instead have received authorization for emergency use by the FDA under an Emergency Use Authorization (EUA) for use in individuals 16 years of age and older and are being injected into millions of people. Dangers arise due to the fast-tracking process that limits the time available for large-scale studies. Owing to the accelerated development process, the interim data from ongoing clinical and preclinical vaccine studies are being published almost in real time. As a result, crucial information about the longevity and quality of vaccine-induced protective immunity is unavailable. Fast-tracking leads companies to push out the vaccine before the results of a large-scale study show the safety and efficacy of the vaccine. Scientists and epidemiologists emphatically confirm that the primary focus of vaccine research is to prove it safe for a large population or group before being unleashed. The trials should offer clear datasets before releasing the vaccine to the public (millions if not billions of people). Without clear time-tested datasets of a large population, it is not possible to ensure that the vaccine is safe for most people in the country.

Pfizer released a Peer Review study entitled Safety and Efficacy of the BNT162b2mRNA Covid-19 Vaccine, recently published in the New England Journal of Medicine.67 In the Pfizer/BioNTech COVID-19 vaccine trials conducted in the United States, there were more allergic reactions reported in the vaccine group than in the placebo control group.68 While allergic reactions occurred in less than one percent of those receiving the COVID vaccine, it is important to note that individuals with a “history of severe adverse reaction associated with a vaccine and/or severe allergic reaction (e.g., anaphylaxis) to any component of the study intervention(s)” were excluded from Pfizer’s clinical trials.69, 70


Further testing and adequate time-testing may also identify specific health conditions, allergies, or related concerns of individuals that may not be qualified to take the vaccine. By fast-tracking the vaccine, the possibility of harm due to allergic reactions, autoimmune reactions, complications with an existing health condition, interactions with certain medications or other related concerns may increase when compared to a longer time frame for trials. In short, tests must prove that the vaccine is safe, which in vaccine time usually requires years rather than months.


Numbers reveal the death rate from COVID resumed to the normal flu death rate in early September 2020. Many scientists now view that the coronavirus pandemic is over. Therefore, a vaccine is no longer needed; it is totally unnecessary and comes with a potential danger. Perhaps the saddest part of this worldwide rush to the vaccine is seeing how little faith people have in their own immune systems. Somehow the powers that should not be have managed to convince the majority of the people that the immune system is just a conspiracy theory, and rather than strengthening our own innate ability to heal and regenerate our bodies, we should give our faith into the hands of pharmaceutical corporations, who profit from sickness.


When we pause for just one moment to marvel the ability of your own skin to heal a wound or a bone to mend itself, we will realize that our bodies have their own bioregulatory intelligence. This organic living intelligence is far beyond the capacities of any nanotechnology or lab-created synthetic concoctions which merely try to mimic nature and its grand design. Our immune system and a healthy biological terrain are our best defense for pathogens and there are several proven ways to keep it active. The mineral zinc is important for numerous immunological enzymes and may be taken daily. Vitamin D3 has been shown to be low or deficient in individuals that develop a serious coronavirus infection. Thus, taking vitamin D3 is preventive and may be taken daily to keep body levels therapeutic. Also, vitamin C has been extensively proven effective for infection protection. Getting fresh air and sunlight, staying active and well hydrated, and enjoying joyous social activities are all helpful in staying well.


Lastly, mRNA vaccines have never been licensed before, and now they are being administered to millions of people with no manufacturer liability. The public has become the testing ground for this new technology. If these coronavirus mRNA vaccines later prove to be harmful to fragile genetic cellular structures, then that cannot be undone. Essentially, we need a much better understanding of their potential side effects, and more evidence of their long-term efficacy. Vaccine development takes time as the vaccines must not only be proven protective but also safe. Unlike other drugs that are delivered into sick patients, vaccines are administered into healthy patients and thus require very high safety margins. There is still a lot of research that should have been done around safety before mRNA vaccines become used on the public. Unfortunately, that is not what is happening now, and consequently this has a potential to turn into a disaster on a massive scale.



Vaccine providers are supposed to report adverse events that occur after vaccinations to VAERS but vaccinated persons who experienced the reaction or a family member also can file a report if a health care provider does not do it. According to one government funded study in 2011, fewer than one percent of all vaccine reactions are reported to VAERS. Report vaccine side effects to the FDA/CDC Vaccine Adverse Event Reporting System (VAERS). The VAERS toll-free number is 1-800-822-7967 or report online to and include ‘Pfizer/BioNTech COVID-19 Vaccine EUA’ in the first line of box #18 of the report form.



  1. Takano, Tomomi, Shinji Yamada, Tomoyoshi Doki, and Tsutomu Hohdatsu. “Pathogenesis of oral type I feline infectious peritonitis virus (FIPV) infection: Antibody-dependent enhancement infection of cats with type I FIPV via the oral route.” Journal of Veterinary Medical Science (2019): 18-0702.

  2. Czub, Markus, Hana Weingartl, Stefanie Czub, Runtao He, and Jingxin Cao. “Evaluation of modified vaccinia virus Ankara based recombinant SARS vaccine in ferrets.” Vaccine 23, no. 17-18 (2005): 2273-2279.

  3. Fett, Craig, Marta L. DeDiego, Jose A. Regla-Nava, Luis Enjuanes, and Stanley Perlman. “Complete protection against severe acute respiratory syndrome coronavirus-mediated lethal respiratory disease in aged mice by immunization with a mouse-adapted virus lacking E protein.” Journal of virology 87, no. 12 (2013): 6551-6559.

  4. Wang, Qidi, Lianfeng Zhang, Kazuhiko Kuwahara, Li Li, Zijie Liu, Taisheng Li, Hua Zhu et al. “Immunodominant SARS coronavirus epitopes in humans elicited both enhancing and neutralizing effects on infection in non-human primates.” ACS infectious diseases 2, no. 5 (2016): 361-376.

  5. Pedersen, Niels C. “An update on feline infectious peritonitis: virology and immunopathogenesis.” The Veterinary Journal 201, no. 2 (2014): 123-132.

  6. Kam, Yiu Wing, François Kien, Anjeanette Roberts, Yan Chung Cheung, Elaine W. Lamirande, Leatrice Vogel, Shui Ling Chu et al. “Antibodies against trimeric S glycoprotein protect hamsters against SARS-CoV challenge despite their capacity to mediate FcγRII-dependent entry into B cells in vitro.” Vaccine 25, no. 4 (2007): 729-740.

  7. Bolles, Meagan, Damon Deming, Kristin Long, Sudhakar Agnihothram, Alan Whitmore, Martin Ferris, William Funkhouser et al. “A double-inactivated severe acute respiratory syndrome coronavirus vaccine provides incomplete protection in mice and induces increased eosinophilic proinflammatory pulmonary response upon challenge.” Journal of virology 85, no. 23 (2011): 12201-12215.

  8. Tirado, S. M. C., & Yoon, K. J. (2003). Antibody-dependent enhancement of virus infection and disease. Viral immunology, 16(1), 69-86.

  9. Takada, Ayato, and Yoshihiro Kawaoka. “Antibody‐dependent enhancement of viral infection: molecular mechanisms and in vivo implications.” Reviews in medical virology 13, no. 6 (2003): 387-398.

  10. Wang, Sheng-Fan, Sung-Pin Tseng, Chia-Hung Yen, Jyh-Yuan Yang, Ching-Han Tsao, Chun-Wei Shen, Kuan-Hsuan Chen et al. “Antibody-dependent SARS coronavirus infection is mediated by antibodies against spike proteins.” Biochemical and biophysical research communications 451, no. 2 (2014): 208-214.

  11. Wan, Yushun, Jian Shang, Shihui Sun, Wanbo Tai, Jing Chen, Qibin Geng, Lei He et al. “Molecular mechanism for antibody-dependent enhancement of coronavirus entry.” Journal of virology 94, no. 5 (2020).

  12. Dutry, Isabelle, Hui-ling Yen, Horace Lee, Malik Peiris, and Martial Jaume. “Antibody-dependent enhancement (ADE) of infection and its possible role in the pathogenesis of influenza.” In BMC proceedings, vol. 5, no. 1, p. P62. BioMed Central, 2011.

  13. Ruckwardt, Tracy J., Kaitlyn M. Morabito, and Barney S. Graham. “Immunological lessons from respiratory syncytial virus vaccine development.” Immunity 51, no. 3 (2019): 429-442.+

  14. Dejnirattisai, Wanwisa, Amonrat Jumnainsong, Naruthai Onsirisakul, Patricia Fitton, Sirijitt Vasanawathana, Wannee Limpitikul, Chunya Puttikhunt et al. “Cross-reacting antibodies enhance dengue virus infection in humans.” Science 328, no. 5979 (2010): 745-748.

  15. Beck, Zoltán, Zoltán Prohászka, and George Füst. “Traitors of the immune system—enhancing antibodies in HIV infection: their possible implication in HIV vaccine development.” Vaccine 26, no. 24 (2008): 3078-3085.

  16. Burke, Donald S. “Human HIV vaccine trials: does antibody-dependent enhancement pose a genuine risk?.” Perspectives in Biology and Medicine 35, no. 4 (1992): 511-530.

  17. Takada, Ayato, Heinz Feldmann, Thomas G. Ksiazek, and Yoshihiro Kawaoka. “Antibody-dependent enhancement of Ebola virus infection.” Journal of virology 77, no. 13 (2003): 7539-7544.

  18. Takada, Ayato, Shinji Watanabe, Katsunori Okazaki, Hiroshi Kida, and Yoshihiro Kawaoka. “Infectivity-enhancing antibodies to Ebola virus glycoprotein.” Journal of virology 75, no. 5 (2001): 2324-2330.

  19. Gauger PC, Vincent AL, Loving CL, Lager KM, Janke BH, Kehrli ME Jr., and Roth JA: Enhanced pneumonia and disease in pigs vaccinated with an inactivated human-like (delta-cluster) H1N2 vaccine and challenged with pandemic 2009 H1N1 influenza virus. Vaccine 2011;29:2712–2719.

  20. Rajão, Daniela S., Hongjun Chen, Daniel R. Perez, Matthew R. Sandbulte, Phillip C. Gauger, Crystal L. Loving, G. Dennis Shanks, and Amy Vincent. “Vaccine-associated enhanced respiratory disease is influenced by haemagglutinin and neuraminidase in whole inactivated influenza virus vaccines.” Journal of General Virology 97, no. 7 (2016): 1489-1499.

  21. Olsen, CHRISTOPHER W., W. V. Corapi, C. K. Ngichabe, J. D. Baines, and F. W. Scott. “Monoclonal antibodies to the spike protein of feline infectious peritonitis virus mediate antibody-dependent enhancement of infection of feline macrophages.” Journal of virology 66, no. 2 (1992): 956-965.

  22. Wang, Sheng-Fan, Sung-Pin Tseng, Chia-Hung Yen, Jyh-Yuan Yang, Ching-Han Tsao, Chun-Wei Shen, Kuan-Hsuan Chen et al. “Antibody-dependent SARS coronavirus infection is mediated by antibodies against spike proteins.” Biochemical and biophysical research communications 451, no. 2 (2014): 208-214.

  23. Wan, Yushun, Jian Shang, Shihui Sun, Wanbo Tai, Jing Chen, Qibin Geng, Lei He et al. “Molecular mechanism for antibody-dependent enhancement of coronavirus entry.” Journal of virology 94, no. 5 (2020).

  24. Jaume, Martial, Ming S. Yip, Chung Y. Cheung, Hiu L. Leung, Ping H. Li, Francois Kien, Isabelle Dutry et al. “Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH-and cysteine protease-independent FcγR pathway.” Journal of virology 85, no. 20 (2011): 10582-10597.

  25. Iwasaki, Akiko, and Yexin Yang. “The potential danger of suboptimal antibody responses in COVID-19.” Nature Reviews Immunology (2020): 1-3.


  27. Pulendran, Bali, and Rafi Ahmed. “Translating innate immunity into immunological memory: implications for vaccine development.” Cell 124, no. 4 (2006): 849-863.

  28. Baxter, David. “Active and passive immunity, vaccine types, excipients and licensing.” Occupational Medicine 57, no. 8 (2007): 552-556.

  29. Sahin, Ugur, Katalin Karikó, and Özlem Türeci. “mRNA-based therapeutics—developing a new class of drugs.” Nature reviews Drug discovery 13, no. 10 (2014): 759-780.

  30. Minor, Philip D. “Live attenuated vaccines: Historical successes and current challenges.” Virology 479 (2015): 379-392.

  31. Lundstrom, Kenneth. “Latest development on RNA-based drugs and vaccines.” Future science OA 4, no. 5 (2018): FSO300.

  32. Sahin, Ugur, Katalin Karikó, and Özlem Türeci. “mRNA-based therapeutics—developing a new class of drugs.” Nature reviews Drug discovery 13, no. 10 (2014): 759-780.

  33. Scorza, Francesco Berlanda, and Norbert Pardi. “New kids on the block: RNA-based influenza virus vaccines.” Vaccines 6, no. 2 (2018): 20.

  34. Brito, Luis A., Sushma Kommareddy, Domenico Maione, Yasushi Uematsu, Cinzia Giovani, Francesco Berlanda Scorza, Gillis R. Otten et al. “Self-amplifying mRNA vaccines.” In Advances in genetics, vol. 89, pp. 179-233. Academic Press, 2015.

  35. Pardi, Norbert, Michael J. Hogan, Frederick W. Porter, and Drew Weissman. “mRNA vaccines—a new era in vaccinology.” Nature reviews Drug discovery 17, no. 4 (2018): 261.

  36. Pardi, Norbert, and Drew Weissman. “Measuring the Adjuvant Activity of RNA Vaccines.” In RNA Vaccines, pp. 143-153. Humana Press, New York, NY, 2017.

  37. Holtkamp, S. et al. (2006) Modification of antigen-encoding RNA increases stability, translational efficacy, and T-cell stimulatory capacity of dendritic cells. Blood 108, 4009–4017.

  38. Geall, A.J. et al. (2012) Nonviral delivery of self-amplifying RNA vaccines. Proc. Natl Acad. Sci. USA 109, 14604–14609.

  39. Lutz J. et al. (2017) Unmodified mRNA in LNPs constitutes a competitive technology for prophylactic vaccines. NPJ Vaccines (2017) 2, 29.

  40. Probst, Jochen, Sonja Brechtel, Birgit Scheel, Ingmar Hoerr, Günther Jung, Hans-Georg Rammensee, and Steve Pascolo. “Characterization of the ribonuclease activity on the skin surface.” Genetic vaccines and therapy 4, no. 1 (2006): 4.

  41. Yang, Qi, and Samuel K. Lai. “Anti‐PEG immunity: emergence, characteristics, and unaddressed questions.” Wiley Interdisciplinary Reviews: Nanomedicine and Nanobiotechnology 7, no. 5 (2015): 655-677.

  42. Garay, Ricardo P., Raafat El-Gewely, Jonathan K. Armstrong, George Garratty, and Pascal Richette. “Antibodies against polyethylene glycol in healthy subjects and in patients treated with PEG-conjugated agents.” (2012): 1319-1323.

  43. Zhang, Peng, Fang Sun, Sijun Liu, and Shaoyi Jiang. “Anti-PEG antibodies in the clinic: Current issues and beyond PEGylation.” Journal of Controlled Release 244 (2016): 184-193.

  44. Ganson, Nancy J., Thomas J. Povsic, Bruce A. Sullenger, John H. Alexander, Steven L. Zelenkofske, Jeffrey M. Sailstad, Christopher P. Rusconi, and Michael S. Hershfield. “Pre-existing anti–polyethylene glycol antibody linked to first-exposure allergic reactions to pegnivacogin, a PEGylated RNA aptamer.” Journal of Allergy and Clinical Immunology 137, no. 5 (2016): 1610-1613.

  45. Richter, Ary Wolfgang, and Eva Åkerblom. “Polyethylene glycol reactive antibodies in man: titer distribution in allergic patients treated with monomethoxy polyethylene glycol modified allergens or placebo, and in healthy blood donors.” International Archives of Allergy and Immunology 74, no. 1 (1984): 36-39.

  46. Ishida, Tatsuhiro, XinYu Wang, Taro Shimizu, Kosuke Nawata, and Hiroshi Kiwada. “PEGylated liposomes elicit an anti-PEG IgM response in a T cell-independent manner.” Journal of controlled release 122, no. 3 (2007): 349-355.

  47. Yang, Qi, Timothy M. Jacobs, Justin D. McCallen, Dominic T. Moore, Justin T. Huckaby, Jasmine N. Edelstein, and Samuel K. Lai. “Analysis of pre-existing IgG and IgM antibodies against polyethylene glycol (PEG) in the general population.” Analytical chemistry 88, no. 23 (2016): 11804-11812.

  48. Rauch, Susanne, Edith Jasny, Kim E. Schmidt, and Benjamin Petsch. “New vaccine technologies to combat outbreak situations.” Frontiers in immunology 9 (2018): 1963.


  50. Pardi, Norbert, Michael J. Hogan, Frederick W. Porter, and Drew Weissman. “mRNA vaccines—a new era in vaccinology.” Nature reviews Drug discovery 17, no. 4 (2018): 261.

  51. Fischer, Silvia, Tibo Gerriets, Carina Wessels, Maureen Walberer, Sawa Kostin, Erwin Stolz, Kirila Zheleva, Andreas Hocke, Stefan Hippenstiel, and Klaus T. Preissner. “Extracellular RNA mediates endothelial-cell permeability via vascular endothelial growth factor.” Blood 110, no. 7 (2007): 2457-2465.

  52. Kannemeier, Christian, Aya Shibamiya, Fumie Nakazawa, Heidi Trusheim, Clemens Ruppert, Philipp Markart, Yutong Song et al. “Extracellular RNA constitutes a natural procoagulant cofactor in blood coagulation.” Proceedings of the National Academy of Sciences 104, no. 15 (2007): 6388-6393.

  53. Tusup, Marina, Thomas Kundig, and Steve Pascolo. “Epitranscriptomics of cancer.” World Journal of Clinical Oncology 9, no. 3 (2018): 42.

  54. Hsu, Phillip J., Hailing Shi, and Chuan He. “Epitranscriptomic influences on development and disease.” Genome biology 18, no. 1 (2017): 197.

  55. Lian, Hao, Qin-Hua Wang, Chang-Bin Zhu, Jie Ma, and Wei-Lin Jin. “Deciphering the epitranscriptome in cancer.” Trends in cancer 4, no. 3 (2018): 207-221.

  56. Dinescu, Sorina, Simona Ignat, Andreea Daniela Lazar, Carolina Constantin, Monica Neagu, and Marieta Costache. “Epitranscriptomic signatures in lncRNAs and their possible roles in cancer.” Genes 10, no. 1 (2019): 52.



  59. Frank, Hans-George, Patrick Bose, Andrea Albieri-Borges, Marcus Borges, Alexandra Greindl, Josepf Neulen, Andy JG Pötgens, and Peter Kaufmann. “Evaluation of fusogenic trophoblast surface epitopes as targets for immune contraception.” Contraception 71, no. 4 (2005): 282-293.

  60. Mi, Sha, Xinhua Lee, Xiang-ping Li, Geertruida M. Veldman, Heather Finnerty, Lisa Racie, Edward LaVallie et al. “Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis.” Nature 403, no. 6771 (2000): 785-789.


  62. Jones, Kathryn L., Debbie Drane, and Eric J. Gowans. “Long-term storage of DNA-free RNA for use in vaccine studies.” Biotechniques 43, no. 5 (2007): 675-681.

  63. Gelles D. How to Ship a Vaccine at -80°C, and Other Obstacles in the Covid Fight. The New York Times [Internet] 2020 Sep 19 [Cited 2020 Oct 11]. Available from:

  64. Brown, T. T. H. “Pfizer’s Major Setback in the COVID-19 Vaccine Race.”

  65. Federal Register :: Amendment to Declaration Under the Public Readiness and Emergency Preparedness Act for Medical Countermeasures Against COVID-19


  67. Polack, Fernando P., Stephen J. Thomas, Nicholas Kitchin, Judith Absalon, Alejandra Gurtman, Stephen Lockhart, John L. Perez et al. “Safety and efficacy of the BNT162b2 mRNA covid-19 vaccine.” New England Journal of Medicine (2020).

  68. FDA. FDA Briefing Document: Pfizer-BioNTech COVID-19 Vaccine. VRBPAC Committee Meeting Dec. 10, 2020.

  69. Pfizer. Study to Describe the Safety, Tolerability, Immunogenicity, and Efficacy of RNA Vaccine Candidates Against COVID-19 in Healthy Adults. Exclusion Criteria. Sept. 28, 2020.

  70. Weintraub K. ‘Very inconsistent’: 2 allergic reactions in the UK to COVID-19 vaccine puzzle researchers.USA Today Dec. 9, 2020.

Recent Posts

Artemisia Annua: A Potent Antimicrobial

Artemisia Annua: A Potent Antimicrobial

August 31, 2020

Artemisia Annua: A Potent Antimicrobial

by James Odell, OMD, ND, L.Ac.

Artemisia annua has been used in China for more than 2000 years to treat fevers and more recently used in the treatment of the chloroquine-resistant and cerebral malaria (Plasmodium falciparum). Much focus has now been paid to its effectiveness in the treatment of SARS-CoV-2 (Covid-19). Its ancient Chinese name Qing Hao literally means “green herb.” Qing Hao was mentioned in the ancient text (168BC) Wu Shi Er Bing Fang or “Recipes for Fifty-Two Ailments”, as a remedy for fevers. The genus Artemisia consists of over 400 species, many of which have an aromatic, bitter taste. Herbal extracts of Artemisia annua have been used for thousands of years in other parts of the world, particularly Southeast Asia, Africa, India, and South America, to treat malaria and a variety of infectious diseases. Apart from its anti-malarial properties, Artemisia annua has been used in traditional Chinese medicine to stimulate hair growth, to promote longevity, as a food additive, as an anti-inflammatory, as well as a treatment for numerous external illnesses including hemorrhoids, lice and boils. 


Botanical Aspects


Artemisia is a large, diverse plant genus with between 200 and 400 species and consists of hardy herbs and shrubs belonging to the Magnoliopsida class of flowering plants. Artemisia annua is an annual shrub of 50–150 cm in height. The shrub grows in temperate climates and is most widespread in China and Vietnam, but is also cultivated in East Africa, the United States, Russia, India, Brazil, and several other countries.1, 2 The reproduction of the shrub occurs by insects, self-pollination, and wind distribution.3


Artemisia annua Chemical Properties


The essential oil of Artemisia annua is rich in mono- and sesquiterpenes with numerous medicinal properties. Significant variations in its percentage and composition have been identified (main constituents may be camphor (up to 48%), germacrene D (up to 18.9%), artemisia ketone (up to 68%), and 1,8 cineole (up to 51.5%)). The oil has been subjected to numerous studies supporting exciting antiparasitic, antibacterial, antiviral, and antifungal activities. One of the more medicinal components found in Artemisia annua is artemisinin, first isolated in China in 1971.4


Artemisinin is the constituent with the greatest antimalarial activity. Up to 42% of the total artemisinin content is found in the upper leaves, where it accumulates in the glandular trichomes of the leaves. Artemisinin has been found in only two other species, Artemisia apiacea and Artemisia lance 5, and since that time its efficacy against malaria has been amply demonstrated.6, 7, 8, 9, 10, 11


The total amount of artemisinin found in different varieties of Artemisia annua varies slightly depending on extraction methods, different collection periods, different sample preparation, and different environmental influences.12 The artemisinin content in the plant exhibits the highest quantities usually just before flowering. Except for Artemisia annua, artemisinin is also present in Artemisia apiacea and Artemisia lancea, but only in minor quantities.13


Nowadays, many researchers are still investigating the effect of artemisinin and its analogues on the malarial parasite (Plasmodium) by modifying the structure of peroxides, ethers and ozonides in artemisinin. This improves the killing rate of plasmodium parasites for both in vitro and in vivo models as well as a faster clinical response for humans.14


Antimalarial Mechanism of Action of Artemisia annua


Malaria is one of the most severe public health problems worldwide. It is a leading cause of death and disease in many developing countries, where young children and pregnant women are the groups most affected. Worldwide an estimated 450,000 deaths annually (around 1200 per day) are attributed to malaria. This infection is caused primarily by the Plasmodium falciparum parasite, which largely reside in red blood cells and contains iron-rich heme-groups (in the form of hemozoin). Such hematophagous organisms digest hemoglobin and release high quantities of free heme, which is the non-protein component of hemoglobin. As a result, hemozoin pigment and other toxic factors such as glycosylphosphatidylinositol (GPI) are also released into the blood. These products, particularly the GPI, activate macrophages and endothelial cells to secrete cytokines and inflammatory mediators such as tumor necrosis factor, interferon-γ, interleukin-1, IL-6, IL-8, macrophage colony-stimulating factor, and lymphotoxin, as well as superoxide and nitric oxide. These inflammatory cytokines and mediators can cause significant damage to organs and tissues.15, 16, 17


The parasite is fairly shielded from attack by the body’s immune system since it resides within the liver and blood cells for much of its human life cycle and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the Plasmodium falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thus sequestering the parasite from passage through the general circulation and the spleen. Sequestered red blood cells can breach the blood-brain barrier and cause cerebral malaria. Artemisinin is also active against other parasite species such as Toxoplasma and Babesia that do not contain hematin.


Chemically, artemisinin is a sesquiterpene lactone that contains an unusual peroxide bridge. This 1, 2, 4-trioxane ring of endoperoxide is responsible for the drug’s mechanism of action.  Thus, the proposed antimalarial mechanism of action of artemisinin involves cleavage of endoperoxide bridges by iron, producing free radicals (hypervalent iron-oxo species, epoxides, aldehydes, and dicarbonyl compounds) which damage biological macromolecules causing oxidative stress in the cells of the parasite.18, 19


Artemisinins have also been investigated for their anti-proliferative activity against a wide range of cancer cell lines. Artemisinin results in decreased proliferation, increased levels of oxidative stress, induction of apoptosis and inhibition of angiogenesis in cancer cells. Artemisinins have also been shown to inhibit the falcipains, a papain family cysteine protease that aids hemoglobin degradation.20




Over the last ten years as the worldwide demand for artemisinin has become evident, Chinese, Vietnamese, African, and Indian plant breeding institutes have developed high-yielding Artemisia hybrids. Factories were developed in all three countries to extract artemisinin and manufacture its anti-malarial compounds. East African factories are currently exporting artemisinin to pharmaceutical factories in India and Europe, where the final products are made.


Drug resistance is a growing issue for the treatment of malaria in the 21st-century. Resistance is now common against all classes of antimalarial drugs except for artemisinins. Artemisinin treatment of resistant drug strains has therefore become increasingly popular. Unfortunately, while the cost of cultivation and production of artemisia is lower than that of other competitive pharmaceuticals, politics involving the pharmaceutical industry have restricted their use in the developing world.

From Quinine to Chloroquine to Hydroxychloroquine to Artemisinin


In 1820, the first antimalarial drug quinine was extracted from cinchona bark by French pharmacists Pelletier and Caventou.21 In the 1940s, limited by the raw materials for quinine extraction, German scientists synthesized chloroquine, which is similar to natural quinine in chemical structure.

In 1950, chemists Alexander Surrey and Henry Hammer published the synthesis of hydroxychloroquine which was even more effective with less toxicity.

By the mid-20th century, malaria was gradually controlled in China. However, parts of Africa still suffer high epidemic proportions of malaria. In the 1960’s an epidemic broke out which spread rapidly in Southeast Asia and South America. In addition, the plasmodium falciparum parasite was developing a resistance to chloroquine and hydroxychloroquine. Inspired by ancient books of traditional Chinese medicine, Youyou Tu, a Chinese scientist, successfully extracted artemisinin from Artemisia annua. With a 100% inhibition rate against plasmodium, artemisinin is now used for chloroquine and hydroxychloroquine resistant malaria. For her work, Tu was awarded the 2011 Lasker Award in clinical medicine and the 2015 Nobel Prize in Physiology or Medicine jointly with William Campbell and Satoshi Ōmura. Tu is the first Chinese Nobel laureate in physiology or medicine and the first female citizen of the People’s Republic of China to receive a Nobel Prize in any category.22

Antiviral Effects of Chloroquine and Hydroxychloroquine


To better understand the therapeutic antiviral similarities of chloroquine derivatives and Artemisia annua extracts it is beneficial to review the antiviral background of chloroquine. Chloroquine has been confirmed to be effective during epidemics of various infectious diseases, especially Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome Coronavirus (MERS). In 2003, SARS broke out in China. According to the World Health Organization, a total of 8,098 people worldwide became sick with SARS during this outbreak, of whom 774 died. In 2004, MarcVan Ranst and colleagues found that chloroquine effectively inhibited SARS coronavirus replication in vitro.23


In 2005, Stuart Nichol and colleagues found that chloroquine suppressed SARS virus replication both before and after infection, suggesting a preventative and therapeutic role of chloroquine against SARS.24


In 2014 Eric Snijder and colleagues successfully inhibited MERS coronavirus replication by chloroquine in monkeys, with similar suppressive effect against SARS and human coronavirus.25 Additionally, chloroquine has also been reported to inhibit Human Immunodeficiency Virus (HIV), Zika virus (ZIKV), and dengue virus (DENV).26 Chloroquine phosphate was also reported to alleviate lung autophagy induced by avian influenza A (H5N1) and reduce alveolar injury in mice.27


February 2020, Wuhan Virus Research Institute of the Chinese Academy of Sciences and other units jointly published the results on cell research, which showed that chloroquine phosphate effectively inhibited SARS-Cov-2 and such inhibition was superior as compared to Remdesivir.28 Other recent studies have validated those findings.29, 30


The antiviral mechanisms of chloroquine and hydroxychloroquine on SARS-Cov-2 is proposed as follows:


1) To weaken the binding of the virus to the receptor by interfering with the terminal glycosylation of the receptor protein angiotensin 2 receptor invertase of coronavirus.

2) As an alkaline drug, chloroquine increases pH value inside endosomes which was not conducive for virus-cell fusion.

3) Inhibits cell autophagy and regulates host immune reaction to suppress viral infection and replication.

4) Suppresses transcription and translation of virus protein by binding to viral protease; and

5) Alleviates cytokine storm through inhibiting the production and release of TNF-α and IL-6.


In June 2020, the U.S. Food and Drug Administration revoked the emergency use authorization that allowed for chloroquine phosphate and hydroxychloroquine sulfate to be used to treat certain hospitalized patients with COVID-19 when a clinical trial was unavailable, or participation in a clinical trial was not feasible. More than 35 states have now restricted prescriptions for hydroxychloroquine, and at least five of those have rules specifically prohibiting prescribing the drug as a preventive measure. Fortunately, we still have artemisia extracts and other immunological nutrients (vitamin D3, zinc, vitamin C) available – for now.


Artemisia annua Extracts Effective Against Viruses


Due to its similar history to chloroquine in the treatment of malaria and viruses, scientists at several institutions have researched whether extracts of Artemisia annua – pure artemisinin and related derivatives – may be effective against the COVID-19 virus. These compounds would be attractive candidates for immediate use as they have an excellent safety profile, are readily available, and are relatively inexpensive.


Numerous in vitro studies have reported that artemisinins have antiviral properties. Artemisinins reduce replication rates of hepatitis B and C viruses 31, 32, a range of human herpes viruses 33, 34, 35, HIV-1 36, influenza virus A 37, 38, and a bovine viral diarrhea virus39, in the low micromolar range. 


Like chloroquine, Artemisia annua extracts have even shown significant activity against the SARS coronavirus. In 2003, Li and colleagues showed that artemisinin was effective in treating SARS-CoV in vitro.40 Since the beginning of the COVID-19 pandemic, formulations of Artemisia annua have been used in Africa, Madagascar, and China for both COVID-19 prevention and treatment.41


Last June 2020, chemists at the Max Planck Institute of Colloids and Interfaces (Potsdam, Germany) in close collaboration with virologists at Freie Universität Berlin demonstrated in laboratory studies that aqueous and ethanolic extracts Artemisia annua are active against the SARS-CoV-2 (COIVID-19) virus. Human clinical trials to test the efficacy of both teas and coffee containing Artemisia annua are about to begin at the University of Kentucky’s academic medical center.42 Artemisia annua leaves, from a cultivated seed line grown by ArtemiLife Kentucky, USA, when extracted with absolute ethanol or distilled water produces the strongest antiviral activity. The addition of either ethanolic or aqueous Artemisia annua extracts prior to the introduction of the virus resulted in significantly reduced plaque formation. The most active extract of both Artemisia annua and coffee was found to be ethanolic. However, artemisinin alone does not present much antiviral activity. “I was surprised to find that A. annua extracts worked significantly better than pure artemisinin derivatives and that the addition of coffee further enhanced the activity” says Klaus Osterrieder, Professor of Virology at Freie Universität Berlin who conducted all activity assays.


In SARS-CoV-2 (COVID-19), cellular adaptive immunity is primarily involved, in particular, CD8 and CD4 lymphocytes that stimulate the B lymphocytes responsible for the production of antibodies targeting the coronavirus. In addition, there is a cytokine storm in patients infected with SARS-CoV-2 which is responsible for a major inflammatory response and their very severe progressive clinical state. The increase in interleukin-10 and TNF alpha reduces CD4 counts, causes functional exhaustion of immune cells, and induces, at their site of action (liver, vascular endothelium), runaway production and action of inflammatory proteins, resulting in secondary aggravation of COVID-19 patients.


Artemisia annua has extensively recognized antiviral activity (anti HSV1, Poliovirus, RSV, hepatitis C anti-virus, type 2 dengue virus, hantavirus, human cytomegalovirus) and anti-HIV in vitro, due in partto the artemisinin, flavonoids, quercetin and dicaffeoylquinic acids it contains. These molecules have been shown to inhibit the enzymatic activity of CLPro (Chymotrypsin-like protease), an enzyme produced by SARS-CoV-2.


The antiviral action of Artemisia annua, which is achieved by stimulating adaptive immunity, regulating the production of the pro-inflammatory cytokines prostaglandin E2 (PGE2), IL-6, IL-10, TNF alpha, and increasing the genesis of CD4, CD8 and interferon gamma, involves many minerals and biomolecules: the properties of flavonoids, polyphenols, triterpenes, sterols, saponins, polysaccharides, artemisinin and its derivatives, the concentration of zinc, gallium and selenium in the plant play a role in the immune, antiviral, antioxidant and anti-inflammatory response.


The plant is rich in vitamins A and E, of which one, when supplemented, is known to reduce morbidity and mortality in viral infections, notably HIV among others, and the other is a powerful antioxidant. Therefore the combination of these biomolecules and the intake of Artemisia annua may strengthen the exhausted adaptive immunity and modulate the runaway inflammatory response during COVID-19 infection, as has already been demonstrated in other serious viral and parasitic infections.


As more research develops it is likely that Artemisia annua extracts will take their place as a first-line defense against coronaviruses. Given that this plant has been extensively used for more than 2000 years in traditional Chinese medicine for treatment of fever, viruses, and malaria, the evidence argues for the inclusion of inexpensive Artemisia annua dried leaf tablets, capsules, or teas into the arsenal of remedies to combat coronavirus.


Lastly, malaria treatment is more complicated for human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) patients. Malaria and HIV co-infection represents a major health burden in Africa, primarily because it is now well known that HIV infection results in a higher incidence and more severe manifestations of malaria. With a compromised immune system, AIDS patients are more susceptible to malaria and respond slower to malaria therapy. In several studies and in clinical observation, Artemisia annua has demonstrated anti-HIV activity.43, 44 Hence, the use of Artemisia annua not only treats malaria but should also enhance the well-being of HIV/AIDS patients.


Preparation and Dosage


Artemisia annua is typically prepared as a tea extracted with water according to the rules of traditional Chinese medicine. There have been few well-controlled studies investigating the extraction, recovery, and stabilization of artemisinin and other compounds in Artemisia annua tea infusions. A systematic study of preparations of Artemisia annua therapeutic tea infusion was performed by van der Kooy and colleagues.45 This study showed that nearly 93% of available artemisinin was extracted from dried Artemisia annua leaves, but only under certain conditions. The best preparation method was: 9 g dried leaves/L, for 5 min at 100 °C. Subsequent storage of the tea infusion at room temperature showed that the concentration of artemisinin was stable for more than 24 hours. This is important for malaria-endemic locations where there is no refrigeration. Other studies using the same extraction protocol also measured the extraction and stability of artemisinin and certain key flavonoids in the tea. Artemisinin was found to be stable at room temperature for up to 48 hours.46 However, some flavonoids were poorly extracted and not stable at room temperature, therefore it may be best to refrigerate after the infusion is complete.47


Clearly, if a tea infusion is to be a therapeutic option, it must be prepared and consumed consistently and reliably.  Artemisia annua is also available commercially in extracts such as capsules and tinctures. As with all herbal remedies, the correct dosage depends on a variety factors such as the illness treated, the age of the person, health status, and number of other conditions.


Herb-Drug Reactions


Artemisinin has no reported toxicity if taken in recommended doses for a limited period of time.51 In animal studies, artemisinin has been used in high oral doses in dogs and rabbits52 and at 200-300 mg/kg BW in mice53 without toxicity. Artemisinin has been effective against Plasmodium in humans at doses of approximately 30 mg/kg BW, but it has poor bioavailability and a short half-life that is quickly eliminated from the body.54, 55 Artemisinin derivatives (dihydroartemisinin, artesunate, artemether, arteether) present better bioavailability and antimalarial activity than artemisinin, but have different safety margins than artemisinin. The bioavailability and half-lives also vary with the delivery mechanism (intramuscular, intravenous, intraperitoneal, oral).




Evidence is mounting for the therapeutic effectiveness of the use of Artemisia annua not only in the treatment of malaria, but also for various viruses, including coronaviruses. The complex mixture of antiparasitic compounds in the plant appears to account for its therapeutic activity with the animal and human trials supporting this claim. It is also clear that the cost of using Artemisia annua is a fraction of that for any other existing or potential antimalarial or antiviral treatment. Considering that for more than 2000 years this plant was used in traditional Chinese medicine for the treatment of fever with little to no significant toxicity and no clear signs of artemisinin drug resistance. Thus, the cumulative evidence argues for the inclusion of Artemisia annua extracts,tinctures, and teas into the arsenal of remedies to not only combat malaria, but also numerous other diseases, particularly viruses.



1. Bhakuni, D.S., Goel, A.K., Jain, S., Mehrotra, B.N., Patnaik, G.K., Prakash, V., 1988. Screening of Indian plants for biological activity: part XIII. Indian Journal of Experimental Biology 26, 883–904.


2. Bhakuni, D.S., Goel, A.K., Jain, S., Mehrotra, B.N., Srimal, R.C., 1990. Screening of Indian plants for biological activity: part XIV. Indian Journal of Experimental Biology 28, 619–637.


3. Bown, Deni. The Royal Horticultural Society encyclopedia of herbs & their uses. Dorling Kindersley Limited, 1995.


4. Klayman, Daniel L. “Qinghaosu (artemisinin): an antimalarial drug from China.” Science 228, no. 4703 (1985): 1049-1055.


5. Tan, Ren Xhiang, W. F. Zheng, and H. Q. Tang. “Biologically active substances from the genus Artemisia.” Planta medica 64, no. 04 (1998): 295-302.


6. Hien, Tran Tinh, and Nicholas J. White. “Qinghaosu.” Lancet (British edition) 8845 (1993): 603-608.


7. Mueller, Markus S., I. B. Karhagomba, Hans Martin Hirt, and Emmanuel Wemakor. “The potential of Artemisia annua L. as a locally produced remedy for malaria in the tropics: agricultural, chemical and clinical aspects.” Journal of ethnopharmacology 73, no. 3 (2000): 487-493.


8. Mueller, Markus S., Nyabuhanga Runyambo, Irmela Wagner, Steffen Borrmann, Klaus Dietz, and Lutz Heide. “Randomized controlled trial of a traditional preparation of Artemisia annua L.(Annual Wormwood) in the treatment of malaria.” Transactions of the Royal Society of Tropical Medicine and Hygiene 98, no. 5 (2004): 318-321.


9. Balint, Gabor A. “Artemisinin and its derivatives: an important new class of antimalarial agents.” Pharmacology & therapeutics 90, no. 2-3 (2001): 261-265.


10. Van Agtmael, Michiel A., Teunis A. Eggelte, and Chris J. van Boxtel. “Artemisinin drugs in the treatment of malaria: from medicinal herb to registered medication.” Trends in Pharmacological Sciences 20, no. 5 (1999): 199-205.


11. De Ridder, Sanne, Frank Van der Kooy, and Robert Verpoorte. “Artemisia annua as a self-reliant treatment for malaria in developing countries.” Journal of ethnopharmacology 120, no. 3 (2008): 302-314.


12. Delabays, N., Simonnet, X., Gaudin, M., 2001. The genetics of artemisinin content in Artemisia annua L. and the breeding of high yielding cultivars. Current Medicinal Chemistry 8, 1795–1801.


13. Hsu, E., 2006. The history of Qing Hao in the Chinese Materia medica. Transactions of the Royal Society of Tropical Medicine and Hygiene 100, 505–508.


14. De Ridder, Sanne, Frank Van der Kooy, and Robert Verpoorte. “Artemisia annua as a self-reliant treatment for malaria in developing countries.” Journal of ethnopharmacology 120, no. 3 (2008): 302-314.


15. Fakhreldin M. Omer, J. Brian de Souza, Eleanor M. Riley. Differential Induction of TGF-{beta} Regulates Proinflammatory Cytokine Production and Determines the Outcome of Lethal and Nonlethal Plasmodium yoelii Infections. J. Immunol. 2003;171;5430-5436.


16. Claire L. Mackintosh, James G. Beeson, Kevin Marsh. Clinical features and pathogenesis of severe malaria. Trends in Parasitology December 2004;20(12):597-603.


17. Ian A Clark, Alison C Budd, Lisa M Alleva, William B Cowden. Human malarial disease: a consequence of inflammatory cytokine release. Malaria Journal. 2006;5:85.


18. Cumming, Jared N., Poonsakdi Ploypradith, and Gary H. Posner. “Antimalarial activity of artemisinin (qinghaosu) and related trioxanes: mechanism (s) of action.” In Advances in pharmacology, vol. 37, pp. 253-297. Academic Press, 1996.


19. Posner, Gary H., and Paul M. O’Neill. “Knowledge of the proposed chemical mechanism of action and cytochrome P450 metabolism of antimalarial trioxanes like artemisinin allows rational design of new antimalarial peroxides.” Accounts of chemical research 37, no. 6 (2004): 397-404.


20. O’neill, Paul M., Victoria E. Barton, and Stephen A. Ward. “The molecular mechanism of action of artemisinin—the debate continues.” Molecules 15, no. 3 (2010): 1705-1721.


21. Pai-Dhungat, J. V. “Caventou, Pelletier &-History Of Quinine.” Journal of the Association of Physicians of India 63 (2015).


22. Chang, Zengyi. “The discovery of Qinghaosu (artemisinin) as an effective anti-malaria drug: a unique China story.” Science China Life Sciences 59, no. 1 (2016): 81-88.


23. Keyaerts, Els, Leen Vijgen, Piet Maes, Johan Neyts, and Marc Van Ranst. “In vitro inhibition of severe acute respiratory syndrome coronavirus by chloroquine.” Biochemical and biophysical research communications 323, no. 1 (2004): 264-268.


24. Vincent, Martin J., Eric Bergeron, Suzanne Benjannet, Bobbie R. Erickson, Pierre E. Rollin, Thomas G. Ksiazek, Nabil G. Seidah, and Stuart T. Nichol. “Chloroquine is a potent inhibitor of SARS coronavirus infection and spread.” Virology journal 2, no. 1 (2005): 1-10.


25. De Wilde, Adriaan H., Dirk Jochmans, Clara C. Posthuma, Jessika C. Zevenhoven-Dobbe, Stefan Van Nieuwkoop, Theo M. Bestebroer, Bernadette G. Van Den Hoogen, Johan Neyts, and Eric J. Snijder. “Screening of an FDA-approved compound library identifies four small-molecule inhibitors of Middle East respiratory syndrome coronavirus replication in cell culture.” Antimicrobial agents and chemotherapy 58, no. 8 (2014): 4875-4884.


26. Al-Bari MAA. Targeting endosomal acidification by Chloroquine analogs as a promising strategy for the treatment of emerging viral diseases. Pharmacol Res Perspect 2017, 5: e00293


27. Yan Y, Zou Z, Sun Y, et al. Anti-malaria drug Chloroquine is highly effective in treating Avian Influenza A H5N1 virus infection in an animal model. Cell Res 2013, 23: 300-2.


28. Wang, Manli, Ruiyuan Cao, Leike Zhang, Xinglou Yang, Jia Liu, Mingyue Xu, Zhengli Shi, Zhihong Hu, Wu Zhong, and Gengfu Xiao. “Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro.” Cell research 30, no. 3 (2020): 269-271.


29. Gao, Jianjun, Zhenxue Tian, and Xu Yang. “Breakthrough: Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies.” Bioscience trends (2020).


30. Gautret, Philippe, Jean-Christophe Lagier, Philippe Parola, Line Meddeb, Morgane Mailhe, Barbara Doudier, Johan Courjon et al. “Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial.” International journal of antimicrobial agents (2020): 105949.


31. Paeshuyse, Jan, Lotte Coelmont, Inge Vliegen, Jan Vandenkerckhove, Eric Peys, Benedikt Sas, Erik De Clercq, and Johan Neyts. “Hemin potentiates the anti-hepatitis C virus activity of the antimalarial drug artemisinin.” Biochemical and biophysical research communications 348, no. 1 (2006): 139-144.


32. Romero, Marta R., Thomas Efferth, Maria A. Serrano, Beatriz Castaño, Rocio IR Macias, Oscar Briz, and Jose JG Marin. “Effect of artemisinin/artesunate as inhibitors of hepatitis B virus production in an “in vitro” replicative system.” Antiviral research 68, no. 2 (2005): 75-83.


33. Efferth, Thomas, Manfred Marschall, Xin Wang, Shu-Mei Huong, Ilona Hauber, Armin Olbrich, Martina Kronschnabl, Thomas Stamminger, and Eng-Shang Huang. “Antiviral activity of artesunate towards wild-type, recombinant, and ganciclovir-resistant human cytomegaloviruses.” Journal of molecular medicine 80, no. 4 (2002): 233-242.


34. Kaptein, Suzanne JF, Thomas Efferth, Martina Leis, Sabine Rechter, Sabrina Auerochs, Martina Kalmer, Cathrien A. Bruggeman, Cornelis Vink, Thomas Stamminger, and Manfred Marschall. “The anti-malaria drug artesunate inhibits replication of cytomegalovirus in vitro and in vivo.” Antiviral research 69, no. 2 (2006): 60-69.


35. Naesens, Lieve, Pascale Bonnafous, Henri Agut, and Erik De Clercq. “Antiviral activity of diverse classes of broad-acting agents and natural compounds in HHV-6-infected lymphoblasts.” Journal of clinical virology 37 (2006): S69-S75.


36. Naesens, Lieve, Pascale Bonnafous, Henri Agut, and Erik De Clercq. “Antiviral activity of diverse classes of broad-acting agents and natural compounds in HHV-6-infected lymphoblasts.” Journal of clinical virology 37 (2006): S69-S75.


37. Efferth, Thomas, Manfred Marschall, Xin Wang, Shu-Mei Huong, Ilona Hauber, Armin Olbrich, Martina Kronschnabl, Thomas Stamminger, and Eng-Shang Huang. “Antiviral activity of artesunate towards wild-type, recombinant, and ganciclovir-resistant human cytomegaloviruses.” Journal of molecular medicine 80, no. 4 (2002): 233-242.


38. Qian, R. S., Z. L. Li, J. L. Yu, and D. J. Ma. “The immunologic and antiviral effect of qinghaosu.” Journal of traditional Chinese medicine= Chung i tsa chih ying wen pan 2, no. 4 (1982): 271.


39. Romero, Marta R., Maria A. Serrano, Marta Vallejo, Thomas Efferth, Marcelino Alvarez, and Jose JG Marin. “Antiviral effect of artemisinin from Artemisia annua against a model member of the Flaviviridae family, the bovine viral diarrhoea virus (BVDV).” Planta medica 72, no. 13 (2006): 1169-1174.


40. Lin, L., Han, Y., & Yang, Z. M. (2003). Clinical observation on 103 patients of severe acute respiratory syndrome treated by integrative traditional Chinese and Western Medicine. Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi= Chinese journal of integrated traditional and Western medicine, 23(6), 409.


41. Suryanarayana, Lakavath, and Dhanalaxmi Banavath. “A Review On Identification of Antiviral Potential Medicinal Plant Compounds Against with COVID-19.” International Journal of Research in Engineering, Science and Management 3, no. 3 (2020): 675-679.


42. Gilmore, K.; Osterrieder, K.; Seeberger, P.H. (2020): “Artemisia annua Plant Extracts are Active Against SARS-CoV-2 In Vitro”, in: submitted for publication


43. Marchand, Els, Magnus A. Atemnkeng, Stijn Vanermen, and Jacqueline Plaizier‐Vercammen. “Development and validation of a simple thin layer chromatographic method for the analysis of artemisinin in Artemisia annua L. plant extracts.” Biomedical chromatography 22, no. 5 (2008): 454-459.


44. Lubbe, Andrea, Isabell Seibert, Thomas Klimkait, and Frank Van der Kooy. “Ethnopharmacology in overdrive: the remarkable anti-HIV activity of Artemisia annua.” Journal of ethnopharmacology 141, no. 3 (2012): 854-859.


45. van der Kooy, Frank, and Robert Verpoorte. “The content of artemisinin in the Artemisia annua tea infusion.” Planta Medica-Natural Products and MedicinalPlant Research 77, no. 15 (2011): 1754.


46. Carbonara, Teresa, Rossana Pascale, Maria Pia Argentieri, Paride Papadia, Francesco Paolo Fanizzi, Luciano Villanova, and Pinarosa Avato. “Phytochemical analysis of a herbal tea from Artemisia annua L.” Journal of Pharmaceutical and Biomedical Analysis 62 (2012): 79-86.


47. Weathers, Pamela J., and Melissa J. Towler. “The flavonoids casticin and artemetin are poorly extracted and are unstable in an Artemisia annua tea infusion.” Planta medica 78, no. 10 (2012): 1024.


48. Xing J, Kirby BJ, Whittington D, et al. Evaluation of P450 inhibition and induction by artemisinin antimalarials in human liver microsomes and primary human hepatocytes. Drug Metab Dispos. 2012 Sep;40(9):1757-64.


49. Burk, O., Arnold, K.A., Nussler, A.K., Schaeffeler, E., Efimova, E., Avery, B.A., Avery, M.A., Fromm, M.F., Eichelbaum, M., 2005. Antimalarial artemisinin drugs induce cytochrome P450 and MDR1 expression by activation of xenosensors pregnane X receptor and constitutive androstane receptor. Molecular Pharmacology 67, 1954–1965.


50. Svensson, Ulrika SH, and M. Ashton. “Identification of the human cytochrome P450 enzymes involved in the in vitro metabolism of artemisinin.” British journal of clinical pharmacology 48, no. 4 (1999): 528.


51. Meshnick, Steven R. “Artemisinin: mechanisms of action, resistance and toxicity.” International journal for parasitology 32, no. 13 (2002): 1655-1660.


52. Zhao, K., Song, Z., 1990. The pharmacokinetics of dihydroqinghaosu given orally to rabits and dogs (chinese). Acta Pharmaceutica Sinica 25:161–163.


53. Shuhua, X., Catto, B.A., 1989. In vitro and in vivo studies of the effect of artemether on Schistosoma mansoni. Antimicrobial Agents and Chemotherapy 33:1557–1562.


54. Titulaer, H.A.C., Zuidema, J., Kager, P.A., Wetsteyn, J.C.F.M., Lugt, C.B., Merkus, F.W.H.M., 1990. The pharmacokinetics of artemisinin after oral, intramuscular and rectal administration to volunteers. J. Pharm. Pharmacol. 42:810–813.


55. Navaratman, V., Mansor, S.M., Chin, L.K., Mordi, M.N., Asokan, M., Nair, N.K., 1995. Determination of artemether and dihydroartemisinin in blood plasma by highperformance liquid chromatography for application in clinical pharmacological studies. J.Chrom. 669:289–294.

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Before we have “Fact-Checkers” taking this down, we are simply posting this video as something that is though-provoking -an opinion piece.

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COVID 19 Vaccine Safety Concerns

COVID 19 Vaccine Safety Concerns

Jun 30

COVID 19 Vaccine Safety Concerns

James Odell, OMD, ND, L.Ac.

The development of antibodies has long been the basis or rationale for vaccine efficacy against a large range of infective agents such as viruses and bacteria. However, it is well known that antibodies, which the immune system develops from natural infections, differ from those that are created from vaccines. (Bear this important difference in mind when reading this article.) Additionally, when vaccines do elicit antibodies, most are only temporary and thus require boosters, unlike lifelong immunity gained from an infectious disease, such as childhood measles. Anthony Fauci and others developing or promoting COVID-19 vaccination are talking about the likelihood that the new coronavirus vaccine will have to be administered in multiple doses, perhaps even annually like the influenza vaccine. This article explores COVID-19 vaccine development and safety concerns around “fast tracking” the manufacturing and testing process.

Antibody-Dependent Enhancement (ADE)

In the 1960s, immunologists discovered the phenomenon of what is now commonly referred to as antibody-dependent enhancement (ADE). Virus ADE is a mechanism in which virus specific antibodies (from an infection or from a vaccine) promote the entry and/or the replication of another virus into white cells such as monocytes/macrophages and granulocytic cells. ADE modulates the immune response and may induce chronic inflammation, lymphopenia, and/or a ‘cytokine storm’, one or more of which have been reported to cause severe illness and even death. Essentially, ADE is a disease dissemination cycle causing individuals with secondary infection to be more immunologically upregulated than during their first infection (or prior vaccination) by a different strain.

A more technical explanation of ADE is that when patients are infected by one stereotype of a virus (whether due to a vaccine or by nature) they produce neutralizing antibodies targeting that particular viral serotype (or distinct variation within a virus species). However, if they are later infected with another viral serotype (i.e., from a secondary infection or vaccine), the preexisting antibodies cannot completely neutralize the virus. Instead, the antibodies first bind to the virus and then bind to the immune cell IgG Fc receptors and mediate viral entry into these cells. For certain cases, however, the ADE of these viruses is responsible for non-neutralizing or binding antibodies.

Early stages of the viral infection cycle requires attachment and entry of viruses into the host cell. Virus attachment is typically mediated by the specific binding of viral surface proteins to host cell receptor molecules, concentrating the virus at the cell plasma membrane. Viruses are often studded with one or more surface proteins, each potentially containing multiple subdomains, to facilitate interaction with cellular receptors and induce the entry of the virus into the cell. However, the surface of the virus is also a highly antigenic structure that can trigger cellular and humoral immune responses that eradicate or neutralize the virus in the host. Antibodies contribute to several levels of antiviral defense to efficiently neutralize the virus and reduce its infectivity. In simple terms, antibody neutralization is good, whereas antibody binding is bad.

After the 1960s, studies on vaccine candidates for diseases such as dengue, respiratory syncytial virus and severe acute respiratory syndrome (SARS) have demonstrated a paradoxical trend. Many animals and humans who received the vaccine and were subsequently exposed to the virus developed a more serious disease than those who had not been vaccinated.1, 2, 3 ADE’s have been observed for a variety of viruses, such as dengue virus, Ross River virus, other alpha and flaviviruses, HIV and influenza viruses.4, 5, 6, 7, 8, 9

Developing the COVID 19 Vaccine

Importantly, during the production of new vaccines for a variety of infectious agents, the ADE effects must be carefully examined to ensure that the vaccines do not harm the recipients. ADE is a clear concern about coronavirus vaccines that are soon to be tested on millions – if not billions – from the healthy to the ill and young to old. As a result of ‘fast-tracking,’dozens of coronavirus manufacturers have been given the green light by the FDA to bypass critical manufacturing safety rules, such as pre-human animal trials and the use of ‘inert’ placebo controls. Most significantly the concept of ‘fast track’ means that the length of the trials will be short; not more than 6 weeks. It can take two to three years to learn if there are negative health effects resulting from a vaccine. Many autoimmune and neurological side effects will not manifest within a few short weeks. Several companies are now cutting corners by conducting phase 1, 2 and 3 human trials simultaneously. Global pharmaceutical and biotech companies are now developing over 100 experimental COVID-19 vaccines, with a few leading the race after securing billions of dollars in funding from the U.S. government, the Gates Foundation, and other organizations.10, 11

At the time of this writing, at least 10 of these vaccine-development programs have reached the clinical stage of evaluation, either phase 1 or phase 2. These include programs led by Western pharmaceutical companies such as AstraZeneca plc (in partnership with the University of Oxford); BioNTech SE partnered with Pfizer, Inc.; Inovio Pharmaceuticals, Inc.; Moderna, Inc. (in partnership with NIAID) and Novavax, Inc. 123 other programs to develop a COVID-19 vaccine remain in preclinical evaluation.

Astonishingly, the University of Oxford’s Jenner Institute and Oxford Vaccine Group in the United Kingdom have announced that their researchers are beginning to recruit children aged 5 to 12 years for phase II and phase III clinical trials of the experimental COVID-19 vaccine developed by the university in collaboration with AstraZeneca plc. Researchers at The University of Oxford and AstraZeneca researchers are proceeding with testing the experimental ChAdOx1 nCov-19 vaccine in children, although a report published on May 13, 2020 indicated that small vaccine trials in mice and monkeys were not successful in proving effectiveness against infection. While the animal studies presented evidence that the experimental vaccine induced a “robust humoral and cell-mediated response” in mice and appeared to protect against development of viral pneumonia in monkeys, it did not prevent infection with COVID-19.12, 13 In other words, the animal studies failed, but the developers intend to continue with human trials.

Some of these coronavirus vaccines being developed will use unlicensed DNA, messenger RNA and nanoparticle technology, oil-based adjuvants and even electricity, to genetically manipulate and hyper-stimulate strong inflammatory immune responses in the body.14 Messenger RNA vaccines, which have never been licensed for use in humans, inject cells with mRNA, usually within lipid nanoparticles, to stimulate cells in the body to become manufacturers of viral proteins. mRNA vaccines like all vaccines stimulate cells in the body to become manufacturers of viral proteins. mRNA vaccines have potential safety issues, including local and systemic inflammation and stimulation of auto-reactive antibodies and autoimmunity, as well as the development of edema (swelling) and blood clots.

Conventional vaccines usually contain inactivated disease-causing organisms or proteins made by the pathogen (antigens) that mimic the infectious agent. These activate the body’s immune response, so it is primed to respond more quickly and efficiently if exposed to the infectious agent in the future. RNA vaccines use a different approach that takes advantage of the process that cells use to make proteins: cells use DNA as the template to make messenger RNA (mRNA) molecules, which are then translated to build proteins. An RNA vaccine consists of an mRNA strand that codes for a disease-specific antigen. Once the mRNA strand in the vaccine is inside the cells of the body, the cells use the genetic information to produce the antigen. This antigen is then displayed on the cell surface, where it is recognized by the immune system.

Safety Issues Bypassed

Vaccine safety experts generally agree that animal studies should always be conducted prior to any human clinical trial with any vaccine; COVID-19 (SARS-CoV-2) vaccines are no exception. Clinical trials should always be double-blind placebo-controlled (with an inert placebo and not with another vaccine or adjuvant as a placebo).Careful assessment of possible immune complications should then be made prior to release of the vaccine to the public. In the case of vaccines, this ‘careful assessment’ is a time of waiting and should be no less than two to three years. Importantly, over the last two decades vaccines manufactures have never been able to develop an effective and safe coronavirus vaccine. Previous coronavirus vaccine animal studies with ferrets and mice have demonstrated significant and serious side-effects. After two decades of failed trials, the question is posed as to why a fast-tracking coronavirus vaccine will now result in a different outcome? Given that many of these fast-track trials have bypassed animal studies, are only performed on healthy volunteers and children (not the elderly or those with pre-morbidities), and that trials are conducted without an inert double-blind placebo-controlled environment, and are not given sufficient time to observe effects on the human trials, there is serious safety concern. Many epidemiologists feel this fast track policy is a recipe for mass disaster. According to Marc Lipsitch, an epidemiologist at the Harvard Chan School of Public Health in Boston, MA, “You really have to test a vaccine carefully and not just roll it out because people are clamoring for it with an epidemic underway.”

National Childhood Vaccine Injury Act and Immunity from Liability for Vaccine Harms

By the early 1980s, pharmaceutical companies faced crippling liability for injuries to children caused by their vaccines. Instead of allowing such market forces to push them to develop safer vaccines, Congress passed the National Childhood Vaccine Injury Act (the 1986 Act) which eliminated the liability of pharmaceutical companies for injuries caused by their vaccine products. After eliminating liability for pharmaceutical companies, the 1986 Act established the Vaccine Injury Compensation Program (Vaccine Court), part of the U.S. Court of Federal Claims, to compensate people injured by vaccines. Under the 1986 Act, the U.S. Department of Health and Human Services (HHS) is the defendant in Vaccine Court and is legally obligated to defend against any claim that a vaccine causes injury. HHS is represented by the formidable resources of the U.S. Department of Justice (DOJ). In nearly every case the injured person must prove the vaccine caused the injury. Notwithstanding these hurdles, since 1986, HHS has paid over $4 billion for vaccine injuries with taxpayers’ money, not with pharmaceutical manufacturers’ dollars. Safety is regulated, not only by comprehensive and thorough manufacturing and testing procedures, but also with liability laws. Without any liability consequences, pharmaceutical vaccine manufacturers are less likely to pay due diligence regarding the safety of the vaccine.

Upon removing the market mechanisms that assured vaccine safety, Congress made HHS exclusively responsible for vaccine safety under the ‘Mandate for Safer Childhood Vaccine’ provision of the 1986 Act. HHS recently conceded in federal court, that it did not comply with the essential provisions of this act, such as submitting reports to Congress on how HHS has improved vaccine safety. Such government neglect of vaccine safety also casts a doubt on the future development of coronavirus vaccines.  

Vaccine-Associated Enhanced Respiratory Disease (VAERD)

Similar to ADE, another immune enhancement phenomena came to the foreground in the 1960s during clinical trials in which young children were immunized with whole-inactivated respiratory syncytial virus (RSV) vaccines.15 When the children contracted RSV naturally a few months after the vaccinations, those who were immunized became significantly sicker than those who had not been vaccinated. In fact, in one trial, 80 percent of children in the youngest cohort had to be hospitalized, and two died.16 The syndrome the hospitalized children developed is sometimes called vaccine-associated enhanced respiratory disease (VAERD). VAERD is like ADE in that a high concentration of binding antibodies do not fully neutralize the virus and results in the formation of binding antibody-virus complexes that elicit a cytokine storm. As a consequence, elevated pro-inflammatory cytokines associated with the innate immune system have been associated with the VAERD phenomenon.17 In these children, the binding-antibody complexes affected the small airways of the lungs, obstructing these spaces and increasing inflammation. 

In another noteworthy study, “Abstract: a formalin-inactivated monkey kidney culture propagated 100-fold concentrated respiratory syncytial (RS) virus vaccine was administered intramuscularly to residents of Harrison and Arthur Cottages in Junior Village, a District of Columbia Welfare Institution for homeless infants and children. No significant local or systemic vaccine reactions were (initially) observed. A sharp outbreak of RS virus infection occurred approximately 9 months after the vaccine study was initiated. Recovery of RS virus was found to be significantly associated not only with the onset of febrile illness but also with the onset of febrile pneumonia illness. The vaccine not only failed to offer protection, but also induced an exaggerated altered clinical response to naturally occurring RS virus infection in the younger vaccines as 9 (69%) of 13 vaccinated and only 4 (9%) of 47 nonvaccinated Harrison Cottage residents, 6–23 months of age developed pneumonia.” The authors concluded, “The paradoxical effect of vaccination suggests that serum antibody may play an active role in the pathogenesis of RS virus disease.”18

Institutions for the homeless and ‘wards of the state’, orphanages, prisons, and developing countries (Uganda, Kenya, Latin America, Caribbean, Thailand) have historically been targeted for experimental vaccine trials. Some larger trials (rarely reported by the media) in Africa have resulted in mass sterility and even death.

The ever-changing mutation terrain of viruses results in ‘vaccine mismatch’ due to the lack of relatedness between the vaccine and the numerous circulating strains. This can potentially create vaccine reactions such as VAERD. Influenza vaccines contain inactivated virus formulated with adjuvants (aluminum, squalene, and several immunological toxins), and this formulation could certainly contribute to the pathology observed in VAERD.19

Another example of VAERD occurred with “Abstract: Field evaluation of two formalin-inactivated respiratory virus vaccines in a selected pediatric population in California during the 1966—1967 respiratory disease season. A total of 441 children ranging in age from four months to nine years were vaccinated: 219 with a respiratory syncytial (RS) virus vaccine and 222 with a trivalent parainfluenza virus (types 1, 2, and 3) vaccine. Very high attack rates of parainfluenza virus types 1 and 3 and RS virus was observed during the study period in infants and children in both vaccine groups. A protective effect was not demonstrable for either vaccine. Infants who received the RS virus vaccine and who subsequently became infected with RS virus tended to have a more severe clinical illness than infants who did not receive this vaccine.”20

There have been numerous studies on VAERD, particularly in children. Unfortunately, mainstream media report little information on this important issue.

COVID-19 Occurrence and Prior Vaccination

One of the more perplexing concerns regarding the current COVID-19 epidemic is the discrepancy between the severity of cases observed in Wuhan, Northern Italy, New York, and those occurring elsewhere in the world. Among the several reasons, such as air pollution, age, and pre-morbidities, another plausible justification is the antibody-dependent enhancement of SARS-CoV-2 due to previous exposure to coronaviruses and widespread influenza vaccine campaigns. Prior to the COVID-19 outbreak, both China and Italy implemented mass influenza vaccination campaigns.21, 22, 23 In one study, ADE was suggested to account for the severity of COVID-19 cases initially observed in China (and elsewhere) relative to other regions of the world.24 The previous infection with other coronaviruses, and/or influenza vaccines may have primed COVID 19 patients, predisposing them to the development of severe disease once infected with SARS-CoV-2.  

ADE and VAERD require prior exposure to viral antigenic epitopes, such as those contained in flu and pneumonia vaccines, making it a possible explanation for the observed geographic limitation of severe cases and deaths, as well as the age discrepancy – affecting primarily the elderly people who have received mandated flu and pneumonia vaccines, particularly in nursing homes. 

Studies have shown that vaccines developed against another coronavirus, feline infectious peritonitis virus, increased the risk for cats to develop disease caused by the virus.25 Similar effects have been seen in animal studies for other viruses, including the coronavirus, which causes SARS.26, 27

Research suggests that prior infection with other coronaviruses, from the agents of the common cold, as well as certain vaccines may have ‘primed’ COVID-19 patients, predisposing them to the development of severe disease once they have been infected with SARS-CoV-2. While severe cases of COVID-19 were reported later from all over the world, this has occurred mainly in the elderly population with pre-morbidities. Thus, the above hypothesis cannot be completey dismissed. Cross-reactivity of antibodies against to SARS-CoV-2 and SARS-CoV spike proteins is common and some preliminary data claim that they seem to be rarely cross-neutralising.28.

Safety Conclusion

Normally, vaccine development is a lengthy and complicated process, often lasting 10-15 years and involving a combination of public and private involvement. Unfortunately, the rapid worldwide competition between pharmaceutical companies to develop a COVID-19 vaccine has bypassed multiple safety controls, rendering the result both dubious and potentially dangerous for the public. Financial interests have taken precedence over the health and safety of the public. Hasty development of vaccines is always risky, and only thorough research employing all the safety precautions will lead to a safe and effective vaccine.

There are other concerns related to the safety of vaccines not discussed here due to space limitations, in particular adjuvants. Adjuvants are used to induce a stronger immune response from vaccines. These chemicals can have a wide range of compositions, including lipids, proteins, nucleic acids, and even inorganic material, such as aluminum salts. What they all have in common is that they hyper stimulate receptors in immune cells and most do this through their cellular toxicity. Animal studies reveal that aluminum adjuvant particles in vaccines deposit in the brain and bones and are neurologically (brain) toxic. Aluminum ingested in the diet has low oral absorption (about 0.3%), is rapidly excreted by the kidneys, is (mostly) excluded from the brain by the blood-brain barrier, and is in a solubilized, ionic (not particulate)Al3+ form. These defenses are adequate for protecting the brain from natural levels of aluminum exposure. These protective mechanisms are unable to protect the brain from injected aluminum adjuvant particles. Aluminum adjuvant particles are too large to be removed by the kidneys and are transmitted across the blood-brain barrier by macrophages.

Regulators (the Center for Biologics Evaluation and Testing of the U.S. Food and Drug Administration are reckless and unethical not to require that vaccine developers check for potentially adverse reactions in animal studies first, and should insist on double-blind, inert placebo controls with human trials that extend at least two to three years, if not longer. The National Institute of Allergy and Infectious Diseases (NIAID), led by Anthony Fauci argue that the risk of delaying vaccine advancement is far greater than the risk of causing illness in healthy volunteers (children remember). Testing vaccines without proper safety precautions or taking the time required to thoroughly analyze the effects of research volunteers could bring untold disastrous consequences on millions of lives well into the future.


  1. Tirado, Sol M. Cancel, and Kyoung-Jin Yoon. “Antibody-dependent enhancement of virus infection and disease.” Viral immunology 16, no. 1 (2003): 69-86.
  2. Takada, Ayato, and Yoshihiro Kawaoka. “Antibody‐dependent enhancement of viral infection: molecular mechanisms and in vivo implications.” Reviews in medical virology 13, no. 6 (2003): 387-398.
  3. Wang, SZ-S., K. E. Rushlow, C. J. Issel, R. F. Cook, S. J. Cook, M. L. Raabe, Y-H. Chong, L. Costa, and R. C. Montelaro. “Enhancement of EIAV replication and disease by immunization with a baculovirus-expressed recombinant envelope surface glycoprotein.” Virology 199, no. 1 (1994): 247-251.
  4. Mascola, John R., Bonnie J. Mathieson, Philip M. Zack, MARY CLARE WALKER, Scott B. Halstead, and Donald S. Burke. “Summary report: workshop on the potential risks of antibody-dependent enhancement in human HIV vaccine trials.” AIDS research and human retroviruses 9, no. 12 (1993): 1175-1184.
  5. Burke, Donald S. “Human HIV vaccine trials: does antibody-dependent enhancement pose a genuine risk?.” Perspectives in Biology and Medicine 35, no. 4 (1992): 511-530.
  6. Guzman, Maria G., Mayling Alvarez, Rosmari Rodriguez-Roche, Lídice Bernardo, Tibaire Montes, Susana Vazquez, Luis Morier et al. “Neutralizing antibodies after infection with dengue 1 virus.” Emerging infectious diseases 13, no. 2 (2007): 282.
  7. Dejnirattisai, Wanwisa, Amonrat Jumnainsong, Naruthai Onsirisakul, Patricia Fitton, Sirijitt Vasanawathana, Wannee Limpitikul, Chunya Puttikhunt et al. “Cross-reacting antibodies enhance dengue virus infection in humans.” Science 328, no. 5979 (2010): 745-748.
  8. Dutry, Isabelle, Hui-ling Yen, Horace Lee, Malik Peiris, and Martial Jaume. “Antibody-dependent enhancement (ADE) of infection and its possible role in the pathogenesis of influenza.” In BMC proceedings, vol. 5, no. 1, p. P62. BioMed Central, 2011.
  9. Takada, Ayato, Heinz Feldmann, Thomas G. Ksiazek, and Yoshihiro Kawaoka. “Antibody-dependent enhancement of Ebola virus infection.” Journal of virology 77, no. 13 (2003): 7539-7544.
  10. Lurie N, Saville M et al. Developing Covid-19 Vaccines at Pandemic Speed. NEJM Mar. 31, 2020.
  11. Fisher BL. COVID-19 Meltdown & Big Pharma’s Big Money Win. The Vaccine Reaction Apr. 13, 2020.
  12. van Doremalen B, Lambe T et al. ChAdOx1 nCoV-19 vaccination prevents SARS-Cov-2 pneumonia in rhesus macaques. bioRxiv May 13, 2020.
  13. Times of India. Coronavirus vaccine current status: Oxford vaccine failed in animal trials; here is what happened. May 21, 2020.
  14. Fisher BL, Raines K Inovio COVID-19 Vaccine Uses Electricity to Drive DNA into Body Cells. The Vaccine Reaction Apr. 18, 2020.
  15. Zimmer, Kathrina. COVID-19 Vaccine Researchers Mindful of Immune Enhancement, The Scientist, 5-26-2020.
  16. KIM, HYUN WHA, JOSE G. CANCHOLA, CARL D. BRANDT, GLORIA PYLES, ROBERT M. CHANOCK, KEITH JENSEN, and ROBERT H. PARROTT. “Respiratory syncytial virus disease in infants despite prior administration of antigenic inactivated vaccine.” American journal of epidemiology 89, no. 4 (1969): 422-434.
  17. Gauger PC, Vincent AL, Loving CL, Lager KM, Janke BH, Kehrli ME Jr., and Roth JA: Enhanced pneumonia and disease in pigs vaccinated with an inactivated human-like (delta-cluster) H1N2 vaccine and challenged with pandemic 2009 H1N1 influenza virus. Vaccine 2011;29:2712–2719.
  18. KAPIKIAN, ALBERT Z., REGINALD H. MITCHELL, ROBERT M. CHANOCK, RUTH A. SHVEDOFF, and C. ELEANOR STEWART. “An epidemiologic study of altered clinical reactivity to respiratory syncytial (RS) virus infection in children previously vaccinated with an inactivated RS virus vaccine.” American journal of epidemiology 89, no. 4 (1969): 405-421.
  19. Rajão, Daniela S., Hongjun Chen, Daniel R. Perez, Matthew R. Sandbulte, Phillip C. Gauger, Crystal L. Loving, G. Dennis Shanks, and Amy Vincent. “Vaccine-associated enhanced respiratory disease is influenced by haemagglutinin and neuraminidase in whole inactivated influenza virus vaccines.” Journal of General Virology 97, no. 7 (2016): 1489-1499.
  20. CHIN, JAMES, ROBERT L. MAGOFFIN, LOIS ANN SHEARER, JACK H. SCHIEBLE, and EDWIN H. LENNETTE. “Field evaluation of a respiratory syncytial virus vaccine and a trivalent parainfluenza virus vaccine in a pediatric population.” American journal of epidemiology 89, no. 4 (1969): 449-463.
  21. Influenza, Vaccination TWG, National Immunization Advisory Committee, and Technical Working Group. “Technical guidelines for seasonal influenza vaccination in China, 2019-2020.” Zhonghua liu xing bing xue za zhi= Zhonghua liuxingbingxue zazhi 40, no. 11 (2019): 1333.
  22. de St. Maurice, Annabelle, and Natasha Halasa. “Preparing for the 2019‐2020 influenza season.” Pediatric Transplantation 24, no. 1 (2020): e13645.
  23. Costantino, Claudio, Vincenzo Restivo, Emanuele Amodio, Giuseppina Maria Elena Colomba, Francesco Vitale, and Fabio Tramuto. “A mid-term estimate of 2018/2019 vaccine effectiveness to prevent laboratory confirmed A (H1N1) pdm09 and A (H3N2) influenza cases in Sicily (Italy).” Vaccine 37, no. 39 (2019): 5812-5816.
  24. Liu, Li, Qiang Wei, Qingqing Lin, Jun Fang, Haibo Wang, Hauyee Kwok, Hangying Tang et al. “Anti–spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection.” JCI insight 4, no. 4 (2019).
  25. Takano, Tomomi, Shinji Yamada, Tomoyoshi Doki, and Tsutomu Hohdatsu. “Pathogenesis of oral type I feline infectious peritonitis virus (FIPV) infection: Antibody-dependent enhancement infection of cats with type I FIPV via the oral route.” Journal of Veterinary Medical Science (2019): 18-0702.
  26. Kam, Yiu Wing, François Kien, Anjeanette Roberts, Yan Chung Cheung, Elaine W. Lamirande, Leatrice Vogel, Shui Ling Chu et al. “Antibodies against trimeric S glycoprotein protect hamsters against SARS-CoV challenge despite their capacity to mediate FcγRII-dependent entry into B cells in vitro.” Vaccine 25, no. 4 (2007): 729-740.
  27. Jaume, Martial, Ming S. Yip, Chung Y. Cheung, Hiu L. Leung, Ping H. Li, Francois Kien, Isabelle Dutry et al. “Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH-and cysteine protease-independent FcγR pathway.” Journal of virology 85, no. 20 (2011): 10582-10597.
  28. Lv N, Wu NC, Tsang OTY, Yuan M, Perera RAPM, Leung WS, et al. Cross-reactive antibody response between SARS-CoV-2 and SARS-CoV infections. BioRxiv 2020.03.15.993097 [Preprint]. 2020 [posted 2020 March 17, cited 2020 April 9]. Available from:
Gain-of-Function Studies and SARS-CoV-2 Virus (COVID-19) Emergence

Gain-of-Function Studies and SARS-CoV-2 Virus (COVID-19) Emergence

Gain-of-Function Studies and SARS-CoV-2 Virus (COVID-19) Emergence

James Odell, OMD, ND, L.Ac.

Editorial – The material published in this editorial is intended to foster scholarly inquiry and rich discussion of the controversial topic of bioethics and health policy. The views expressed in this article are solely the authors and do not represent the policy or position of the Bioregulatory Medicine Institute (BRMI), nor any of its Board Advisors or contributors. The views expressed are not intended to malign any religious or ethnic group, organization, company, individual, or any other.Every effort has been made to attribute the sources of this article to the rightful authors

Gain-of-function (GOF) research involves experimentation that aims to (and actually does) increase the transmissibility and/or virulence of pathogenic viruses. GOF research typically involves mutations that confer altered functionality of a protein, molecule, or organism such as a virus. Such research (when safely conducted by responsible scientists) allegedly intends to improve the understanding of disease-causing agents, their interaction with human hosts, and/or even their potential to cause pandemics. But concerns about the safety of GOF studies have been voiced by numerous scientists from their very beginning. No matter how anyone justifies it or spins it, GOF studies manipulate pathogenic, deadly viruses to increase their transmissibility or virulence. Within the field of virology, these studies create ‘chimeric viruses’ defined as a new hybrid microorganism.  These are created by joining nucleic acid fragments, from two or more different microorganisms, in which each of at least two of the fragments contains essential genes necessary for replication.  This type of research has proven to be historically unsafe. Serious questions arise as to whether GOF research and the development of chimeric viruses are necessary for understanding viruses considering its potential for deadly contamination (pandemics) and bioterrorism. 

The term “potential pandemic pathogen (PPP)” was coined for such manufactured viruses. The first suspected experimental effort to create a PPP occurred in 2005 with a laboratory re-creation of a strain of influenza, H1N1 from 1918, by Tumpey and colleagues. This was based on synthesizing nucleic acid sequences obtained from partially preserved viral RNA in frozen corpses from 1918, and then creating infectious viruses by reverse genetics. The pandemic influenza virus of 1918–1919 killed an estimated 20 to 50 million people worldwide. The question was raised as to whether it was wise to construct a virus that was historically associated with the worst pandemic in modern history and somewhat different from any virus currently circulating. However, the debate seems to have been internal to the US Department of Health and Human Services (HHS), particularly the National Institutes of Health (NIH), and it was judged that the work should proceed.

In the United States, more GOF study controversy occurred in 2011 when two laboratories published reports of mutational screens of H5N1 avian influenza viruses, identifying variants which proved transmissible through the air between ferrets. The Dutch virologist Ron Fouchier, based at Erasmus Medical Center in Rotterdam, and Yoshihiro Kawaoka at the University of Wisconsin-Madison announced that they had successfully mutated H5N1, a strain of bird flu, to pass through the air between ferrets, in two separate experiments. Ferrets are considered one of the best flu models because their respiratory systems react to the flu much like humans. The mutations that gave the virus its ability to be airborne transmissible were gain-of-function mutations. Of course, the concern then became that if their mutated H5N1 ever left the lab it could cause a pandemic.

Around this time more scientists raised concerns about the potential of a laboratory accident that could lead to the release of a pathogen that, by design, combined high virulence and antigenic novelty with high human-to-human transmissibility. These early critiques also questioned whether the scientific and public health value of such research justified the risks involved. One of the first major discussion meetings on this topic, to my knowledge, was held at the Royal Society of London in 2012 (, with mainly UK and North American speakers.

In 2012 and 2013, contamination and safety concerns continued to be published throughout the media and voiced by the international scientists.1 Then in 2014, as many as 75 scientists at the Center of Disease Control and Prevention were exposed to anthrax. A few weeks later, FDA officials discovered 16 forgotten vials of smallpox in storage. Meanwhile, the largest, most severe, and most complex Ebola outbreak in history was raging across West Africa, and the first patient to be diagnosed in the US had just been announced. On October 16, 2014 following these biosafety mishaps involving anthrax, smallpox, and H5N1 in government laboratories, the White House Office of Science and Technology Policy announced the launch of the U.S. Government in implementing a deliberative process to re-evaluate the potential risks and benefits associated with certain GOF experiments. The then Obama administration paused the release of federal funding for GOF studies anticipated to enhance the pathogenicity or transmissibility of respiratory influenza droplets among mammals and, in particular the COVID viruses – SARS and MERS. Thus, there was a moratorium on GOF between 2014 and 2017on the grounds of safety concerns and views of many top scientists who considered this type of viral research ‘unnecessarily dangerous’ – with potential risks of accidental release of pandemic potential viruses.

Following the funding pause, two major discussion meetings were held by the US National Academy of Sciences, and multiple meetings were held by the NSABB. A few ethicists, and others, debated the scientific and public health rationale for GOF or PPP experiments, the risks they posed, and the ethics of performing research that poses potentially major risks to unaware persons not involved in the studies. This process raised awareness of many issues that had not been previously highlighted, notably the lack of a framework for assessing research risks to persons who are not research participants, the very poor availability of data on biosafety in biological laboratories in the US and elsewhere, and the consequent uncertainty in risk-benefit calculations.

GOF Research in Europe

The debate on the risks and merits of GOF research has not been limited to the United States, as the Dutch Court of Appeals recently handed down a verdict concerning Erasmus University Medical Centers (EMC) objection to export license rules regarding the publication of highly pathogenic avian influenza virus GOF research. Export licenses are in place in the European Union to prevent the proliferation of weapons of mass destruction and apply to specific biological agents, chemical agents, and technologies. In 2012, the Dutch government ruled that EMC had to apply for an export license to publish their GOF work, which they had done in order to expedite publication. However, EMC later filed an objection, maintaining that GOF research in this context was for “basic scientific research.” The Dutch Court of Appeals ruled that EMC had no legal standing to contest the export license regulations, but did not address the legality of the export license itself, leaving the issue open for further debate. Currently, all GOF research within the European Union requires an export license for publication.

Laboratory Mishaps

GOF laboratory contamination mishaps have historically occurred on more than one occasion. In 1975 smallpox, the deadly infectious disease that killed about 30 percent of those who contracted it, finally became eradicated from the world. Around 300 million-plus people died of smallpox in the century before it was annihilated. In 1978, smallpox suddenly appeared again in Birmingham, England when Janet Parker, a photographer at Birmingham Medical School developed a horrifying rash. 2 The doctors initially mistakenly diagnosed it as chickenpox. Parker’s condition worsened and she was admitted to the hospital, where testing determined she had smallpox. Unfortunately, she died of the disease a few weeks later. People then questioned how she acquired smallpox that was supposed to have been eradicated. It turned out that the building Parker worked in also contained a research laboratory, one of a handful in the world where smallpox was still studied. Some papers reported the lab was badly mismanaged 3, with important safety precautions being ignored. Interestingly, the doctor who ran the lab died by alleged suicide shortly after Parker was diagnosed. So somehow, smallpox escaped the lab to infect this individual elsewhere in the building. Through sheer luck and a rapid response from health authorities, including quarantine of more than 300 people, the deadly error did not turn into an outright pandemic.

As previously mentioned, in 2014 the FDA did a cleanup for a planned move to a new office. They found hundreds of unclaimed vials of virus samples in a cardboard box in the corner of a cold storage room.4 Six of them, it turned out, were vials of smallpox. No one had been keeping track of them and no one apparently even knew they were there. They may have been there since the 1960s. The surprised and panicked scientists put the materials in a box, sealed it with clear packaging tape, and carried it to a supervisor’s office. This of course is not approved handling of dangerous biological materials. It was later found that the integrity of one vial was compromised, luckily, not one containing a ‘deadly’ virus. Additionally, there is also strong circumstantial evidence that the reintroduction of H1N1 into human circulation in 1977 after its disappearance in 1950 began with the accidental release of a laboratory strain.5, 6

Lab mishaps continue to occur and with GOF studies creating more virulent and pathogenic organisms, it becomes only a matter of time before dangerous organisms escape into the world or are used in bioterrorism. Highly transmissible, highly virulent GOF viruses like the modified H5N1 strains that have been created have the ability to infect millions and potentially kill a large fraction of those afflicted.

Current GOF Risks and Policy

GOF risks fall into two general categories which are separate but related: namely, biosecurity and biosafety. Biosecurity risk is the likelihood that someone would use the products or information obtained regarding a more pathogenic virus from GOF experiments that led to a more pathogenic virus that caused intentional damage in the form of bioterrorism. Biosafety risk is the likelihood of accidental escape that could trigger an outbreak and epidemic.

Here is a more in-depth review of the risk of GOF studies:

• Biosafety—i.e. health dangers associated with laboratory accidents

• Biosecurity—i.e., health dangers associated with crime and terrorism if pathogens are not physically secure and/or if malevolent actors gain access to them.

• Proliferation—i.e., dangers that might grow proportionally with an increased rate of GOF, potentially in different settings with varying biosafety standards.

• Information risk—i.e., if published studies facilitate malevolent action (e.g., by terrorists) or, possibly, breach of intellectual property.

• Agricultural—i.e., risks to agriculturally-relevant animals if enhanced pathogens arising from GOF are accidentally or intentionally released into animal populations, and possible implications for human health.

• Economic risks—i.e., financial implications of (accidental or intentional) pathogen release with resulting stock market collapse, business bankruptcies, job losses with increasing unemployment, starvation increases, suicides, and overall health-care downfall.

• Loss of public confidence—i.e., compromise of trust (in the scientific enterprise) that could result from (accidental or intentional) pathogen release.

Resuming Gain-of Function Studies

On Dec 19, 2017, the US National Institutes of Health (NIH) announced that they would resume funding GOF experiments involving influenza, Middle East respiratory syndrome coronavirus, and severe acute respiratory syndrome coronavirus. This ended the safety moratorium.

In review, during the GOF moratorium, a panel called the National Science Advisory Board for Biosecurity spent months designing a new process for determining the risks and benefits of GOF studies that could make pathogens more likely to spread and cause serious disease in humans. That led to a December 2017 HHS review framework for research on what the government now calls enhanced potential pandemic pathogens (enhanced PPPs). The policy stipulates that after a proposed enhanced PPP experiment passes NIH scientific peer review, an HHS panel of federal officials with wide-ranging expertise weighs the risks and benefits. If the committee approves, it can then receive NIH funding.

Then in February 2019, the magazine Science reported that the HHS review panel had approved two H5N1 projects in labs in Wisconsin and the Netherlands.7 These approvals and funding were for the same labs (Kawaoka and Fouchier labs) that created the controversy in 2011. Remembering that in 2011, Fouchier and Kawaoka alarmed the world by revealing they had separately modified the deadly avian H5N1 influenza virus so that it spread between ferrets.8 The news greatly disturbed opponents of such research, and they criticized federal officials for not disclosing the approvals in an op-ed in The Washington Post.9 HHS and NIH soon publicized the two approved projects, but did not release the risk reviews.

Today, much of this GOF research has little to zero transparency, particularly what is funded by the NIH and conducted in China at the Wuhan Institute of Virology. This P4 lab in Wuhan (P4 is an exceedingly high biosafety level designation) is not only the first of its kind in China, but also the first in Asia. When it opened in 2017, U.S. scientists expressed concerns that, considering China’s opaque administrative structure, if one of those killer viruses “escaped” from the lab, it could cause a doomsday disaster.

Wuhan Institute of Virology, a biosafety level 4 laboratory located in Jiangxia District, Wuhan that has engaged in gain-of-function research.

Hector Retamal/AFP/Getty Images

Dr. Marc Lipsitch is Professor of Epidemiology and Director of the Center for Communicable Disease Dynamics at the Harvard School of Public Health. He is an author of more than 100 peer-reviewed publications on antimicrobial resistance, mathematical modeling of infectious disease transmission, bacterial and human population genetics, and immunity to Streptococcus pneumoniae. Dr. Lipsitch was quoted,7 “I still do not believe a compelling argument has been made for why these studies (GOF) are necessary from a public health point-of-view; all we have heard is that there are certain narrow scientific questions that you can ask only with dangerous experiments”, he said. “I would hope that when each HHS review is performed someone will make the case that strains are all different, and we can learn a lot about dangerous strains without making them transmissible.” Lipsitch pointed out that every mutation that has been highlighted as important by a gain-of-function experiment has been previously highlighted by completely safe studies. “There is nothing for the purposes of surveillance that we did not already know”, said Dr. Lipsitch. “Enhancing potential pandemic pathogens in this manner is simply not worth the risk.”10

Gain-of-Function – Chimera Virus Research in China

Since the SARS virus of 2003 China launched extensive virology research programs. These occurred through their military labs (People’s Liberation Army) and other labs such as the P4 virology lab in Wuhan located, apparently, just 280 meters away from the Hunan Seafood Market. The P4 lab in Wuhan was initially started as a joint venture with the French government. Chinese authorities switched the management of the project to a firm with close ties to the Chinese military complex. The Lab is a subsidiary of the Wuhan Institute of Virology managed by the China Academy of Sciences. The Chinese government has been working on GOF coronavirus studies for well over a decade. One of the most renowned Chinese virologists of this field is Shi Zhen-Li (surname Shi 石) who is renowned for her extensive research of SARS-like coronaviruses of bat origin. Since the SARS virus outbreak in 2003, Shi Zhengli and her team have conducted research on coronaviruses. In 2005, Shi and colleagues found that bats are a natural reservoir of SARS-like coronaviruses.11 To further determine the mechanism by which a SARS-associated coronavirus (SARS-CoV) may infect humans, Shi led a research team that studied the binding of spike proteins (s-protein) of both natural and chimeric SARS-like coronaviruses to ACE2 receptors in human, civet, and horseshoe bat cells.12, 13 ACE2’s functions include ultimately acting as a vasodilator that influences blood flow. It is located on cells all around the body, but ACE2 receptors also occur in many organs. It is especially common on cells lining air sacs (pneumocytes) in the lungs, which is partly why infection is associated with respiratory symptoms like pneumonia.

From 2010 onwards, Shi and her team have been primarily focused on identifying the capacity for coronavirus transmission across species, specifically putting the emphasis of study on the s-protein, or spike protein, of the coronaviruses. To successfully initiate an infection, viruses need to overcome the cell membrane barrier. Enveloped viruses achieve this by membrane fusion, a process mediated by specialized viral fusion proteins.

For coronaviruses, this fusion occurs through its spike protein. Each spike protein consists of three components that combine to form a ‘trimer’ structure with two parts or ‘subunits’, S1, and S2. You can think of the spike as a multistage rocket, with S1 being the boosters and S2 as a space shuttle: once attached to the ACE2 receptor, a spike sheds its S1 subunit and the remaining S2 part changes its shape or ‘conformation’ to enable the viral envelope to fuse with the outer membrane and drop the virus’ genetic material inside the cell.

The spike proteins (shown sticking out from the round virus) have high homology with the SARS virus. These are the proteins that make up the “key” that binds with the ACE2 receptors in humans to enter the cell. This contributes to the organ failure we see with infected persons as it drives the virus into the cells of the lungs and other organs such as the heart and kidneys, which also have ACE2 receptors.

Coronavirus​ / CC BY-SA

Thus, for SARS-CoV entry into a host cell, its s-protein needs to be cleaved by cellular proteases at 2 sites, termed S protein priming, so the viral and cellular membranes can fuse.14 In other words, Shi and her research team has been dedicated to finding ways that can better allow bat coronavirus to be transmissible to other animals.

In June of 2010, Shi’s team published a paper that describes research to understand the susceptibility of angiotensin-converting enzyme 2 (ACE2) proteins of different bat species to the s-protein of the SARS virus.15 With their chimeric research, they also modified key amino acid components to mutate the bats’ ACE2 receptor in order to examine compatibility with the SARS s-protein. This paper demonstrated their awareness of the relationship between the s-protein and the ACE2 receptor.

It is now understood that 2019-nCoV can infect the human respiratory epithelial cells through interaction with the human ACE2 receptor. Indeed, the recombinant spike protein can bind with the recombinant ACE2 protein. Shi and her colleagues’ paper also signified that they had discovered the passageway for coronaviruses to infect human bodies.

Angiotensin-converting enzyme 2, a monocarboxylase that degrades angiotensin II to angiotensin 1–7, is also the functional receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) and is highly expressed in the lungs and heart. Patients with SARS also suffered from cardiac disease including arrhythmias, sudden cardiac death, and blood pressure -systolic and diastolic dysfunction.

In 2013, Shi and her team published a paper in the journal Science China Life Sciences in which they isolated and identified numerous bat viruses (bat lyssaviruses, bat paramyxoviruses, bat filoviruses, bat reoviruses, and others).Bats are the only mammals capable of sustained flight and are notorious ‘reservoir hosts’ for some of the world’s most highly pathogenic viruses, including Nipah, Hendra, Ebola, and SARS.16 A reservoir is one or several animal species that are not or not very sensitive to the virus, which will naturally host one or several viruses. The absence of symptoms of the disease is explained by the effectiveness of their immune system, which allows them to fight against too much viral proliferation.

Bats Have Been Linked with Seven Major Epidemics Over the Past Three Decades.

In October 2013 Shi and her team published their findings in the prestigious journal Nature and claimed a breakthrough in coronavirus research.17 They provide evidence that SARS-CoV originated in bats. They concluded, “Our results provide the strongest evidence to date that Chinese horseshoe bats are natural reservoirs of SARS-CoV, and that intermediate hosts may not be necessary for direct human infection by some bat SL-CoVs.” In their research, they isolated three bat viruses, one of which had an s-protein that integrated with human ACE2 receptors. This effectively demonstrated the direct human infection of SARS-like viruses to humans without the need for an intermediate host. Then in 2014, Shi and her team collaborated on additional gain-of-function experiments led by Ralph S. Baric of the University of North Carolina, which showed that two critical mutations that the MERS coronavirus possesses allow it to bind to the human ACE2 receptor.18 In 2015, She and colleagues further showed that SARS had the potential to re-emerge from coronaviruses circulating in bat populations in the wild.19

Then in November 2015, Shi and her team from Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology together with scientists from the Department of Epidemiology at the University of North Carolina at Chapel Hill, published a paper in the journal Nature Medicine describing their joint gain of function coronaviruses research and new chimeric virus creation. According to Ralph Baric, an infectious-disease researcher at the University of North Carolina at Chapel Hill and co-author of the study, this study began before the US moratorium was enacted. So, the US National Institutes of Health (NIH) allowed it to proceed while it was under review by the agency. Baric claims the NIH eventually concluded that the work was not ‘so risky’ as to fall under the moratorium.20

They revealed the formation of a new synthetic virus or self-replicating chimeric virus. This chimeric virus had SARS virus as the framework with the key s-protein replaced by one they had found in a coronavirus, she mentioned in her 2013 paper. They concluded “we synthetically re-derived an infectious full-length SHC014 recombinant virus and demonstrate robust viral replication both in vitro and in vivo (mice).” In short, they took genes from a bat coronavirus spike-protein and spliced it to a mouse coronavirus genome, then tested this for its ability to infect human airway cells through their ACE-2 receptors. This chimeric recombinant coronavirus was tested in mice with significant deadly infections occurring. According to their paper, “all mouse studies were performed at the University of North Carolina, prior to the 2014 GOF moratorium involving influenza, MERS and SARS viruses.” This new virus demonstrated a powerful ability for cross species infection. The mice infected with this chimeric virus showed severe lung damage with no cure. Shi Zhengli’s team and her US colleagues’ successful recombinant splicing of the SARS virus was strategically important to the development of cross-species transmission. Their study eerily concluded that there was “a significant risk of a SARS coronavirus re-emergence”.

The fact that scientists are deliberately manipulating the genetics of deadly viruses to manufacture chimeric viruses and then test them for their ability to cause human disease should have created an outrage in the scientific community. This event was not even reported in mainstream media. The medium (chimeric coronavirus) from transfected cells was harvested and served as seed stocks for subsequent experiments (to be performed later).

An additional piece of vaccination information emerged from their 2015 study entitled ‘A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence’. They revealed that in order “to evaluate the efficacy of existing vaccines against infection with SHC014-MA15 (chimeric coronavirus), we vaccinated aged mice with double-inactivated whole SARS-CoV (DIV). Previous work showed that DIV could neutralize and protect young mice from challenge with a homologous virus; however, the vaccine failed to protect aged animals in which augmented immune pathology was also observed, indicating the possibility of the animals being harmed because of the vaccination. Here we found that DIV did not provide protection from challenge with SHC014-MA15 with regards to weight loss or viral titer. Consistent with a previous report with other heterologous groups 2b CoVs, serum from DIV-vaccinated, aged mice also failed to neutralize SHC014-MA15. Notably, DIV vaccination resulted in robust immune pathology and eosinophilia). Together, these results confirm that the DIV vaccine would not be protective against infection with SHC014 and could possibly augment disease in the aged vaccinated group.”21 The phenomena that specific viral vaccines can exacerbate an existing viral disease is well documented, particularly with influenza vaccines.22, 23, 24, 25, 26, 27

In summary, the researchers created and examined the disease potential of a synthetic SARS-like virus, SHC014-MA15, which was chimerically created from viruses found in Chinese horseshoe bat populations. Using what they described as “SARS-CoV reverse genetics system”, the researchers said that they generated and characterized a “chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone.” The mice died a grim death and the experiment was hailed a success by the researchers.

Back in Wuhan, Shi and her team then focused their chimeric viral research on primates. At this stage, some scientists took notice and became genuinely concerned, understanding this development was a dangerous move towards simulating the infection in humans. Academic debates on GOF studies one again began worldwide.

Dr. Wain-Hobson of the Pasture Institute in France expressed his disapproval and concern. In an article, he told Nature, “If the virus escaped, nobody could predict the trajectory.” Richard Ebright, a molecular biologist and biodefence expert at Rutgers University in Piscataway, New Jersey agrees and said, “The only impact of this work is the creation, in a lab, of a new, non-natural risk.”28 Both Drs Ebright and Wain-Hobson are long-standing critics of GOF research.

In October of 2014, the Obama Administration wary of the potential threats to public health and GOF research suspended funding to these research projects. Funding cuts and scientific criticism of GOF studies however did not stop Shi Zhengli’s team research. She and her colleagues continued under the cover and funding of the Chinese Government.

The question then is why would anyone be creating a virulent designer coronavirus that can infect humans? For what purpose is this research? Is it for a bioweapon? Is it so that you can create a vaccine and be the recipient of the profits? The standard pro-gain-of-function narrative is that the ultimate objective of such research is to better inform public health and preparedness efforts and/or development of medical countermeasures. Many scientists disagree. As Dr. Marc Lipsitch pointed out, every mutation that has been highlighted as important by a gain-of-function experiment has been previously brought to light by completely safe studies.

NIH Funding Resumes

On Dec 19, 2017, the NIH announced that they would again resume funding gain-of-function experiments involving influenza, Middle East respiratory syndrome coronavirus, and severe acute respiratory syndrome coronavirus ending the safety moratorium.29 This once again opened the door to NIH funding to GOF studies China. As a safety condition, the federal government then began requiring that any National Institutes of Health grant proposals involving gain-of-function research undergoes a review by an expert panel to evaluate the risk of such work against the potential gains. But the names of the expert-panel members are not publicly available, nor are its reviews of study proposals. “We’re not trying to say the policy is wrong, we’re trying to say the policy is ambiguous,” says Dr. Marc Lipsitch, an epidemiologist at the Harvard T.H. Chan School of Public Health in Boston, Massachusetts, and one of the researchers calling for greater transparency around such work.

In 2019, the NIH committed $3.7 million over six years for research on bat coronaviruses in China. The program followed a previous $3.7 million, a 5-year project for collecting and studying bat coronaviruses, which ended in 2019, bringing the total to $7.4 million. One primary concern by many scientists is some of this newest additional 3.7 million was directed to the Wuhan Institute of Virology for coronavirus GOF studies. When the NIH was questioned about the grants they responded, “The grant you are referencing is a multi-site, multi-country project supporting research that aims to understand what factors allow coronaviruses, including close relatives to SARS, to evolve and jump into the human population and cause disease. Specifically, the project includes studying viral diversity in animal (bats) reservoirs, surveying people that live in high-risk communities for evidence of bat-coronavirus infection, and conducting laboratory experiments to analyze and predict which newly-discovered viruses pose the greatest threat to human health.”30 The National Institute of Allergy and Infectious Diseases (NIAID), under Anthony Fauci’s leadership, has financially supported six studies of bats and their connection to coronavirus.

SARS-CoV-2 Origin Debate

Many rumors and debates have persisted as to the origins of the SARS-CoV-2 virus. Most claim it came from bats and jumped into humans, acquiring new genomic features through adaptation during undetected human-to-human transmission. The official narrative from the WHO and the CDC is that the SARS-CoV-2 virus was a natural development or mutation, from a still-unknown animal source. An excerpt from the website states, “The SARS-CoV-2 virus is a betacoronavirus, like MERS-CoV and SARS-CoV-1. All three of these viruses have their origins in bats. The sequences from U.S. patients are similar to the one that China initially posted, suggesting a likely single, recent emergence of this virus from an animal reservoir. Early on, many of the patients at the epicenter of the outbreak in Wuhan, Hubei Province, China had some link to a large seafood and live animal market, suggesting animal-to-person spread. Later, a growing number of patients reportedly did not have exposure to animal markets, indicating person-to-person spread.”

The Chinese government from the beginning has claimed the virus originated in the Hunan Seafood Market in Wuhan in December 2019. This was propagated by mainstream media and at first, was believable because 27 of the first 41 people hospitalized (66 percent) passed through a market located in the heart of Wuhan city. Yet, later it was discovered that there is also genomic evidence and reports of the virus having circulated earlier in November. A molecular dating estimate based on the SARS-CoV-2 genomic sequences indicate an origin in November 2019.31 They also concluded, “ that the human SARS‐CoV‐2 virus, which is responsible for the current outbreak of COVID‐19, did not come directly from pangolins.” Interestingly, bats were not sold in the Hunan Seafood Market. This raises questions about the link between this COVID-19 epidemic and wildlife in the Hunan Seafood Market.

Thus, the Hunan Seafood Market origin scenario is highly unlikely, particularly now that other evidence exists of numerous individuals before December with the virus who had no contact with anyone from the market. Theories about laboratory contamination surfaced immediately in China, primarily because of the proximity of the Hunan Seafood Market from the Wuhan Institute of Virology. Particularly with the ongoing history of chimeric bat coronaviruses being studied and created there.

The Chinese government has strongly pushed back conjecture that the virus was lab leaked or lab manufactured. Wuhan Institute of Virology director Wang Yanyi recently told state broadcaster CGTN that the theory Covid-19 leaked from a lab in Wuhan is “pure fabrication.” Wang adds “her lab was studying three live strains of bat coronaviruses, but none matched Covid-19.”32 An analysis by a team from the Wuhan Institute of Virology, posted to the preprint server bioRxiv, claimed that the genome of this coronavirus (the seventh known to infect humans) is 96% identical to that of a bat coronavirus, suggesting that species is the original source.33

A recent study was published in the Nature Medicine journal34 in which the authors investigated the genetic code of a key part of the coronavirus and compared this to other known coronaviruses. They concluded that “Human-SARS CoV-2 was a natural mutation from one of several possible animal sources, of which still has not been identified.” The figure below from this study demonstrates the genetic code differences between the different animal coronavirus types and the 2002 SARS coronavirus as well. The marked and different colored areas show genetic differences.

The foremost problem with the scientists’ conclusion is the insertion of a 12-nucleotide section in the “Human-SARS CoV-2” coronavirus sequence which is completely missing from every other coronavirus type known. Such a large genetic difference (insertion) does not suddenly happen at random or naturally. This sequence was not even present in the alleged bat coronavirus as the source of this pandemic. Thus, this insertion strongly suggests that this Human-SARS CoV-2 was manufactured in a lab. The researchers claim the functional consequence of this inserted sequence (polybasic cleavage site) is unknown, but that it appears to enhance infection in human cells. They still contend that this virus originating from a laboratory is “improbable” – that means possible.

They stated,

“Polybasic cleavage sites have not been observed in related ‘lineage B’ beta coronaviruses, although other human beta coronaviruses, including HKU1 (lineage A), have those sites, and predicted O-linked glycans. Given the level of genetic variation in the spike, it is likely that SARS-CoV-2-like viruses with partial or full polybasic cleavage sites will be discovered in other species. The functional consequence of the polybasic cleavage site in SARS-CoV-2 is unknown, and it will be important to determine its impact on transmissibility and pathogenesis in animal models. Experiments with SARS-CoV have shown that insertion of a furin cleavage site at the S1–S2 junction enhances cell-cell fusion without affecting viral entry.”35

a, Mutations in contact residues of the SARS-CoV-2 spike protein. The spike protein of SARS-CoV-2 (red bar at the top) was aligned against the most closely related SARS-CoV-like coronaviruses and SARS-CoV itself. Key residues in the spike protein that make contact to the ACE2 receptors are marked with blue boxes in both SARS-CoV-2 and related viruses, including SARS-CoV (Urbani strain).

b, Acquisition of polybasic cleavage site and O-linked glycans. Both the polybasic cleavage site and the three adjacent predicted O-linked glycans are unique to SARS-CoV-2 and were not previously seen in lineage B beta coronaviruses.

Studies show that the s-protein of the new SARS-CoV-2 virus, like 2002 SARS-CoV-1 counterpart binds angiotensin-converting enzyme 2 (ACE-2), but with much higher affinity and faster binding kinetics.36, 37 This finding is particularly interesting, remembering how Shi Zhengli and her team previously investigated ways their chimeric virus could better infect the ACE-2 receptors of human and animal cells.38

Recently, Dr. Luc Montagnier during a TV interview with a French TV channel stated that elements of the HIV-1 retrovirus, which he co-discovered in 1983, can be found in the genome of the new SARS-CoV-2. Along with Françoise Barré-Sinoussi and Harald Zur Hause, Luc Montagnier won the 2008 Nobel Prize for Medicine for the discovery of human immunodeficiency virus (HIV).

Dr. Montagnier said “There has been a manipulation of the virus: at least part of it, not all of it. There is one model, which is the classic virus, which comes mainly from bats, but to which HIV sequences have been added,” he said. “In any case, it’s not natural,” he continued. “It’s the work of professionals, of molecular biologists. Very meticulous work. For what purpose? I don’t know. One hypothesis is that they wanted to create an AIDS vaccine.”

To support his theory, Montagnier cited the study by a group of researchers at the Indian Institute of Technology in New Delhi titled, “Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp 120 and Gag,”

The abstract of the article read, “We are currently witnessing a major epidemic caused by the 2019 novel coronavirus (2019- nCoV). The evolution of 2019-nCoV remains elusive. We found 4 insertions in the spike glycoprotein (S) which are unique to the 2019-nCoV and are not present in other coronaviruses. Importantly, amino acid residues in all the 4 inserts have identity or similarity to those in the HIV-1 gp120 or HIV-1 Gag. Interestingly, despite the inserts being discontinuous on the primary amino acid sequence, 3D-modelling of the 2019-nCoV suggests that they converge to constitute the receptor binding site. The finding of 4 unique inserts in the 2019-nCoV, all of which have identity /similarity to amino acid residues in key structural proteins of HIV-1 is unlikely to be fortuitous in nature. This work provides yet unknown insights on 2019-nCoV and sheds light on the evolution and pathogenicity of this virus with important implications for diagnosis of this virus.”

The study was criticized by authorities and later withdrawn by its authors. Dr. Montagnier also predicted the imminent disappearance of the virus, because its supposedly artificial origin would be weakening it.“One can do anything with nature, but if you make an artificial construction, it is unlikely to survive. Nature loves harmonious things; what is alien, like a virus coming from another virus, for example, is not well tolerated,” he said. For the scientist, the parts of the virus into which HIV was inserted are rapidly mutating, causing it to self-destruct.

In a separate podcast episode with a different outlet, Montagnier further said the virus had escaped in an “industrial accident” from the Wuhan city laboratory when Chinese scientists were attempting to develop a vaccine against HIV. Dr. Montagnier claims have since been strongly attacked by the media and his TV interview censored.

Based on the history trail of bat COVID research, and reports from microbiologists, it suspiciously ‘appears’ that the SARS CoV-2 is not a natural mutation of any known coronavirus strain but in fact, a manmade – chimeric – strain that likely escaped the Wuhan lab. Time will tell the truth.

Biosafety Laboratories on the Rise – Regulations are Questionable

According to a 2011 report by the National Research Council, an arm of the U.S. National Academy of Sciences, hundreds of BSL-3 laboratories may be unknown, because “no federal agency is required to track the number of biocontainment labs.” 39, 40 Globally, BSL-3 labs have recently been built or are under construction in Bangladesh, India, Indonesia, China, Brazil, and Mexico, among others. Yet many countries have few or no regulations, the NRC concluded. The more secure but dangerous BSL-4 labs are also proliferating. A 2011 workshop in Istanbul organized by the NRC was told that there are 24 BSL-4 facilities, including in Germany, Gabon, Sweden, Russia, South Africa, and Canada. The United States has six BSL-4 laboratories.

In 2019 the BSL-4 Army laboratory at Fort Detrick that studies deadly infectious organisms like Ebola, anthrax and smallpox was shut down for a period of time after a CDC inspection, with many projects being temporarily halted. The lab itself reported that the shutdown order was due to ongoing infrastructure issues with wastewater decontamination, and the CDC declined to provide the reason for the shutdown due to national security concerns.41

While excellent biosafety conditions in the laboratories performing GOF studies are certainly important, it is not a panacea for guaranteeing safety. Of the major mishaps at US government labs in recent years, nearly all involved removing the infectious agent from the high-containment lab where it was under study to another, lower-containment lab because it was thought to be inert. High-tech containment cannot prevent the deliberate removal of supposedly safe material from a laboratory, and so human error remains a source of potential missteps, regardless of the quality of the laboratory facilities.

GOF studies have been one of the most hotly debated science policy issues during the 21st century, with the controversy surrounding a series of published experiments with potential implications for biological weapons-making. Such studies include the genetic engineering of a superstrain of the mousepox virus in 200142, the artificial synthesis (via synthetic genomics) of a “live” poliovirus from chemical components in 200243, and the reconstruction (via synthetic genomics) of the 1918 “Spanish Flu” virus in 2005.44 Though all of these studies involved claimed legitimate aims, critics argued that they should not have been conducted and/or published. Some argued that publishing studies like these in full detail provided “recipes” for especially dangerous potential biological weapons agents to would-be bioterrorists. Whether or not COVID-19 is eventually determined to have originated from gain-of-function research, this pandemic should be a stark reminder of the dangers it poses.

Considering the recent COVID-19 pandemic, GOF studies with the potential to enhance the pathogenicity or transmissibility of potential pandemic pathogens have once again raised biosafety and biosecurity fear and apprehension. Of concern in the context of life science research is that GOF advances in biotechnology may enable the development and use of a new generation of biological weapons of mass destruction. GOF studies can add to the evidence base, but it cannot qualitatively change that evidence base. Empirically, the contribution of such studies to applied public health goals has been far more modest than claimed. Vast advances in the most essential questions of influenza virology and in the public health goal of pandemic preparedness can be achieved without undertaking experiments that, if an accident occurs, could start a new pandemic. Until more evidence is shown that GOF studies can be conducted safely, or are even necessary, it would be wise and prudent to enact another moratorium on all GOF funding and studies.


1.; 2012.




5. Webster, Robert G., William J. Bean, Owen T. Gorman, Thomas M. Chambers, and Yoshihiro Kawaoka. “Evolution and ecology of influenza A viruses.” Microbiology and molecular biology reviews 56, no. 1 (1992): 152-179.

6. Wertheim, Joel O. “The re-emergence of H1N1 influenza virus in 1977: a cautionary tale for estimating divergence times using biologically unrealistic sampling dates.” PloS one 5, no. 6 (2010).




10. Lipsitch, Marc, and Barry R. Bloom. “Rethinking biosafety in research on potential pandemic pathogens.” MBio 3, no. 5 (2012): e00360-12.

11. Li, Wendong, Zhengli Shi, Meng Yu, Wuze Ren, Craig Smith, Jonathan H. Epstein, Hanzhong Wang et al. “Bats are natural reservoirs of SARS-like coronaviruses.” Science 310, no. 5748 (2005): 676-679.

12. Yu, Meng, Mary Tachedjian, Gary Crameri, Zhengli Shi, and Lin-Fa Wang. “Identification of key amino acid residues required for horseshoe bat angiotensin-I converting enzyme 2 to function as a receptor for severe acute respiratory syndrome coronavirus.” Journal of General Virology 91, no. 7 (2010): 1708-1712.

13. Hou, Yu-xuan, Cheng Peng, Zheng-gang Han, Peng Zhou, Ji-guo Chen, and Zheng-li Shi. “Immunogenicity of the spike glycoprotein of Bat SARS-like coronavirus.” Virologica Sinica 25, no. 1 (2010): 36-44.

14. Belouzard, Sandrine, Victor C. Chu, and Gary R. Whittaker. “Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites.” Proceedings of the National Academy of Sciences 106, no. 14 (2009): 5871-5876.

15. Hou, Yuxuan, Cheng Peng, Meng Yu, Yan Li, Zhenggang Han, Fang Li, Lin-Fa Wang, and Zhengli Shi. “Angiotensin-converting enzyme 2 (ACE2) proteins of different bat species confer variable susceptibility to SARS-CoV entry.” Archives of virology 155, no. 10 (2010): 1563-1569.

16. Shi, ZhengLi. “Emerging infectious diseases associated with bat viruses.” Science China Life Sciences 56, no. 8 (2013): 678-682.

17. Ge, Xing-Yi, Jia-Lu Li, Xing-Lou Yang, Aleksei A. Chmura, Guangjian Zhu, Jonathan H. Epstein, Jonna K. Mazet et al. “Isolation and characterization of a bat SARS-like coronavirus that uses the ACE2 receptor.” Nature 503, no. 7477 (2013): 535-538.

18. Yang, Yang, Chang Liu, Lanying Du, Shibo Jiang, Zhengli Shi, Ralph S. Baric, and Fang Li. “Two mutations were critical for bat-to-human transmission of Middle East respiratory syndrome coronavirus.” Journal of virology 89, no. 17 (2015): 9119-9123.

19. Menachery, Vineet D., Boyd L. Yount Jr, Kari Debbink, Sudhakar Agnihothram, Lisa E. Gralinski, Jessica A. Plante, Rachel L. Graham et al. “A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence.” Nature medicine 21, no. 12 (2015): 1508.

20. Menachery, V.D., Yount, B.L Jr, Debbink, K., Agnihothram, S., Gralinski, L.E., Plante, J.A., Graham, R.L., Scobey, T., Ge, X-Y., Donaldson, E.F., Randell, S.H., Lanzavecchia, A., Marasco, W.A., Shi, Z-L., & Baric, R.S. (2015). A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence. Nature Medicine, 21, 1508– 1513. Doi: 10.1038/nm.3985 – Funding for this US/China joint chimeric research was supported by grants from the National Institute of Allergy & Infectious Disease, the National Institute of Aging of the US National Institutes of Health (NIH), the National Natural Science Foundation of China, and by USAID-EPT-PREDICT funding from EcoHealth Alliance.

Researchers and their affiliated institutions:

∙ Vineet D Menachery, Department of Epidemiology, University of North Carolina at Chapel Hill, USA.

∙ Boyd L Yount Jr, Department of Epidemiology, University of North Carolina at Chapel Hill, USA.

∙ Kari Debbink, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, USA.

∙ Lisa E Gralinski, Department of Epidemiology, University of North Carolina at Chapel Hill, USA.

∙ Jessica A Plante, Department of Epidemiology, University of North Carolina at Chapel Hill, USA.

∙ Rachel L Graham, Department of Epidemiology, University of North Carolina at Chapel Hill, USA.

∙ Trevor Scobey, Department of Epidemiology, University of North Carolina at Chapel Hill, USA.

∙ Xing-Yi Ge, Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.

∙ Eric F Donaldson, Department of Epidemiology, University of North Carolina at Chapel Hill, USA.

∙ Scott H Randell, Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, USA.

∙ Antonio Lanzavecchia, Institute for Research in Biomedicine, Bellinzona Institute of Microbiology, Zurich, Switzerland.

∙ Wayne A Marasco, Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA

∙ Zhengli-Li Shi, Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.

∙ Ralph S Baric, Department of Epidemiology, University of North Carolina at Chapel Hill, USA

21. IBID. Menachery, V.D.

22. Cowling, Benjamin J., and Hiroshi Nishiura. “Virus interference and estimates of influenza vaccine effectiveness from test-negative studies.” Epidemiology 23, no. 6 (2012): 930-931.

23. Viboud, Cecile, and Lone Simonsen. “Does seasonal influenza vaccination increase the risk of illness with the 2009 A/H1N1 pandemic virus?.” Plos medicine 7, no. 4 (2010).

24. Janjua, Naveed Z., Danuta M. Skowronski, Travis S. Hottes, William Osei, Evan Adams, Martin Petric, Suzana Sabaiduc et al. “Seasonal influenza vaccine and increased risk of pandemic A/H1N1-related illness: first detection of the association in British Columbia, Canada.” Clinical Infectious Diseases 51, no. 9 (2010): 1017-1027.

25. Rikin, Sharon, Haomiao Jia, Celibell Y. Vargas, Yaritza Castellanos de Belliard, Carrie Reed, Philip LaRussa, Elaine L. Larson, Lisa Saiman, and Melissa S. Stockwell. “Assessment of temporally-related acute respiratory illness following influenza vaccination.” Vaccine 36, no. 15 (2018): 1958-1964.

26. Skowronski, Danuta M., Gaston De Serres, Natasha S. Crowcroft, Naveed Z. Janjua, Nicole Boulianne, Travis S. Hottes, Laura C. Rosella et al. “Association between the 2008–09 seasonal influenza vaccine and pandemic H1N1 illness during spring–summer 2009: four observational studies from Canada.” PLoS medicine 7, no. 4 (2010).

27. Wolff, Greg G. “Influenza vaccination and respiratory virus interference among Department of Defense personnel during the 2017–2018 influenza season.” Vaccine 38, no. 2 (2020): 350-354.

28. Butler, Declan. “Engineered bat virus stirs debate over risky research.” Nature News.



31. Li, Xingguang, Junjie Zai, Qiang Zhao, Qing Nie, Yi Li, Brian T. Foley, and Antoine Chaillon. “Evolutionary history, potential intermediate animal host, and cross‐species analyses of SARS‐CoV‐2.” Journal of medical virology (2020).


33. Zhou, P., Yang, X., Wang, X. et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 579, 270–273 (2020).

34. Andersen, Kristian G., Andrew Rambaut, W. Ian Lipkin, Edward C. Holmes, and Robert F. Garry. “The proximal origin of SARS-CoV-2.” Nature medicine 26, no. 4 (2020): 450-452.

35. IBID Anderson, K.

36. Wu, C., Yang, Y., Liu, Y., Zhang, P., Wang, Y., Wang, Q., Xu, Y., Li, M., Zheng, M., Chen, L., & Li, H. (2020). Furin, a potential therapeutic target for COVID-19. Retrieved 14th May 2020 from

37. Ortega, Joseph Thomas, Maria Luisa Serrano, Flor Helene Pujol, and Hector Rafael Rangel. “Role of changes in SARS-CoV-2 spike protein in the interaction with the human ACE2 receptor: An in silico analysis.” EXCLI journal 19 (2020): 410.

38. Ren, W., Qu, X., Li, W., Han, Z., Yu, M., Zhou, P., Zhang, S-Y., Wang, L-F., Deng, H., & Shi, Z. (2008). Difference in Receptor Usage between Severe Acute Respiratory Syndrome (SARS) Coronavirus and SARS-Like Coronavirus of Bat Origin. Journal of Virology, 82 (4), 1899-1907: doi:10.1128/JVI.01085-07.




42. Jackson, R.J. et al., 2001. Expression of mouse interleukin-4 by a recombinant ectromelia virus overcomes genetic resistance to mousepox. Journal of Virology, 75, pp. 1205-1210.

43. Cello, J. et al., 2002. Chemical synthesis of poliovirus cDNA: generation of infectious virus in the absence of natural template. Science, 297, pp. 1016-1018.

44. Tumpey, T.M. et al. 2005. Characterization of the reconstructed 1918 Spanish influenza pandemic virus. Science, 310(5745), pp. 77–80.


Vaccine Viral Interference

Vaccine Viral Interference

May 8, 2020

Vaccine Viral Interference

Here is an excellent and thought-provoking article by Dr. Allan S. Cunningham, retired pediatrician dated 02/23/2020 entitled “TAMIFLU & INFLUENZA VACCINES: MORE HARM THAN GOOD?”

Dr. Cunningham discusses how flu vaccines increase the risk of illness from noninfluenza virus infections such as rhinoviruses, coronaviruses, RS viruses, parainfluenza viruses, adenoviruses, HMP viruses and enteroviruses. After reading this think of the tri-and particularly quadrivalent flu vaccines administered in Italy in 2019 to thousands of elderlies. According to data most of the people who received flu vaccination were over 65 years old. Particularly, implicated as potentially causing was this newly concocted quadivalent flu vaccine that contained influenza A-(H1N1)pdm09; influenza A(H3N2); influenza B/Yamagata and influenza B/Victoria together with proprietary adjuvants. Adjuvants are substances, like aluminum, added to vaccines to boost immune response Did this flu (influenza) vaccine campaign cause Vaccine Interference and increase the coronavirus pandemic numbers across Italy recently?

More References of Vaccination Viral Interference:

Cowling, Benjamin J., and Hiroshi Nishiura. “Virus interference and estimates of influenza vaccine effectiveness from test-negative studies.” Epidemiology 23, no. 6 (2012): 930-931.

Authors concluded, “In a separate placebo-controlled trial of influenza vaccination, we reported that recipients of influenza vaccine had significantly higher risk of non-influenza respiratory virus infections.”

Viboud, Cecile, and Lone Simonsen. “Does seasonal influenza vaccination increase the risk of illness with the 2009 A/H1N1 pandemic virus?.” Plos medicine 7, no. 4 (2010).

Authors concluded, “In summary, we report findings from four epidemiologic studies in Canada showing that prior receipt of 2008–09 TIV was associated with increased risk of medically attended pH1N1 illness during the spring–summer 2009.”

Janjua, Naveed Z., Danuta M. Skowronski, Travis S. Hottes, William Osei, Evan Adams, Martin Petric, Suzana Sabaiduc et al. “Seasonal influenza vaccine and increased risk of pandemic A/H1N1-related illness: first detection of the association in British Columbia, Canada.” Clinical Infectious Diseases 51, no. 9 (2010): 1017-1027.

Authors concluded, “In this article, we present the first observation of an unexpected association between prior seasonal influenza vaccination and pH1N1 illness during the spring and summer of 2009 in Canada. Specifically, outbreak investigation conducted during the early stages of the pandemic in a northern BC community identified that participants reporting pH1N1-related ILI during the period 1 April through 5 June 2009 were more than twice as likely to report having previously received seasonal influenza vaccine.”

Rikin, Sharon, Haomiao Jia, Celibell Y. Vargas, Yaritza Castellanos de Belliard, Carrie Reed, Philip LaRussa, Elaine L. Larson, Lisa Saiman, and Melissa S. Stockwell. “Assessment of temporally-related acute respiratory illness following influenza vaccination.” Vaccine 36, no. 15 (2018): 1958-1964.

Authors concluded, “Vaccinated individuals were no more likely to get influenza after influenza vaccination; however, patients’ experiences of illness after vaccination may be validated by these results which suggest increased risk of ARI caused by non-influenza respiratory pathogens following influenza vaccination among children <18 years.”

Skowronski, Danuta M., Gaston De Serres, Natasha S. Crowcroft, Naveed Z. Janjua, Nicole Boulianne, Travis S. Hottes, Laura C. Rosella et al. “Association between the 2008–09 seasonal influenza vaccine and pandemic H1N1 illness during spring–summer 2009: four observational studies from Canada.” PLoS medicine 7, no. 4 (2010).

Authors concluded, “we report findings from four epidemiologic studies in Canada showing that prior receipt of 2008–09 Trivalent Inactivated Influenza Vaccine (TIV) was associated with increased risk of medically attended pandemic-H1N1 illness during the spring–summer 2009.

Wolff, Greg G. “Influenza vaccination and respiratory virus interference among Department of Defense personnel during the 2017–2018 influenza season.” Vaccine 38, no. 2 (2020): 350-354.

Authors concluded, “Examining virus interference by specific respiratory viruses showed mixed results. Vaccine derived virus interference was significantly associated with coronavirus and human metapneumovirus; however, significant protection with vaccination was associated not only with most influenza viruses, but also parainfluenza, RSV, and non-influenza virus coinfections.”

Recent Posts

Thriving Through Corona: Practical Tips For People And Pets

Thriving Through Corona: Practical Tips For People And Pets

April 28, 2020

Thriving Through Corona: Practical Tips For People And Pets

Marlene Siegel, DVM

Who would have ever imagined a worldwide crisis that would bring the WORLD to a halt!


Not minimizing the gravity of health concerns, there were other “pan epidemics” going on even before this Corona Virus threat. Most people were overworked, stressed all the time, sleep-deprived, deeply in debt with no emergency fund reserves and distracted from focusing on the meaning of “life and happiness”. Too many people were tied to the hamster wheel they were running on, working in jobs that were not fulfilling but paid the bills. Few people had a spiritual understanding of “who they were” or “what their purpose and passion in life” was. Even fewer people were living the life of their dreams.


The worldwide response to this flu epidemic has destroyed the world as we knew it, but is that a totally bad thing? If we only focus on the negative, the fear, doubt, and uncertainty, we drown in the quicksand of low vibration and become stuck there. We can not find answers, problem solve and bring our greatest gifts to light when we are contracted and stuck in a dark place.


Technically, most people have their basic human needs met, adequate food, water, and shelter. “Essential” businesses are open, and many others are finding creative ways to continue operations using a virtual platform.


Meanwhile, millions of people find themselves with a ton of free time, quarantined in their homes. This can be a positive or negative experience depending on how we choose to perceive it (note the operative word here is choose).


There are only 2 emotions that stimulate behavior: Fear and Love


Fear triggers the sympathetic part of the nervous system and releases cortisol, the stress hormone. Also known as the fight/flight response, the purpose of the sympathetic nervous system is to enable survival during life-threatening situations. Interestingly, the body doesn’t know the difference between being chased by a sabertooth tiger and the fear state created by the coronavirus threat. The end result is the same, the parasympathetic system is turned off and all resources are diverted to the sympathetic nervous system to enable the body to survive the “threat”. In this fear state, people feel depressed, stuck, energetically contracted, unable to problem solve and create solutions. People feel like victims with no control over the circumstances.


Love stimulates the parasympathetic nervous system. It creates a high vibration, an expanded energetic state, leading to feeling empowered and creative, resulting in possibilities and solutions.


It is human nature to need motivation. Contrast (experiencing what is NOT wanted) and adversity stimulate the co-creative mind to find solutions to problems the world needs. Every one of us has unique skills and passion, enabling everyone to be a part of the “new world” that will emerge as we transform and grow from where we were to where we are going.


Change is good. We are leaving a world of competition and entering a world where cooperation will be the key to survival. Embrace it, go inwards to connect to your spiritual self, because it is there that our superpowers live. It is time to birth a new vision of the world and our role in it.


Step #1 Take back your power. No one and no circumstance can make you feel any way unless you allow it. Choose to find the blessings in every moment. Even if you can’t “see” the blessing, have trust and faith that what is happening is for the highest and best purpose, you just haven’t seen what that is yet…but you will!


Step #2 Let go…let go of the “stuff” you have been chained to. Now is the time to create the “more” that is REALLY wanted and desired. Letting go is the gift, giving birth to FREEDOM from the shackles. Anything is possible if you think it is!


Step #3 Have a plan and take action. Create action plans for yourself, your family, your business/job and your pets.


You And The Family

The oxygen mask needs to go on you first or you can’t be available to help others. Take care of your health, both mental and physical.


Eat the rainbow, nutritionally healthy organic foods (no processed sugar, processed foods, and toxic drinks). Grow some of your food! Herbs, greens, and vegetables are easy and now is the time to start. There are Grow Towers, Earth boxes and tubes, hydroponics, aquaponics, raised beds, microgreens, regenerative farming, permaculture, planting food-bearing trees in your yard and community gardening.


Water is the second most critical nutrient (air is the first). Today’s tap water has over 65,000 (yes, not a typo) toxic chemicals. Criteria for water should be: highly filtered, structured (small particle size) and contain molecular hydrogen. There are 2 systems I recommend, one does not use electricity ( ) great during power outages, hydrogen water is still produced), it uses a chemical reaction with magnesium (this is great because many people are magnesium deficient). The other system uses electrolysis and does require power. This system also produces hypochlorous acid water, which is 4X stronger than bleach with no side effects. Call me to see which system is best for you.


Air quality is extra important now that people are in their homes more. Check for mold (home kits are available to test) and be aware of toxins (products impregnated with formaldehyde or fire retardants, petroleum-based candles, chemical air fresheners, and non-green household cleaners. I recommend 2 companies that both do a great job cleaning the air. has free consumer information and product ratings. Rule of thumb, if you can’t pronounce the ingredients, don’t use it. Call me to discuss companies and their products. Air Doctor offers a $300 discount when you use this link. has air and water systems.


Gut support is critical to maintaining a healthy immune system. At least 70% of the immune system lives in the gut. Foods like bone broth (easily make at home), kefir or other fermented foods should be consumed daily.

Preserve food. Consider investing in a dehydrator, freeze dryer, vacuum sealing or canning. This allows you to buy food on sale and in bulk and minimize waste. Make sauerkraut, it is inexpensive, easy and a superfood, helping to restore good gut bacteria. A healthy immune system begins in the gut with the right bacteria! Make a goal of having 2 months’ worth of food preserved which is a good idea due to natural disasters too.


Pet and Livestock Needs.

I believe they are fur angels. They model unconditional love and help lighten the heavy burden of this physical dimension. Now is a great time to learn how to keep your fur child healthy and happy. Broke care is when we wait for a health challenge and chase the symptom with a pill for an ill or a diet for disease. Health care is understanding the body’s biology, how the body works and maintaining the body for optimum health. This starts with a species-appropriate diet. Visit my websites for information blogs, articles, and videos. for education on species-appropriate diets and essential nutrients. Have a month’s supply of feed, hay, and medications. Find online resources that can deliver. My site offers grass-fed/grass-fed out raw pet food and essential supplements along with an online grass-fed meat source for humans, all delivered to your door. ( Share your bone broth and kefir or other fermented foods with the fur fam, they need to support their microbiome too!


Telemedicine. On line health care may be an option for some pet and human emergencies. Call ahead and see who is offering that service. offers basic over the phone health coaching sessions. Understand that nothing is better than a hands-on physical exam and accurate diagnosing utilizing proper testing.


Sleep. 6-8 hours a night. There are many online resources to educate and aid in how to get healthy sleep. One of my favorite products is music which has special frequencies to calm and relax the body. Contact me for details.


Exercise. At a minimum, be active for an hour a day. Mix in strength training with aerobic and high intensity plus yoga, qi gong and pilates. Youtube has loads of follow-along video training for free and Planet Fitness is offering free online classes too!


Detoxification. We (and our pets) have 6 organs of elimination. The kidney, colon, lungs, liver, skin, and lymphatics. All are important but the liver and lymphatics do a LOT of work! Herbs, homeopathic, breathing exercises, salt therapy, infrared sauna, dry brushing, rebounding exercises, coffee enemas and more (much of which can be done at home). For specific questions or resources, contact me at


Stimulate the parasympathetic nervous system at minimum twice daily, when waking up and before sleeping. The parasympathetic nervous system controls rest, digest, repair and detoxification. Deep breathing exercises and meditation are easy and readily available. There are many foods and teas to stimulate the parasympathetic nervous system. Magnesium and the amino acid Glycine are wonderful for helping the body relax. Google resources and try a variety of methods.


EMF and other household toxins. I have blogs on how to reduce toxic exposures at Make your own supplies (house cleaners and sanitizers). Great family projects that are fun, empowering and inexpensive.


Clean and organize. Remove the clutter to make room for the new. Go through closets, pantries, the “junk drawer”. Box up the things you have not used in a year and donate them to shelters, ministries or online community platforms. Things of value can be used for trade and barter.


Learning. All the things on the “bucket list” that there was no time to do, now you have the time to do! Books, video programs, youtube, the resources are endless!


Spiritual awakening. This is the deeper inner work that many did not dare to explore. Now is the time to seek the answers to “who am I”, “why am I here in this particular time and place”, “what is my purpose(s)”. Serve. What does the world need that you can provide through your unique gifts and talents? Now is the time to “just do it”


Barter. “Money” is simply a value trade for things you have that others want or what you want to have. Be creative on things you can use as barter, including your skillset. This could be physical services, emotional intelligence or intellectual property.


Conserve. Undoubtedly we as a society have been wasteful of our resources. Time to conserve and repurpose. Limit showers to conserve water. Raise (or lower) the thermostat a few degrees to conserve electricity.

Practice intermittent fasting (it is super healthy for the body) by limiting eating to a 4-6 hour window and missing a meal. Create a compost pile outside (google or YouTube if needed) to feed your garden (the one you started in step one).


Emergency kit. Thermometers, bandages, natural remedies (for colds, cough and headaches). Consider ozone for home use (ozone is the strongest sterilizer in the world) and laser therapies. Contact me for specific recommendations at


Financial emergency kit. Cut out unnecessary spending and get some liquid assets (things easily converted to cash with direct access to it). Have 2 months of emergency money set aside for paying utilities, gas and other unexpected items. Consider re financing home or business and taking out cash equity.


Homeschooling children

It is the children who will take the baton and run with it. There is a Devine blessing here. They will not be doomed to the “rat race” and ties to “things” that are not really important. Connect to your kids and explore all the above steps together. The best learning is the skills that enable optimum survival.


Children take on the beliefs and behaviors their caregivers express. Be mindful of your mindset and behavior.


Limit TV and computer time and dedicate time to hands-on exploring and creating. Arts, crafts, scrapbooking, cooking, gardening, exercising and talking about meaningful things.


Create space and alone time, this is just as important as creating quality together time.


Here is my favorite GEM (genuine encounter moment) that I do whenever possible with family and friends. This can be done before a meal, before a discussion or meeting, or as a bedtime ritual.

Each person starts with one of the phrases below: “What I love (like, appreciate, am grateful for) about you (or the situation or experience) is…’They say 1 or 2 things about each person (using the above starter sentence) AND end with themselves.



“What I love about you is… (naming character traits about that person) how creative, generous, kind…. “What I love about myself is…(naming your character traits)”


Business / Professional Life

For many people, this is going to be brand new. What was may no longer be. Allow yourself the time to feel the emotions, detach from the identity of what was and then create a plan to deal with it and future possibilities. Again, this may not be a bad thing if it makes room for something better.


1. Find your purpose. This is the perfect opportunity to get off the hamster wheel and follow your passion. What do you want? Create from a place where anything is possible. Identify your end goal, then be creative and flexible on how you get there.


2. Identify limiting beliefs and resistance that has been holding you back, then release it!


3. What does the world need that you can provide? Make a plan. Utilize the internet for resources and training. These are interesting times, ones that test the foundations of our morals, beliefs and integrity.



Without a doubt, we as a collective world, have strayed far from our sustainable roots. We have allowed fast, cheap and convenient to lure us into a false state of pleasure and security. We have been massively distracted by social media and mindless entertainment. We have become dangerously disconnected from the present by electronics and social media and we have become dependent on “the market place” for our basic survival needs. In truth, most people have been disconnected and isolated for years, not really knowing their “purpose”.


It is human nature to need motivation. Contrast (experiencing what is NOT wanted) and adversity stimulate the co-creative mind to find solutions to problems the world needs. Every one of us has unique skills and passion, enabling everyone to be a part of the “new world” that will emerge as we transform and grow from where we were to where we are going.


This worldwide crisis is an opportunity for positive change. Choose to be a part of the solution, embracing the fact that it will be far different than the “life” we have come to know. Connect deeply within, to the spiritual truths and core values, to create a world of kindness and compassion while awakening the core values of life itself, honoring mankind and mother earth.


We have 2 feet to move our bodies, but animals have 4 feet to move our soul…


For specific questions and resources, contact me at

Marlene Siegal, DVM. BRMI Veterinary Advisor

Recent Posts

Lianhua Qingwen Capsule (granule) Approved for Treatment of COVID-19

Lianhua Qingwen Capsule (granule) Approved for Treatment of COVID-19

April 22, 2020

Lianhua Qingwen Capsule (granule) Approved for Treatment of COVID-19

Dr. James Odell, ND, OMD, L.Ac.

On April 14, 2020, Yiling Pharmaceutical announced that the traditional Chinese medicine herbal formulation Lianhua Qingwen capsules (granules) were approved by The State Administration for Market Regulation People’s Republic of China to add functional indications to the originally approved indications: “In the conventional treatment of novel coronavirus pneumonia, Lianhua Qingwen can be used for common type of fever, cough, and fatigue, in treatment lasting for 7-10 days.”


During the epidemic in China, Lianhua Qingwen capsules (granules) became the most frequently recommended Chinese herbal patent medicine for treatment of COVID 19. The efficacy of the Lianhua Qingwen capsule (granule) in the treatment of COVID and influenza viruses has been previously confirmed by numerous in vitro, animal and clinical studies (see references). In studies it exerted broad-spectrum antiviral effects on a series of influenza viruses and immune regulatory effects Recently, Runfeng, Li, and his team published a paper entitled “Lianhuaqingwen exerts anti-viral and anti-inflammatory activity against novel coronavirus (SARS-CoV-2).” in the international journal Pharmacology Research. This is the first basic research article demonstrating the effectiveness of this Chinese patent herbal medicine against SARS-Cov-2. In this study, it was found that “Lianhua Qingwen exerted its anti-coronavirus activity by inhibiting virus replication and reducing the cytokine release from host cells, which supported the clinical application of LH in combination with existing therapies to treat COVID-2019.” The authors further concluded, “ These findings indicate that LH protects against the virus attack, making its use a novel strategy for controlling the COVID-19 disease.”


Composition of Formula:


Lianhua-Qingwen capsule (LQC), developed from the two classical traditional Chinese medicine (TCM) formulae Maxing-Shigan-Tang and Yinqiao-San, both which have a long history of clinical application in the treatment of influenza. It has become a popular and commonly used traditional Chinese herbal preparation to treat viral influenza. It especially played an important role in the fight against severe acute respiratory syndrome (SARS) in 2002-2003 in China. LQC is composed of 11 herbs including Fructus Forsythiae (Lianqiao), Flos Lonicerae Japonicae (Jinyinhua), Herba Ephedrae (Mahuang), Semen Armeniacae Amarum (Kuxingren), Radix Isatidis (Banlangen), Rhizoma Dryopteridis Crassirhizomatis (Mianmaguanzhong), Herba Houttuyniae (Yuxingcao), Herba Pogostemonis (Guanghuoxiang), Radix et Rhizoma Rhei (Dahuang), Radix et Rhizoma Rhodiolae Crenulatae (Hongjingtian), and Radix et Rhizoma Glycyrrhizae (Gancao), along with menthol and a traditional Chinese mineral medicine, Gypsum Fibrosum (Shigao).




Unfortunately, this formula must be ordered online. Thus, it may be a month or more wait when ordering this formula online.




Ding, Yuewen, Lijuan Zeng, Runfeng Li, Qiaoyan Chen, Beixian Zhou, Qiaolian Chen, Pui leng Cheng et al. “The Chinese prescription lianhuaqingwen capsule exerts anti-influenza activity through the inhibition of viral propagation and impacts immune function.” BMC complementary and alternative medicine 17, no. 1 (2017): 130.


Duan, Zhong-ping, Zhen-hua Jia, Jian Zhang, Liu Shuang, Chen Yu, Lian-chun Liang, Chang-qing Zhang et al. “Natural herbal medicine Lianhuaqingwen capsule anti-influenza A (H1N1) trial: a randomized, double blind, positive controlled clinical trial.” Chinese medical journal 124, no. 18 (2011): 2925-2933.


Hai, Guo, Yang Jin, Gong Jiening, and Zhang Qinghong. “Effect of Lianhua Qingwen Capsule on Pulmonary Index of Mice with Viral Infection [J].” Henan Traditional Chinese Medicine 3 (2007).


Jia, Weina, Chunhua Wang, Yuefei Wang, Guixiang Pan, Miaomiao Jiang, Zheng Li, and Yan Zhu. “Qualitative and quantitative analysis of the major constituents in Chinese medical preparation Lianhua-Qingwen capsule by UPLC-DAD-QTOF-MS.” The Scientific World Journal 2015 (2015).


Mo, Hongying, Changwen KE, Jingping ZHENG, and Nanshan ZHONG. “Anti-viral Effects of Lianhua Qingwen Capsule Against Influenza A Virus in Vitro [J].” Traditional Chinese Drug Research & Clinical Pharmacology 1 (2007).


Ouyang, Huixiang, Qingyan TANG, Yongzhong CHEN, Yu WEI, and Guoshu LI. “Clinical observation of Lianhua Qingwen Department of Emergency, Capsules in treatment of the influenza A/H1N1 [J].” China Medical Herald 30 (2010).


Runfeng, Li, Hou Yunlong, Huang Jicheng, Pan Weiqi, Ma Qinhai, Shi Yongxia, Li Chufang et al. “Lianhuaqingwen exerts anti-viral and anti-inflammatory activity against novel coronavirus (SARS-CoV-2).” Pharmacological research (2020): 104761.


Wang, Chun-Hua, Yi Zhong, Yan Zhang, Jin-Ping Liu, Yue-Fei Wang, Wei-Na Jia, Guo-Cai Wang, Zheng Li, Yan Zhu, and Xiu-Mei Gao. “A network analysis of the Chinese medicine Lianhua-Qingwen formula to identify its main effective components.” Molecular BioSystems 12, no. 2 (2016): 606-613.


Yang, Libo, J. I. Zhenhui, Xuedong Gao, and G. U. Chunhua. “Phase Ⅱ Clinical Study of Lianhua Qingwen Capsule for Influenza.” Traditional Chinese Drug Research & Clinical Pharmacology 04 (1993).


Yan-xia, LIU Geng-xin ZHANG, and Y. A. N. G. Ji-qing. “The randomized controlled study of Lianhuaqingwen capsule in treating A/H1N1 influenza.” Chinese Journal of Difficult and Complicated Cases 1 (2010): 9.

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BRMI is a non-commercial website and does not specifically endorse any products or services mentioned in this biography (or on this site generally).

Coronavirus: Overcome Fear with Facts & Confidence

Coronavirus: Overcome Fear with Facts & Confidence

March 17, 2020

Coronavirus: Overcome Fear with Facts & Confidence

Naturopathic Newsletter Alpstein Clinic Gais, Switzerland (17.3.2020)

Naturopathic Newsletter Alpstein Clinic Gais, Switzerland (17.3.2020)


Data, background, active prevention, and treatment with integrative biological medicine


As we all know, large parts of Europe and North America are in a pandemic state of emergency. The reason for it is the supposedly high levels of aggressiveness and death rates from Coronavirus. But in our expert medical opinions, the unprecedented media madness and intensity is the biggest problem – causing unnecessary and cumbersome levels of fear and hysteria across the globe.


So, what are the real facts and causes? How dangerous is Coronavirus compared to the annual influenza virus/flu? Why isn’t a major emphasis being placed on the vast population’s capability to remain healthy and our immune system’s ability to defend itself against viruses, including Coronavirus – while also using natural, biological methods to help strengthen and empower the immune system?


Alpstein Clinic is here to help eliminate unnecessary fear and hysteria regarding this extraordinary Coronavirus topic. We are also grateful for the opportunity to greet you and share competent advice that will allow us to help safeguard everyone’s health, families, friends, communities, and vitality.


True Facts


The COVID-19 Coronavirus was first diagnosed in the Chinese city of Wuhan in December 2019. Since then, approximately 80,000 cases of illness and approximately 3,000 deaths have been recorded in this city. The rate of newly infected persons in China appears to be regressing. As is typical for a flu-like virus, the Coronavirus incubation period is 3-14 days and, clinically, symptoms include body aches, runny nose, fever, cough, and shortness of breath.


In very rare cases, severe respiratory failure may occur due to pneumonia, circulatory collapse, and kidney failure. As of today, 7,272 positive Coronavirus infections have been confirmed in Germany — and 17 cases with fatality (= 0.233%) have been registered. In Switzerland, the numbers are 2,330, cases with 19 fatalities (= 0.815%) and in the US, the numbers are 4,661, cases with 85 fatalities (= 1.823%) reported (source: John Hopkins Institute, New York, 3467b48e9ecf6


According to sensible estimations, a very small number of cases vary from the data of past flu outbreaks. Central Europe experienced an unusually strong wave of influenza in the 2017/2018 season, which affected around 25,100 Germans, who have consequently lost their lives (Quelle: Deutsches Ärzteblatt,


In 2019, approximately 19 million were affected by the flu virus in the USA, of which 180,000 required hospitalization and approximately 10,000 died (source: Statistica 2019).


In 2018, the World Health Organization registered 140,000 deaths from measles, 405,000 deaths from malaria, and 1.5 million deaths from tuberculosis. The flu outbreak from 2108 claimed approximately 650,000 lives. These numbers are countered by the above-mentioned figures of Coronavirus. Readers should make judgments and comparisons for themselves. . .


How does our virus and immune defense work?


It is very unfortunate that the media rarely focuses on the scientific evidence that the human body has a highly effective and intelligent defense system against viruses and invaders. As the first illustration depicts, viruses are tackled by our humoral and cellular immune response. This is preceded by our mucous membranes, which inhibit the penetration of the viruses via an antibody-containing mucus layer. Since viruses can only multiply in a host cell, it is essential that the cell wall of mucous membranes must not be destabilized by external and internal toxins (and a lack of unsaturated fatty acids).

The majority of our immune cells are located in the lymph system, lymph nodes, and immune organs, which are primarily the spleen, thymus, intestine, and bone marrow. The secondary immune organs, such as tonsils, appendix, and copper-like star cells of the liver are important and must not be left out. Since most children have a high immune activity via the primary and secondary immune organs compared to adults and elderly people, children are less sensitive to developing life-threatening virus complications. Additionally, since almost 60 percent of our lymph and immune cells are located in the abdomen, our digestive tract is very important in the defense against mucous membranes. Thus, the intestine is a key element of risk control and infection prevention, with a view at the major complication of the viral flu – pneumonia.


Effective flu prevention and virus defense is natural and always possible


Let’s differentiate between general and specific therapy components, which enable preventive and therapeutic measures against viruses. Figure 2 sums up all essential and scientificallybased factors that trigger and influence activity and efficiency of our immune system. It is important to emphasize a famous principle “The microbe is nothing, the milieu is everything” (Dr. A. Bechamp); viruses are less the cause of disease BUT the symptom of an imbalance of other primary components. Only with a causative-oriented approach as is the principle of Alpstein Clinic (i.e. whole-body medicine), can we succeed against any systemic disease, including the Coronavirus-related flu.


These causative triggers are also responsible for and lead to chronic illness, comprised immune system, and especially elderly people having the greatest risk of dying from virusrelated compli




The graphics below demonstrate our primary recommendations to diminish coronavirus risks, fear, and anxiety. Most measures are simple, inexpensive, and possible without requiring a doctor’s visit or a major clinic. We recommend these exceptional naturopathic remedies for immediate use.


1. Cistus Incanus (CYSTUS 052®) pastille, forms a protective layer on oral/pharynx mucosa and digestive tract mucosa, for prevention: 3×1 pastille per day or suck one every hour if a sore throat begins;


2. OSCILLOCOCCINUM®, homeopathic organ preparation from spleen and liver, stimulation of primary lymph organs, for prevention: allow 5 globules to dissolve in the mouth daily, take one tube per day if flu-like symptoms begin;


3. Glandula Thymi D6 Capsules (Sanum-Kehlbeck), homeopathic organ preparation from thymus, stimulation of the thymus and maturation of T-lymphocytes, for prevention: 2 capsules per week, 1 capsule daily in case of health complaints;


4. GRIPP-Heel® tablets (Heel), homeopathic complex: for prevention, suck 2-3x 1 tablet; or 6 tablets daily when symptomatic;


5. METAVIRULENT® drops (meta Fackler), homeopathic complex with Influenzinum nosode and lactic acid additionally: for prevention, use 3×10 drops or 12×5-10 drops when health complaints are present.


Offer for multi-morbid and high-risk patients to actively prevent virus flu outbrea


As always, we are here to provide guidance and therapeutic remedies and treatments. Each day, we are fulfilling and shipping remedies to patients, individuals, and families across the globe to help strengthen the immune system. For new Alpstein patients, all that is required is a consultation, which can be scheduled as a phone call or as a web-based Zoom Video Conference.


For an intensive (and onsite) active prevention package, we offer the Alpstein “Immune Building Day”. It contains highly effective therapies that last for approximately five hours, including a 60-minute Iratherm® whole-body hyperthermia (for fever therapy); high-dose infusions with antiviral, lymph activating, and immune system-relevant amino acids; intramuscular injection of thymus and spleen organo-peptide extracts; and a medical colon cleansing with ozone and gentle hydrotherapy as well as special acupuncture/acupressure therapies.


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Triclosan Free Hand Sanitizer Recipe:

Triclosan Free Hand Sanitizer Recipe:

March 11, 2020

Triclosan Free Hand Sanitizer Recipe:

Recipe by Dr. James Odell, ND, OMD, L.Ac

Everclear Alcohol (190 proof): 3/4 parts


Aloe Vera juice: 1/4 parts


Tea Tree Oil and Lemon Oil – several drops for scent and antimicrobial and anti-parasitic effect.

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