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-2 ‘vaccines’ 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?
Conclusion
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.
References
Ehrenfeld M, Tincani A, Andreoli L, et al. Covid-19 and autoimmunity. Autoimmun Rev 2020;19:102597.https://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-S1568997220301610/first-page-pdf
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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7271072/
Shoenfeld, Yehuda, and David A. Isenberg. "The mosaic of autoimmunity." Immunology today 10, no. 4 (1989): 123-126. https://www.sciencedirect.com/science/article/abs/pii/0167569989902454
COHEN, ARNON DOV, and YEHUDA SHOENFELD. "The viral-autoimmunity relationship." Viral immunology 8, no. 1 (1995): 1-9. https://www.liebertpub.com/doi/abs/10.1089/vim.1995.8.1?journalCode=vim
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). https://www.medrxiv.org/content/medrxiv/early/2020/05/01/2020.04.27.20077180.full.pdf
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). https://ascpt.onlinelibrary.wiley.com/doi/pdf/10.1111/cts.12805
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. https://www.sciencedirect.com/science/article/abs/pii/0002934376907622
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. https://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.903.366&rep=rep1&type=pdf
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. https://jamanetwork.com/journals/jama/fullarticle/199859
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. https://academic.oup.com/cid/article/54/6/800/290493?fbclid=IwAR3sAcwhLS-WMjPn8DyBGSPxtqbGJHTHGrnP4io9nYVroZQG5t0sJHtcMNc
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.
Haber, Penina, James Sejvar, Yann Mikaeloff, and Frank DeStefano. "Vaccines and guillain-barre syndrome." Drug Safety 32, no. 4 (2009): 309-323. https://link.springer.com/article/10.2165/00002018-200932040-00005
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. https://encephalitis.by/wp-content/uploads/2020/02/vaccines-and-the-risk-of-guillain-barr-syndrome-2019.pdf
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. https://academic.oup.com/jid/article/200/3/321/900101
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. https://www.sciencedirect.com/science/article/abs/pii/S1473309910701407
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. https://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.903.366&rep=rep1&type=pdf
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. https://www.sciencedirect.com/science/article/pii/S0264410X10013319
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. https://academic.oup.com/aje/article/175/11/1100/140453
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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7092860/
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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7092860/
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. https://www.jimmunol.org/content/jimmunol/181/9/6337.full.pdf
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). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6478436/
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. http://sa.uploads.ru/SU2xL.pdf
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. https://www.nature.com/articles/nm918
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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5858873/
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. https://link.springer.com/article/10.1007%2Fs00705-013-1645-3
Iwasaki, Akiko, and Yexin Yang. "The potential danger of suboptimal antibody responses in COVID-19." Nature Reviews Immunology 20, no. 6 (2020): 339-341. https://www.nature.com/articles/s41577-020-0321-6?fbclid=IwAR2OHhAhzFzJpqZOEI_ifMLBpihW-beWYoGQ0L4XJ5cDQRpleOQ5kQ9lH28
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. https://jvi.asm.org/content/jvi/89/6/2995.full.pdf
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. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0035421&fbclid=IwAR2uGSe8kP-_ceHlnwMqM-H-MvUksEdg80MS5lCrAIGvne00B08bIScOn-M
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 https://jvi.asm.org/content/jvi/88/15/8597.full.pdf
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. https://jvi.asm.org/content/jvi/85/23/12201.full.pdf
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. https://www.nature.com/articles/s41586-020-2538-8?ref=theprepping-com
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. https://arthritis-research.biomedcentral.com/articles/10.1186/ar4500
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. https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.22739
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. https://www.tandfonline.com/doi/pdf/10.1517/17425247.2012.720969
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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6512330/
Douglas, R. Gordon, and Vijay B. Samant. "The vaccine industry." Plotkin's Vaccines (2018): 41. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7151793/
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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247514/
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). https://www.nejm.org/doi/full/10.1056/NEJMoa2022483
Sahin, U. et al. Concurrent human antibody and TH1 type T-cell responses elicited by a COVID-19 RNA vaccine. Preprint at https://www.medrxiv.org/content/10.1101/2020.07.17.20140533v1 (2020).
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. https://www.medrxiv.org/content/10.1101/2020.09.23.20199604v1 (2020)
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. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31208-3/fulltext?fbclid=IwAR0D3ml3K1WdmZ-G_WfyPh2M5dpwqDXdcntJHvw7U0SbD3Rzm5OoYb69XkA
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.
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.