James Odell, OMD, ND, L.Ac.
Many claims are being made about COVID-19 inoculations, (misnamed “vaccines”) and what they do and do not do. The problem is that measurements are constantly being manipulated and misrepresented. What is clear is that inoculation adverse reactions and deaths are exponentially increasing at a terrifying rate. In addition to the hundreds of thousands of adverse events reported to the CDC Vaccine Adverse Event Reporting System (VAERS) and the European EndraVigilance Database Management System, as of March 2022, more than 1000 peer-reviewed studies have evidenced a multitude of adverse events in COVID-19 inoculation recipients.1 Such studies report severe adverse reactions following the shot, including thrombosis, thrombocytopenia, myocarditis, pericarditis, cardiac arrhythmias, nervous system disorders, and other alterations. It is noteworthy that several of the aforesaid side effects had already been reported in the confidential post-authorization cumulative analysis released as part of a Freedom of Information Act (FOIA) procedure, which provides data on deaths and adverse events recorded by Pfizer from 14 December 2020 to 28 February 2021.2
Additionally, numerous clinicians and studies have been reporting that COVID-19 mRNA genetic experimental inoculations are depleting specific cellular immunity in certain individuals and causing pathological autoimmunity and tumor development in others., 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22
These gene-based biologicals are not vaccines, as research has shown that the inoculations do not prevent infection or transmission and that their effectiveness against symptomatic coronavirus infection wanes progressively over time.23 This loss of effectiveness instead of being realistically viewed as “vaccine” failure and abandoned is instead propagated by the pharmaceutical industry that boosters will be needed every 3 to 6 months.
With waning effectiveness, the rise in serious adverse event risk and deaths, and the potential that inoculations over time are dysregulating and depleting cellular immunity, many scientists and doctors strongly believe this experimental COVID-19 inoculation program should be immediately halted until further research is performed. This paper highlights important cellular immune mechanisms and abnormal cellular immune responses related to COVID-19 inoculations.
Cellular Immunity Overview
The immune system comprises a complex network of cellular and molecular components subdivided into thymus-independent (innate) and thymus-dependent (adaptive) arms which function synergistically in all immune responses. Innate immunity constitutes the first line of defense and is mediated by innate immune cells (white cells) such as tissue macrophages and granulocytes which elicit their function within minutes to hours following antigen-pathogen exposure. Once activated these innate immune cells can effectively clear toxic antigens through a process called phagocytosis. Dendritic cells take up and process these antigens and serve as antigen-presenting cells for the priming of the adaptive immune system. In this way, the early innate response is coupled to and facilitates adaptive immunity.
Lymphocytes are a type of white blood cell that helps the body fight infection and play a major role in adaptive immunity. There are two main types of lymphocytes: B-lymphocytes and T-lymphocytes and they differ in their structure and function. The B cells are responsible for humoral immunity and T cells are required for cell-mediated immunity. The B cells secrete antibodies, which are transported by blood, hence they can work over a long distance, whereas T cells can migrate to the target tissues and act locally.
There are surface proteins present, which differentiate the subtypes of lymphocytes. They are known as the cluster of differentiation or CD markers. Thus, T and B lymphocytes express specific antigen recognition receptors and develop highly specialized effector functions with the ability to form long-term immunological memory. Lymphocytes are primarily concentrated in the lymphoid organs, e.g., spleen, lymph nodes, tonsils, etc., and initiate the immune response against the foreign pathogen.
The normal lymphocyte count is 1000 to 4800 per µl. An increase or decrease in the lymphocyte count has clinical significance. The increase in lymphocyte count is known as lymphocytosis. It is an indication of cytotoxicity (biological terrain toxicity) and can indicate leukemia. The decrease in the lymphocyte count from the normal range is known as lymphocytopenia. It is associated with immune deficiency diseases, malnutrition, and certain inherited disorders.
T Cell Lymphocytes
T lymphocytes differentiate into subtypes. For the purpose of this discussion, I will focus on CD4 and CD8 T-Cell lymphocytes. CD4 T-cells, also known as T-helper cells, are T-lymphocytes that have molecules called CD4 on their surface. They start the immune response by signaling other defensive immune cells (white cells) like macrophages, B lymphocytes, and cytotoxic T-cells to act against toxic antigens.
CD8 T-cells, also known as cytotoxic T cells, contain CD8 membrane glycoprotein on their surface.
CD8 T-cells (cytotoxic T cells) are key lymphocytes of the adaptive immune system. Cytotoxic T cells are also known as ‘killer’ T cells thanks to their role in the destruction of infected cells, pathogens, and tumor cells. The main way they do this is via the transfer of cytotoxic granules to infected target cells, which kill the cell and any pathogens it contains.
Cytotoxic T cells attack infected cells and cancer cells.
When overactive they participate in autoimmune diseases.
Like helper T cells, cytotoxic T cells are activated by antigen-presenting cells in the lymph nodes. However, whereas helper T cells mediate the activity of other immune cells against a pathogen, cytotoxic T cells directly attack and destroy infected host cells. Cytotoxic T cells contain cytotoxic granules containing proteins called perforin and granzymes, which work together to destroy target cells. When they encounter an infected cell, cytotoxic T cells bind to the major histocompatibility complexes via their TCR receptors and release their cytotoxic granules. There are two types of major histocompatibility complexes found on the surface of APCs; these are MCHI and MCHII. The key difference in the activation of helper T cells vs. cytotoxic T cells is that they each bind to a different type of MCH receptor. Cytotoxic T cells bind to MHCI complexes, whereas helper T cells can only bind to MHCII complexes.
Perforin creates holes in the cell membrane of the target cell, and granzymes enter the cell via these pores. Once inside, the granzymes initiate apoptosis (programmed cell death) which kills the cell and any pathogens it contains. Thus, upon recognition, their purpose becomes the removal of damaged infected cells, bacteria, and tumor fragments (such as cancer cells) through apoptosis. Perforin and granzyme secretion is the main weapon of the cytotoxic T cell, but it is not their only function. Cytotoxic T cells also secrete cytokines, which contribute to the adaptive immune response in several ways.
One of these cytokines (IFN-γ) directly inhibits viral replication, which helps to slow the spread of infection in the body. IFN-γ also activates macrophages and stimulates them to migrate to sites of infection, where they function both as effector cells (as they engulf and destroy pathogens) and as antigen-presenting cells.
Activation of Cytotoxic T Cells
All T cells are considered ‘naïve’ until they encounter their specific antigen. Like helper T cells, cytotoxic T cells are specific to just one type of antigen. However, they cannot bind to their antigen directly; instead, they rely on assistance from antigen-presenting cells (APCs). APCs (such as dendritic cells, macrophages, and B cells) find and engulf invading pathogens before digesting them into protein fragments. Some of these fragments are displayed on their surface as part of a structure called the Major Histocompatibility Complex (MCH) and presented to T cells in the lymph nodes. When a cytotoxic T cell encounters its specific antigen on the surface of an APC, its TCR binds to the MHC and the T cell is activated.
Cytotoxic T cells are key players in the adaptive immune response and are highly effective in clearing infected cells from the body. However, if left unchecked, cytotoxic T cells can contribute to an excessive immune response (autoimmunity), resulting in damage to healthy host cells and tissues. Until recently, little was known about the importance of cytotoxic T cells (CD8+ T cells) in promoting autoimmune disease development. Later in this article, I present Dr. Professor Arne Burkhardt’s information that relates the “vaccine” adverse reaction to overactive cytotoxic T cells causing vasculitis and autoimmune systemic inflammation.
Cytotoxic T cells use perforin and granzymes to destroy target cells
Memory Cytotoxic T Cells
Memory cytotoxic T cells are the small percentage of cytotoxic T cells that remain in the body following the contraction phase. These cells persist in the immune system for a long time, and quickly recognize and launch an attack against the pathogen in the event of re-infection.
Absolute CD4 Count
The absolute CD4 count is a measurement of how many functional CD4 T-cells are circulating in the blood. The lower the absolute CD4 count, the weaker the innate immune response. The absolute CD4 count is measured by a simple blood test, the results of which are reported as the number of CD4 cells per cubic millimeter of blood.
Absolute CD4 Counts:
Normal: 600 to 1200 cells per cubic millimeter
Immune suppressed: Less than 500 cells per cubic millimeter
Critically suppressed: Less than 200 cells per cubic millimeter. Per the CDC, one of the indications for the diagnosis of AIDS is when the CD4 cell count drops below 200 cells/mm^3. The decline of CD4 T cells can lead to opportunistic infections and increases mortality.
The CD4 Percentage
The CD4 percentage represents the percentage of total lymphocytes that are CD4 cells and is measured using the same blood test as that for the absolute CD4 count. A normal CD4 percentage of about 40%, while a suppressed CD4 percentage can be as low as 25% or less. Clearly, the higher the percentage, the more robust the immune response.
CD4/CD8 Ratio as a Snapshot of Immune Health
Another way to gain better insights into the immune function is to additionally examine the CD4/CD8 percentage. This assesses the number of CD4 T-cells compared to the number of CD8 T-cells (cytotoxic T cells). This test can determine if the disease is progressing by tracking the depletion of cytotoxic T cells in blood samples. Historically, the immunological progression of the human immunodeficiency virus (HIV) is monitored by comparing the proportion of “helper” CD4 T cells to “killer” CD8 T cells, the value of which can help predict the likely course of the disease. Typically, in advancing disease, as the immune system becomes exhausted, it is less able to produce helper CD4 T-cells to defend itself. A CD4/CD8 ratio is considered normal when the value is between 1.0and 4.0. In a healthy individual, that translates to roughly 30-60% CD4 T cells in relationship to 10-30% CD8 T cells. Clinicians who have been monitoring the COVID inoculation adverse reactions have observed a significant drop in CD4 T cells and an increase in the CD8 T cells in these individuals.
COVID Inoculation Associated “Lymphocytic Amok” and Prolonged Autoimmune Development as Described by Dr. Professor Arne Burkhardt
[Dr. Arne Burkhardt, German pathologist, researcher; certified in medicine University Kiel, Germany; certified pathologist University Hamburg; Recipient Konjetzny prize Cancer Liga Hamburg, 1980; Member International Association Oral Pathologists (councilor 1992-1996).]
Dr. Professor Arne Burkhardt of Germany has performed detailed histological research with autopsies on patients who died after COVID-19 inoculations from such conditions as strokes, pericarditis, myocarditis, etc. In these individuals he documented with histology slides consistent dense infiltration of cytotoxic T-cells and specific lymphocytic pathological changes in the heart, small and large intestine, brain (dura), kidney, uterus, and lungs. Basically, he described this pathophysiological
inflammation and necrosis. He called this phenomenon “Lymphocyte-Amok” or lymphocyte-predominant tissue destruction/inflammation with imminent prolonged auto-immune disease development. He observed this lymphocytic infiltration in organs and soft tissues not normally associated with lymphocyte accumulation and concluded this infiltration to be related to the shot. The most common cause of death from this lymphocytic infiltration was myocarditis and the second cause of death was lymphocytic lung pneumonitis or alveolitis. He further noted that this lymphocytic alveolitis is often not diagnosed but is instead written off as COPD. Lymphocytic interstitial pneumonia or alveolitis is frequently associated with autoimmune diseases.
Not only did he show accumulations of lymphocytes in a wide variety of tissues, from the heart muscle to the kidney, liver, spleen, and uterus; he also showed images in which the tissue was massively attacked as a result, and a whole series of lymphocyte follicles, which are, as it were, small, developing lymph nodes in completely the wrong place, for example in lung tissue. It also showed detachments of endothelial cells – which are the smooth cells that form the wall of blood vessels – clumps of red blood cells that ultimately cause thrombosis, and giant cells that formed around trapped foreign bodies.
He concludes histopathologic analysis shows clear evidence of vaccine-induced autoimmune-like pathology in multiple organs. Those myriad adverse events deriving from such auto-attack processes must be expected to frequently occur in all individuals, particularly following booster injections, which is self-evident.
Without any doubt, the injection of these gene-based COVID-19 biological agents places lives under the threat of illness and death. We note that both mRNA and vector-based vaccines are represented among these cases, as are all four major manufacturers. Dr. Burkhardt strongly feels that this inoculation associated with “lymphocytic amok” is a very alarming finding particularly since millions of people worldwide have received these experimental inoculations.24
(Dr. Burkhardt’s videos are linked in the references)
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 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. Since the beginning of the Covid 19 mRNA gene inoculation rollout in 2020, it has been proposed that antibodies produced from the inoculations might contribute to the development of more severe and lethal presentations of COVID-19 possibly by triggering ADE.
Technically, the binding of virions complexed with antibodies to Fcγ receptors on the target cells initiates receptor-mediated signaling events, leading to enhanced expression of inflammatory cytokines and suppression of intracellular antiviral responses at the transcriptome level, followed by endocytosis of the virus and subsequent activation of immune cells. The activated immune cells accumulate in the lung, liver, or elsewhere and promote cytokine storm and lymphopenia. Furthermore, the formation of immune complexes can promote complement activation and subsequent tissue damage.25
This ADE phenomenon is apparently what Dr. Professor Arne Burkhardt’s histological findings have revealed. Thus, “Lymphocytic Amok” is another biological manifestation of ADE. The severity and potential fatality of ADE are greater in the aged and immune-compromised and those that have had repeated exposure to the COVID-19 inoculations (boosters).
Inoculations Causing Immune Exhaustion
More than three shots have been shown to deplete humoral immunity. In a February 2022 study entitled "Four doses of the inactivated SARS-CoV-2 vaccine redistribute humoral immune responses away from the Receptor Binding Domain”, the authors concluded “our data indicate that the 3rd dose is the turning point for repeated vaccination of inactive SARS vaccines made from ancestral viral strain. We observed a clear suppression of humoral immunity after the 4th dose.” They went on to say, “As a result of such suppression, peak levels of S binding, RBD binding, and RBD-Nabs (neutralizing antibodies) were all inferior to their counterparts after the 3rd dose. Our data reveal that immune responses cannot be endlessly elevated, while suppression of heightened immune responses focusing on one subunit together with a shift of immune responses to other subunits would occur after repeated vaccination.”26
Recently, this immune exhaustion conclusion has been vindicated by European Union regulators who warned that frequent COVID-19 booster shots could adversely affect the immune response and may not be feasible. The European Medicines Agency now claims, “repeat booster doses every four months could eventually weaken the immune response and tire out people.”27
CD4 Depletion Post Inoculation
Many doctors worldwide have been monitoring lymphocytes and particularly the CD4/CD8 dynamic in the COVID-19 mRNA inoculated population. They have observed a pattern of low CD4 numbers in many inoculated patients. Doctors are calling this low CD4 T-helper cell phenomenon in the repeatedly inoculated “immune erosion”, or “vaccine acquired immune deficiency syndrome” (VAIDS). This hematology pattern is associated with a post-inoculation illness that can either affect them more rapidly as with myocarditis and even death or more slowly, resulting in chronic infections and illnesses. Depleted or suppressed absolute CD4 counts from COVID-19 inoculations are a particular concern with those already immune-compromised or in patients on immunosuppressive drugs.28, 29, 30, 31, 32 Bear in mind, pharmaceutical financed “Fact Checker” services claim there is no such thing as a “vaccine-acquired immunodeficiency syndrome” or “VAIDS.”
Toxicity of Spike Protein (Spikopathy) and Lipid Nanoparticles
Both the spike proteins elicited by the mRNA inoculations and the lipid nanoparticles that enshroud the mRNA can damage cells and tissues of the body. Spike proteins are produced in the body after taking a Covid-19 mRNA jab, and they can fuse to cell membranes. The cells making the spike protein are then targeted by the immune system in an effort to destroy the spike protein. Thus, the immune system’s response to spike proteins can damage cells. The spike protein is the pathogen and can damage the body in several ways:
The spike protein can damage the endothelium of blood vessels creating microcirculatory clots that in turn can damage tissues and important vascular organs (lungs, heart, brain). Emerging evidence on “spikopathy” suggests that effects related to inflammation and micro-clotting may occur in any tissue in which the spike protein accumulates.
The spike protein via lipid nanoparticles can penetrate the blood-brain barrier, important for protecting the brain. Peer-reviewed studies have found that the spike protein is capable of crossing the blood-brain barrier.33 Thus, in humans, it could potentially lead to central nervous system damage (strokes, motor, and sensory nerve impairments).
The spike protein behaves as a hapten, a small molecule that binds to the surface of organs, leading to an autoimmune response and possible antibody-dependent enhancement (ADE). (As previously described.)
The mRNA spike protein can incorporate into human DNA through a process called reverse transcription.
The spike protein evokes the release of destructive anti-spike-antibodies, [anti-S-Ab]. The antibodies can also cross-react with 28 different human tissue types, establishing a mechanism for multi-system autoimmune disorders and multi-organ failure.33
Covid mRNA inoculations use only part of the virus’s genetic code. The mRNA inoculation carries code into the body, where it enters the cell and instructs those cells to create spike proteins that are allegedly associated with COVID-19 (the computer model). However, these inoculations “mis-train” the immune system to recognize only a small part of the virus (the spike protein). Variants that differ, even slightly, in this protein can escape the narrow spectrum of antibodies created by the inoculations (called vaccine escape).
According to the preeminent virologist and vaccine expert Dr. Geert Vanden Bossche:34
"As of the early days of the mass vaccination campaigns, at least a few experts
have been warning against the catastrophic impact such a program could have
on global and individual health. Mass vaccination in the middle of a pandemic
is prone to promoting selection and adaptation of immune escape variants that
are featured by increasing infectiousness and resistance to spike protein (S)-
directed antibodies (Abs), thereby diminishing protection in vaccinees and
threatening the unvaccinated."
"This already explains why the WHO’s mass vaccination program is not only unable to generate herd immunity but even leads to substantial erosion of the population’s immune protective capacity," he continues. "As the ongoing universal mass vaccination program will soon promote dominant propagation of highly infectious, neutralization escape mutants (i.e., so-called ‘S Ab-resistant variants’), naturally acquired, or vaccinal neutralizing Abs, will, indeed, no longer offer any protection to immunized individuals whereas high infectious pressure will continue to suppress the innate immune defense system of the nonvaccinated.”
"This is to say that every further increase in vaccine coverage rates will further contribute to forcing the virus into resistance to being neutralizing, S-specific Abs. Increased viral infectivity, combined with evasion from antiviral immunity, will inevitably result in an additional toll taken on human health and human lives."
Doctors are discovering more autoimmunity in their COVID-19 inoculated patients. This pathology appears to be partly associated with the toxic spike protein produced or introduced by the shot. Researchers are unsure how long this autoimmune response to the coronavirus spike protein may last. A paper entitled "A possible role for anti-idiotype antibodies in SARS-CoV-2 infection and vaccination”, published in the New England Journal of Medicine concluded: “Ab2 antibodies binding to the original receptor on normal cells, therefore, have the potential to mediate profound effects on the cell that could result in pathologic changes, particularly in the long term — long after the original antigen itself has disappeared.” 35
Thus, an indefinite, uncontrolled autoimmune response to the coronavirus spike protein may produce a wave of antibodies called anti-idiotype antibodies or Ab2s that continue to damage human bodies long after clearing either Sars-Cov-2 itself or those spike proteins that the shots cause the body's cells to produce. In other words, spike protein antibodies may themselves produce a second wave of antibodies, called anti-idiotype antibodies or Ab2s. Those Ab2s may modulate the immune system’s initial response by binding with and destroying the first wave of antibodies. It is speculated that these antibodies produced by the inoculation could be responsible for the current unprecedented wave of myocarditis and neurological illnesses, and deaths.
Lipid Nanoparticles in the Inoculation
In addition to the cellular toxicity of the spike protein, there are also toxic lipid nanoparticles.36, 37 An alleged goal of wrapping this mRNA in lipid nanoparticles is to optimize its cellular deliverability. However, certain lipid components are toxic to cells and may activate host immune responses following systemic or local administration. Thus, a major liability of liposome-based drug delivery is their potential to cause inflammatory toxicities through activation of the innate immune response.38
Innate immunity is triggered by the recognition of nonself particulate matter by macrophages and other hematopoietic cell populations through the engagement of pattern recognition receptors. TLR engagement promotes phagocytosis and the release of inflammatory intermediates such as chemokines and cytokines. This inflammatory response leads to tissue infiltration of monocytes and neutrophils, which ultimately causes tissue necrosis, hypotension, and other potentially severe sepsis-like toxicities. In addition, liposomes have also been shown to activate components of the complement pathway in blood, which increases the risk of anaphylactic shock.39
The COVID-19 mRNA inoculation contains a composition of four different lipids. One of the lipids used in the mRNA inoculation is a “cationic/ionizable lipid” (e.g., DOTMA, DOTAP/MC3, C12-200), and can disrupt cellular membranes. Cationic and ionizable lipids have also been reported to stimulate the secretion of pro-inflammatory cytokines and reactive oxygen species.40, 41, 42, 43
Another toxic lipid used in the jab’s lipid nanoparticle composition is polyethylene glycol (PEG) which has an extensively documented history of inducing hypersensitivity reactions by stimulating the complement system.44, 45 Thus, these lipid nanoparticles among other potentially toxic mechanisms, have the ability to disrupt cellular membranes, cause inflammation, and oxidative stress.
Organ and Tissue Biodistribution and Duration of mRNA Inoculation
Biodistribution studies are fundamental to determine in which tissues and organs an injected compound travels and accumulates. Up to now, no such evaluation has been carried out on humans for any of the emergency use approved COVID-19 vaccines. As concerns the Pfizer/BioNTech BNT162b2 vaccine, it is injected into the deltoid muscle, which drains primarily to the axillary lymph nodes. Theoretically, the lipid nanoparticles (LNPs) in which the mRNA is encapsulated should have a very restricted biodistribution, targeting the draining axillary lymph nodes. However, a pharmacokinetic study performed by Pfizer for the Japanese regulatory agency shows that the LNPs display an off-target distribution in rodents, accumulating in organs such as the spleen, liver, pituitary gland, thyroid, ovaries, and other tissues.46
Similarly, the results of the European Medicines Agency assessment reports show an off-target distribution of the LNPs used by Pfizer/BioNTech and Moderna, in the liver and other organs of rodents.47
In another study published in November 2021 in the Journal of Immunology, the spike proteins made in the body after receiving a Pfizer COVID-19 shot have been found on tiny membrane vesicles called exosomes, that mediate cell-to-cell communication by transferring genetic materials to other cells, for at least four months after the second vaccine dose.48
It is vitally important to understand that every human cell that intakes the LNPs and translates the viral spike protein (in case of the mRNA vaccines), or that gets infected by the adenovirus and expresses and translates the viral spike protein (in case of the adenovirus-based vaccines), is inevitably recognized as a threat by the immune system and killed. There are no exceptions to this mechanism. The severity of the resulting damage and the consequences for health depend on the quantity of the cells involved, on the type of tissue, and on the strength of the following autoimmune reaction. For instance, if the mRNA contained in the LNPs would get internalized by cardiac myocytes, and such cells would produce the spike protein, the resulting inflammation would likely lead to the necrosis of the myocardium, with an extent proportional to the number of involved cells.49
The persistence of the spike protein in the body “raises the prospect of sustained inflammation within and damage to organs which express the spike protein,” according to Michael Palmer, MD, and Sucharit Bhakdi, MD at Doctors for COVID Ethics, an organization consisting of physicians and scientists “seeking to uphold medical ethics, patient safety, and human rights in response to COVID-19.”50, 51
Thus, it has been revealed that the spike protein on its own is enough to cause inflammation and damage to the vascular system, even independent of a virus. It is neurotoxic and these spike proteins can continue to generate and circulate in the body long after injection, causing chronic damage to cells, tissues, and organs.
mRNA Reverse Transcription
Pharmaceutically funded Fact Checker services and the CDC still claim that the mRNA COVID-19 gene inoculations “do not change or interact with your DNA in any way.” The CDC says on a web page titled “Myths and Facts about COVID-19 Vaccines'' that the “genetic material delivered by mRNA vaccines never enters the nucleus of your cells.” However, a new Swedish study finds Pfizer’s shot indeed enters liver cells and converts or reverse transcribes to DNA. The researchers found that when the mRNA material enters the human liver cells, it triggers the cell’s DNA, which is inside the nucleus, to increase the production of the LINE-1 gene expression to make mRNA.52
The mRNA then leaves the nucleus and enters the cell’s cytoplasm, where it translates into LINE-1 protein. A segment of the protein called the open reading frame-1, or ORF-1, then goes back into the nucleus, where it attaches to the vaccine’s mRNA and reverse transcribes into spike DNA. Reverse transcription is when DNA is made from RNA, whereas the normal transcription process involves a portion of the DNA serving as a template to make an mRNA molecule inside the nucleus.
They conclude, “In this study, we present evidence that COVID-19 mRNA vaccine BNT162b2 is able to enter the human liver cell line Huh7 in vitro,” the researchers wrote in the study, published in Current Issues of Molecular Biology. “BNT162b2 mRNA is reverse transcribed intracellularly into DNA as fast as 6 [hours] after BNT162b2 exposure.” BNT162b2 is another name for the Pfizer-BioNTech COVID-19 vaccine that is marketed under the brand name Comirnaty.
Additionally, the Swedish study also found spike proteins expressed on the surface of the liver cells that researchers say may be targeted by the immune system and possibly cause autoimmune hepatitis, as “there [have] been case reports on individuals who developed autoimmune hepatitis after BNT162b2 vaccination.”
The Swedish authors also reported of a healthy 35-year-old female who developed autoimmune hepatitis a week after her first dose of the Pfizer COVID-19 vaccine said that there is a possibility that “spike-directed antibodies induced by vaccination may also trigger autoimmune conditions in predisposed individuals” as it has been shown that “severe cases of SARS-CoV-2 infection are characterized by an autoinflammatory dysregulation that contributes to tissue damage,” for which the virus’s spike protein appears to be responsible.53
Whether the findings of the study will occur in living organisms or if the DNA converted from the vaccine’s mRNA will integrate with the cell’s genome is unknown. The authors said more investigations are needed, including in whole living organisms such as animals, to better understand the potential effects of the mRNA vaccine. They write, “At this stage, we do not know if DNA reverse transcribed from BNT162b2 is integrated into the cell genome. Further studies are needed to demonstrate the effect of BNT162b2 on genomic integrity, including whole-genome sequencing of cells exposed to BNT162b2, as well as tissues from human subjects who received BNT162b2 vaccination.”
Dr. Peter McCullough, internist, cardiologist, and epidemiologist, who is one of the leading critics of the COVID-19 “vaccines”, said the findings have “enormous implications of permanent chromosomal change” that could drive a “whole new genre of chronic disease.”54
Monitoring Laboratory Values
Many clinicians monitor CD4 and CD8 T cell lymphocyte ratios and numbers, as well as clot markers such as D-dimer, platelet count, fibrinogen, and the inflammation marker C-reactive protein in Covid-19, inoculated individuals. Some have also ventured into conducting what is termed a Cytokine 14 panel. This is often helpful in better understanding the immunological pathophysiology of a Covid 19 inoculation reaction.
This panel includes IL-2, IL-4, IL-6, IL-8, IL-10, IL-13, GM-GSF, SCD40L, CCL3 (MIP-1 ALPHA), CCL4 (MIP-1 BETA), CCL5 (RANTES), TNF-ALPHA, IFN-GAMMA, and VEGF.
Abnormalities in the levels of these specific 14 cytokines and chemokines have been identified in “cytokine storms” associated with the Covid spike protein and associated vasculitis. Preliminary findings show IL-2, IL-4, CCL3, IL-6, IL-10, IFN-gamma, and VEGF are often elevated in chronically Covid impaired patients. Conversely, CCL4 and GM-GSF are often found to be diminished.
Brief Overview of the Panel:
IL-2 is responsible for the proliferation and activation of T cells, B cells, and NK cells.
IL-4 is a cytokine that induces the differentiation of naïve T cells to Th2 cells. Upon activation by IL-4, Th2 cells subsequently produce additional IL-4 in a positive feedback loop. IL-4 is produced primarily by mast cells, Th2 cells, eosinophils, and basophils.
IL-6 is a pro-inflammatory cytokine whose major function is the differentiation of B-cells into plasma cells and IgG production. IL-6 has been associated with oxidative stress, inflammation, endothelial dysfunction, and thrombogenesis.
IL-8 is a chemokine that is released early post-injury mainly by macrophages and is one of the major mediators of the inflammatory response. It is secreted by several cell types such as epithelial cells, airway smooth muscle cells, and endothelial cells, and functions as a chemoattractant and as a potent angiogenic factor. It is like IL-6 but has a longer half-life.
IL-10 is an anti-inflammatory cytokine that maintains the balance of the immune response, allowing the clearance of infection while minimizing damage to the host. IL-10 can also dampen the harmful immune responses elicited in autoimmunity and allergy. However, the consequence of this activity is that IL-10 when elevated can contribute to chronic infection.
IL-13 is closely related to IL-4 in biological function but, in general, the responses of cells to IL-13 are smaller in magnitude. It is secreted by T helper type 2 (Th2) cells, CD4 cells, natural killer T cell, mast cells, basophils, and eosinophils. Interleukin-13 is a central regulator in IgE synthesis, goblet cell hyperplasia, mucus hypersecretion, airway hyperresponsiveness, fibrosis, and chitinase up-regulation. It is a mediator of allergic inflammation and different diseases including asthma as it regulates the function of human B cells and monocytes.
GM-GSF or Granulocyte-macrophage colony-stimulating factor, also known as colony-stimulating factor 2, is a monomeric glycoprotein secreted by macrophages, T cells, mast cells, natural killer cells, endothelial cells, and fibroblasts that functions as a cytokine.
CCL3 (macrophage inflammatory protein-1 α, MIP-1α), belonging to the CC chemokine family, is involved in the acute inflammatory state and in the recruitment and activation of polymorphonuclear leukocytes and in macrophage and NK-cell migration as well as T-cell dendritic cell interactions.
CCL4 (Macrophage inflammatory protein-1β (MIP-1β), belonging to the CC chemokine family, is involved in macrophage and NK-cell migration as well as T-cell/dendritic interactions. It is a chemoattractant for natural killer cells, monocytes, and a variety of other immune cells.
CCL5 (also known as RANTES) may promote the infiltration of NK cells into the liver during acute and chronic liver injury via interaction with CCR1 expressed on NK cells. Thus, it is involved in macrophage and NK-cell migration as well as T-cell /dendritic cell interactions. Emerging studies show that changes to CCL5 or CCR5 at the DNA, RNA, and/or protein level may be associated with the development or progression of cancer.
TNF-alpha (Tumor necrosis factor-alpha) was initially recognized as a factor that causes the necrosis of tumors, but it has been recently identified to have additional important functions as a pathological component of autoimmune diseases. It is a pro-inflammatory cytokine, associated with phagocyte cell activation and endotoxic shock. It is mainly produced by activated macrophages, T lymphocytes, and natural killer (NK) cells.
It is beyond terrifying that these inoculations are now shown to deplete CD4 cells (helper T cells) and cause CD8 infiltrates to attack organs and tissues leading to autoimmune vasculitis, heart attacks, strokes, etc. It is undetermined how long the body continues to manufacture the toxic spike protein after injection. The biodistribution of the spike protein is systemically extensive and can accumulate in organs such as the brain, spleen, liver, pituitary gland, thyroid, ovaries, testes, and other tissues. Equally disturbing is that the inoculation can potentially cause permanent changes in the cellular DNA. Lastly, I previously wrote of the concern of graphene oxide being added to some of the inoculations. That article may be accessed here:
(At the time of this writing, the FDA has approved a second booster dose (that is four total) of the experimental EUA Pfizer or Moderna COVID-19 inoculation for Americans over 50.)
A new scientific study published on the 21st of April 2022, has concluded that Covid-19 vaccination can elicit a distinct T cell-dominant immune-mediated hepatitis (liver inflammation) with a unique pathomechanism associated with vaccination-induced antigen-specific tissue-resident immunity requiring systemic immunosuppression.
The findings come just days after the World Health Organization issued a ‘global alert’ about a new form of severe hepatitis affecting children; and after the UK Government announced it was launching an urgent investigation after detecting higher than usual rates of liver inflammation (hepatitis) among children, after having ruled out the common viruses that cause the condition.
Study title: SARS-CoV-2 vaccination can elicit a CD8 T-cell dominant hepatitis
Highlights of the Study
- Identification of immune correlates in a case of mRNA vaccine-associated autoimmune hepatitis
- Imaging mass cytometry identifies intrahepatic panlobular enrichment of activated cytotoxic CD8 T cells
- Flow cytometry identifies intrahepatic enrichment of activated CD8 T cells with SARS-CoV-2-specificity
- Peripheral SARS-CoV-2-specific CD8 T cell activation correlates with ALT levels
CA. 1000 Peer Reviewed Studies Questioning Covid-19 Vaccine Safety. Informed choice; 2022, Accessed March 7, 2022. https://www.informedchoiceaustralia.com/post/1000-peer-reviewed-studies-questioning-covid-19-vaccine-safety
CUMULATIVE ANALYSIS OF POST-AUTHORIZATION ADVERSE EVENT REPORTS OF PF-07302048 (BNT162B2) RECEIVED THROUGH 28-FEB-2021. Public Health and Medical Professionals for Transparency - https://phmpt.org Google Scholar
Rela, Mohamed, Dinesh Jothimani, Mukul Vij, Akila Rajakumar, and Ashwin Rammohan. "Auto-immune hepatitis following COVID vaccination." Journal of Autoimmunity 123 (2021): 102688.
Patil, Sakshi, and Anant Patil. "Systemic lupus erythematosus after COVID‐19 vaccination: A case report." Journal of Cosmetic Dermatology 20, no. 10 (2021): 3103.
Avci, Enver, and Fatma Abasiyanik. "Autoimmune hepatitis after SARS-CoV-2 vaccine: New-onset or flare-up?." Journal of autoimmunity 125 (2021): 102745.
Vuille-Lessard, Élise, Matteo Montani, Jaume Bosch, and Nasser Semmo. "Autoimmune hepatitis triggered by SARS-CoV-2 vaccination." Journal of autoimmunity 123 (2021): 102710.
Ghielmetti, Michele, Helen Dorothea Schaufelberger, Giorgina Mieli-Vergani, Andreas Cerny, Eric Dayer, Diego Vergani, and Benedetta Terziroli Beretta-Piccoli. "Acute autoimmune-like hepatitis with atypical anti-mitochondrial antibody after mRNA COVID-19 vaccination: A novel clinical entity?." Journal of Autoimmunity 123 (2021): 102706.
Londoño, Maria-Carlota, Jordi Gratacós-Ginès, and Joaquín Sáez-Peñataro. "Another case of autoimmune hepatitis after SARS-CoV-2 vaccination–still casualty?." Journal of hepatology 75, no. 5 (2021): 1248-1249.
Torrente, Silvia, Agustin Castiella, Maddi Garmendia, and Eva Zapata. "Probable autoimmune hepatitis reactivated after COVID-19 vaccination." Gastroenterologia y hepatologia (2021).
Grieco, Teresa, Alfredo Rossi, Patrizia Maddalena, Alvise Sernicola, Luca Ambrosio, Pasquale Fino, and Vito Gomes. "COVID-19 infection and BNT162b2 vaccine triggering sarcoid-like lesions in the same patient. Response to: Sarcoid-like reaction in a patient recovering from COVID-19 pneumonia." JAAD Case Reports (2022).
Grieco, Teresa, Patrizia Maddalena, Alvise Sernicola, Rovena Muharremi, Stefania Basili, Domenico Alvaro, Roberto Cangemi, Alfredo Rossi, and Giovanni Pellacani. "Cutaneous adverse reactions after COVID‐19 vaccines in a cohort of 2740 Italian subjects: An observational study." Dermatologic Therapy 34, no. 6 (2021): e15153.
Temiz, Selami Aykut, Ayman Abdelmaksoud, Uwe Wollina, Omer Kutlu, Recep Dursun, Anant Patil, Torello Lotti, Mohamad Goldust, and Michelangelo Vestita. "Cutaneous and Allergic reactions due to COVID‐19 vaccinations: A review." Journal of cosmetic dermatology 21, no. 1 (2022): 4-12.
Maldonado, María Dolores, and J. Romero-Aibar. "The Pfizer-BNT162b2 mRNA-based vaccine against SARS-CoV-2 may be responsible for awakening the latency of herpes varicella-zoster virus." Brain, Behavior, & Immunity-Health 18 (2021): 100381.
Alpalhão, Miguel, João Maia-Silva, and Paulo Filipe. "Severe acute respiratory syndrome coronavirus 2 vaccines and cutaneous adverse reactions: a review." Dermatitis 32, no. 3 (2021): 133-139.
Föhse, F. Konstantin, Büsranur Geckin, Gijs J. Overheul, Josephine van de Maat, Gizem Kilic, Ozlem Bulut, Helga Dijkstra et al. "The BNT162b2 mRNA vaccine against SARS-CoV-2 reprograms both adaptive and innate immune responses." (2021).
Al Soub, Hussam, Wanis Ibrahim, Muna Al Maslamani, Gawahir A. Ali, and Waseem Ummer. "Kikuchi-Fujimoto disease following SARS CoV2 vaccination: Case report." IDCases 25 (2021): e01253.
Iwanaga, Joe, Hiroshi Fukuoka, Nobuko Fukuoka, Hirokazu Yutori, Soichiro Ibaragi, and R. Shane Tubbs. "A narrative review and clinical anatomy of herpes zoster infection following COVID‐19 vaccination." Clinical Anatomy 35, no. 1 (2022): 45-51.
Patil, Sakshi, and Anant Patil. "Systemic lupus erythematosus after COVID‐19 vaccination: A case report." Journal of Cosmetic Dermatology 20, no. 10 (2021): 3103.
Finsterer, Josef. "Neurological side effects of SARS‐CoV‐2 vaccinations." Acta Neurologica Scandinavica 145, no. 1 (2022): 5-9.
Li, Minghui, Jing Yuan, Gang Lv, Jacob Brown, Xiangxiang Jiang, and Zhiqiang Kevin Lu. "Myocarditis and Pericarditis following COVID-19 Vaccination: Inequalities in Age and Vaccine Types." Journal of personalized medicine 11, no. 11 (2021): 1106.
Lane, Samantha, and Saad Shakir. "Reports of myocarditis and pericarditis following mRNA COVID-19 vaccines: A review of spontaneously reported data from the UK, Europe, and the US." medRxiv (2021).
Nordström, Peter, Marcel Ballin, and Anna Nordström. "Effectiveness of Covid-19 vaccination against risk of symptomatic infection, hospitalization, and death up to 9 months: a Swedish total-population cohort study." Hospitalization, and Death Up to 9 (2021).
Dr. Professor Arne Burkhardt’s findings may be viewed here: https://www.bitchute.com/video/aBhVDNdu6vnf/
Farshadpour, Fatemeh, and Reza Taherkhani. "Antibody-Dependent Enhancement and the Critical Pattern of COVID-19: Possibilities and Considerations." Medical Principles and Practice 30, no. 5 (2021): 422-429.
Wang, Ji, Caiguanxi Deng, Ming Liu, Yihao Liu, Liubing Li, Zhangping Huang, Liru Shang et al. "Four doses of the inactivated SARS-CoV-2 vaccine redistribute humoral immune responses away from the Receptor Binding Domain." medRxiv (2022).
Collier, A. Y., Jingyou Yu, Katherine Mcmahan, Jinyan Liu, Caroline Atyeo, Jessica L. Ansel, Zachary P. Fricker et al. "COVID-19 mRNA Vaccine Immunogenicity in Immunosuppressed Individuals." The Journal of infectious diseases (2021).
Ehmsen, Sidse, Anders Asmussen, Stefan S. Jeppesen, Anna Christine Nilsson, Sabina Østerlev, Hanne Vestergaard, Ulrik S. Justesen, Isik S. Johansen, Henrik Frederiksen, and Henrik J. Ditzel. "Antibody and T cell immune responses following mRNA COVID-19 vaccination in patients with cancer." Cancer Cell 39, no. 8 (2021): 1034-1036.
Lombardi, Andrea, Giacomo M. Butta, Lorena Donnici, Giorgio Bozzi, Massimo Oggioni, Patrizia Bono, Malvina Matera et al. "Anti-spike antibodies and neutralising antibody activity in people living with HIV vaccinated with COVID-19 mRNA-1273 vaccine: a prospective single-centre cohort study." The Lancet Regional Health-Europe 13 (2022): 100287.
Plymate, Lisa C., Gregory Pepper, Maxwell P. Krist, and David M. Koelle. "Immunogenicity of repeat COVID-19 mRNA vaccinations in a patient with myasthenia gravis receiving mycophenolate, prednisone, and eculizumab." Journal of Translational Autoimmunity 4 (2021): 100114.
Nordström, Peter, Marcel Ballin, and Anna Nordström. "Effectiveness of Covid-19 vaccination against risk of symptomatic infection, hospitalization, and death up to 9 months: a Swedish total-population cohort study." Hospitalization, and Death Up to 9 (2021).
Li Liu, et al. “Anti–spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection. JCI Insight. 2019;4(4):e123158. https://doi.org/10.1172/jci.insight.123158
Murphy, William J., and Dan L. Longo. "A possible role for anti-idiotype antibodies in SARS-CoV-2 infection and vaccination." New England Journal of Medicine 386, no. 4 (2022): 394-396.
Hou, Xucheng, Tal Zaks, Robert Langer, and Yizhou Dong. "Lipid nanoparticles for mRNA delivery." Nature Reviews Materials 6, no. 12 (2021): 1078-1094.
Schoenmaker, Linde, Dominik Witzigmann, Jayesh A. Kulkarni, Rein Verbeke, Gideon Kersten, Wim Jiskoot, and Daan JA Crommelin. "mRNA-lipid nanoparticle COVID-19 vaccines: Structure and stability." International Journal of Pharmaceutics 601 (2021): 120586.
Sakurai, Haruna, Kenji Kawabata, Fuminori Sakurai, Shinsaku Nakagawa, and Hiroyuki Mizuguchi. "Innate immune response induced by gene delivery vectors." International journal of pharmaceutics 354, no. 1-2 (2008): 9-15.
Szebeni, Janos. "Complement activation-related pseudoallergy: a new class of drug-induced acute immune toxicity." Toxicology 216, no. 2-3 (2005): 106-121.
Kedmi, Ranit, Noa Ben-Arie, and Dan Peer. "The systemic toxicity of positively charged lipid nanoparticles and the role of Toll-like receptor 4 in immune activation." Biomaterials 31, no. 26 (2010): 6867-6875.
Dokka, Sujatha, David Toledo, Xianglin Shi, Vincent Castranova, and Yon Rojanasakul. "Oxygen radical-mediated pulmonary toxicity induced by some cationic liposomes." Pharmaceutical research 17, no. 5 (2000): 521-525.
Abrams, Marc T., Martin L. Koser, Jessica Seitzer, Stephanie C. Williams, Martha A. DiPietro, Weimin Wang, Andrew W. Shaw et al. "Evaluation of efficacy, biodistribution, and inflammation for a potent siRNA nanoparticle: effect of dexamethasone co-treatment." Molecular therapy 18, no. 1 (2010): 171-180.
Sedic, Maja, Joseph J. Senn, Andy Lynn, Michael Laska, Mike Smith, Stefan J. Platz, Joseph Bolen et al. "Safety evaluation of lipid nanoparticle–formulated modified mRNA in the sprague-dawley rat and cynomolgus monkey." Veterinary pathology 55, no. 2 (2018): 341-354.
Knop, Katrin, Richard Hoogenboom, Dagmar Fischer, and Ulrich S. Schubert. "Poly (ethylene glycol) in drug delivery: pros and cons as well as potential alternatives." Angewandte chemie international edition 49, no. 36 (2010): 6288-6308.
Lila, Amr S. Abu, Hiroshi Kiwada, and Tatsuhiro Ishida. "The accelerated blood clearance (ABC) phenomenon: clinical challenge and approaches to manage." Journal of Controlled Release 172, no. 1 (2013): 38-47.
https://pandemictimeline.com/2021/05/japan-shares-biodistribution-study-of-pfizer-covid-19-vaccine/ (In Japanese) https://pandemictimeline.com/wp-content/uploads/2021/07/Pfizer-report_Japanese-government.pdf
Bansal, Sandhya, Sudhir Perincheri, Timothy Fleming, Christin Poulson, Brian Tiffany, Ross M. Bremner, and Thalachallour Mohanakumar. "Cutting Edge: Circulating Exosomes with COVID Spike Protein Are Induced by BNT162b2 (Pfizer–BioNTech) Vaccination prior to Development of Antibodies: A Novel Mechanism for Immune Activation by mRNA Vaccines." The Journal of Immunology 207, no. 10 (2021): 2405-2410.
Polykretis, P. "The role of the antigen presentation process in the immunization mechanism of the genetic vaccines against COVID‐19 and the need for biodistribution evaluations." Scandinavian Journal of Immunology (2022): e13160.
Long-term persistence of the SARS-CoV-2 spike protein: evidence and implications – Doctors for COVID Ethics (icourban.com) https://www.semanticscholar.org/paper/Long-term-persistence-of-the-SARS-CoV-2-spike-and-Palmer-Bhakdi/b5206b42361313804165542d2635608352185a36
Aldén, Markus, Francisko Olofsson Falla, Daowei Yang, Mohammad Barghouth, Cheng Luan, Magnus Rasmussen, and Yang De Marinis. "Intracellular reverse transcription of Pfizer BioNTech COVID-19 mRNA vaccine BNT162b2 in vitro in human liver cell line." Current Issues in Molecular Biology 44, no. 3 (2022): 1115-1126.
Aldén, Markus, IBID