What my analysis precipitated was a flurry of studies, including laboratory work that confirmed that pathogenic priming was likely to happen.
My findings, as well as those by others who did subsequent similar analyses, point to autoimmunity as a prime driver of COVID-19 disease and of long-term reactions to COVID-19 “vaccination”.
One of the very best summaries was published in a beautiful opus by Seneff and Nigh in the journal “International Journal of Vaccine Theory, Research and Practice” about a year after my initial predictions. That article, entitled “Worse Than the Disease? Reviewing Some Possible Unintended Consequences of the mRNA Vaccines Against COVID-19”, is as comprehensive a piece as you will find warning against the dangers of widespread exposure to the SARS-CoV-2 spike protein. I recently had occasion to re-read the article while preparing written testimony for one of the lawsuits in which I serve as expert witness, and it is absolutely, an “If you read one thing.”
“Pathogenic Priming, Multisystem Inflammatory Disease, and Autoimmunity
Pathogenic priming is a concept that is similar in outcome to ADE, but different in the underlying mechanism. We discuss it here as a unique mechanism through which the mRNA vaccines could provoke associated pathologies.
In April 2020 an important paper was published regarding the potential for self reactive antibodies to be generated following exposure to the spike protein and other antigenic epitopes spread over the length of SARS-CoV-2. Lyons-Weiler (2020) coined the phrase ‘pathogen priming’ because he believed the more commonly used ‘immune enhancement’ fails to capture the severity of the condition and its consequences. In his in silico analysis, Lyons-Weiler compared all antigenic SARSCoV-2 protein epitopes flagged in the SVMTriP database (http://sysbio.unl.edu/SVMTriP/) and searched the p-BLAST database (https://blast.ncbi.nlm.nih.gov/Blast.cgi) for homology between those epitopes and endogenous human proteins. Of the 37 SARS-CoV-2 proteins analyzed, 29 had antigenic regions. All but one of these 29 had homology with human proteins (putative self-antigens) and were predicted to be autoreactogenic. The largest number of homologies were associated with the spike (S) protein and the NS3 protein, both having 6 homologous human proteins.
A functional analysis of the endogenous human proteins homologous with viral proteins found that over 1/3 of them are associated with the adaptive immune system. The author speculates that prior virus exposure or prior vaccination, either of which could initiate antibody production that targets these endogenous proteins, may be playing a role in the development of more severe disease in the elderly in particular. In this case the pre-existing antibodies act to suppress the adaptive immune system and lead to more severe disease.
Another group (Ehrenfeld et. al., 2020), in a paper predominantly about the wide range of autoimmune diseases found in association with a prior SARS-CoV-2 infection, also investigated how the spike protein could trigger such a range of diseases. They report, in Table 1 of that reference, strings of heptapeptides within the human proteome that overlap with the spike protein generated by SARS-CoV-2. They identified 26 heptapeptides found in humans and in the spike protein. It is interesting to note that 2 of the 26 overlapping heptapeptides were found to be sequential, a strikingly long string of identical peptides to be found in common between endogenous human proteins and the spike protein. Commenting on the overlapping peptides they had discovered and the potential for this to drive many types of autoimmunity simultaneously, they comment, ‘The clinical scenario that emerges is upsetting.’ Indeed, it is.
In May of 2020 another important paper in this regard was published by Vojdani and Kharrazian (2020). The authors used both mouse and rabbit monoclonal antibodies against the 2003 SARS spike protein to test for reactivity against not only the spike protein of SARS-CoV-2, but also against several endogenous human proteins. They discovered that there was a high level of binding not only with the SARS-CoV-2 spike protein, but against a wide range of endogenous proteins. ‘[W]e found that the strongest reactions were with transglutaminase 3 (tTG3), transglutaminase 2 (tTG2), ENA, myelin basic protein (MBP), mitochondria, nuclear antigen (NA), α-myosin, thyroid peroxidase (TPO), collagen, claudin 5+6, and S100B.’ (Vojdani and Kharrazian, 2020).
These important findings need to be emphasized. Antibodies with a high binding affinity to SARSCoV-2 spike and other proteins also have a high binding affinity with tTG (associated with Celiac Disease), TPO (Hashimoto’s thyroiditis), myelin basic protein (multiple sclerosis), and several endogenous proteins. Unlike the autoimmune process associated with pathogen priming, these autoimmune diseases typically take years to manifest symptomatically.
The autoantibodies generated by the spike protein predicted by Lyons-Weiler (2020) and described above were confirmed with an in vitro study published more recently. In this follow-on paper, Vojdani et. al., (2021) looked again at the issue of cross reactivity of antibodies, this time using human monoclonal antibodies (mAbs) against the SARS-CoV-2 spike protein rather than mouse and rabbit mAbs. Their results confirmed and extended their prior findings. ‘At a cutoff of 0.32 OD [optical density], SARS-CoV-2 membrane protein antibody reacted with 18 out of the 55 tested antigens.’ These 18 endogenous antigens encompass reactivity to tissue in liver, mitochondria, the nervous and digestive system, the pancreas, and elsewhere in the body.
In a report on multisystem inflammatory syndrome in children (MIS-C), Carter et. al. (2020) studied 23 cases. Seventeen of 23 (68%) patients had serological evidence of prior SARS-CoV-2 infection.
Of the three antibodies assessed in the patient population (nucleocapsid, RBD, and spike), IgG spike protein antibody optical density (which quantifies antibody concentrations against a standardized curve (Wikipedia, 2021)), was highest (see Figure 1d in Carter et al., 2020).
MIS-C is now commonly speculated to be an example of immune priming by prior exposure to SARS-CoV-2 or to other coronaviruses. Buonsenso et. al. (2020) reviewed multiple immunologic similarities between MIS-C and disease related to prior β hemolytic Group A streptococcal infection (GAS). The authors write, ‘We can speculate that children’s multiple exposition to SARS-CoV-2 with parents with COVID-19 can work as a priming of the immune system, as happens with GAS infection and, in genetically predisposed children, lead to [MIS-C] development. Another hypothesis is that previous infections with other coronaviruses, much more frequent in the pediatric population, may have primed the child immune system to SARS-CoV-2 virus.’
In June 2019 Galeotti and Bayry (2020) reviewed the occurrence of both autoimmune and inflammatory diseases in patients with COVID-19. They focus their analysis on MIS-C. After reviewing several previously published reports of a temporal link between COVID-19 and onset of MIS-C and describing a number of possible mechanistic connections between the two, the authors noted that no causal link had been established. In a somewhat prescient recommendation, they wrote, ‘A fine analysis of homology between various antigens of SARS-CoV-2 and self-antigens, by use of in silico approaches and validation in experimental models, should be considered in order to confirm this hypothesis.’ It is precisely this type of in silico analysis (that had already been) carried out by Lyons-Weiler (2020) and by Ehrenfeld et. al. (2020) described in the opening paragraphs of this section which found the tight homology between viral antigens and self-antigens. While this may not definitively confirm the causal link hypothesized by Galeotti and Bayry, it is strong supporting evidence.
Autoimmunity is becoming much more widely recognized as a sequela of COVID-19. There are multiple reports of previously healthy individuals who developed diseases such as idiopathic thrombocytopenic purpura, Guillain-Barré syndrome and autoimmune haemolytic anaemia (Galeotti and Bayry, 2020). There are three independent case reports of systemic lupus erythemosus (SLE) with cutaneous manifestations following symptomatic COVID-19. In one case a 39-year-old male had SLE onset two months following outpatient treatment for COVID-19 (Zamani et.al., 2021).
Another striking case of rapidly progressing and fatal SLE with cutaneous manifestations is described by Slimani et.al. (2021).
Autoantibodies are very commonly found in COVID-19 patients, including antibodies found in blood (Vlachoyiannopoulos et. al., 2020) and cerebrospinal fluid (CFS) (Franke et. al., 2021).
Though SARS-CoV-2 is not found in the CSF, it is theorized that the autoantibodies created in response to SARS-CoV-2 exposure may lead to at least some portion of the neurological complications documented in COVID-19 patients. One important Letter to the Editor submitted to the journal Arthritis & Rheumatology by Bertin et. al. (2020) noted the high prevalence and strong association (p=0.009) of autoantibodies against cardiolipin in COVID-19 patients with severe disease.
Zuo et. al. (2020) found anti-phospholipid autoantibodies in 52% of hospitalized COVID-19 patients and speculated that these antibodies contribute to the high incidence of coagulopathies in these patients. Schiaffino et. al. (2020) reported that serum from a high percentage of hospitalized COVID-19 patients contained autoantibodies reactive to the plasma membrane of hepatocytes and gastric cells. One patient with Guillain-Barre Syndrome was found to have antibody reactivity in cerebrospinal fluid (CFS), leading the authors to suggest that cross-reactivity with proteins in the CFS could lead to neurological complications seen in some COVID-19 patients. In a more recent review, Gao et. al. (2021) noted high levels of autoantibodies in COVID-19 patients across multiple studies. They conclude, ‘[O]ne of the potential side effects of giving a mass vaccine could be an emergence [sic] of autoimmune diseases especially in individuals who are genetically prone for autoimmunity.’
A recent publication compiles a great deal of evidence that autoantibodies against a broad range of receptors and tissue can be found in individuals who have had previous SARS-CoV-2 infection. ‘All 31 former COVID-19 patients had between 2 and 7 different GPCR-fAABs [G-protein coupled receptor functional autoantibodies] that acted as receptor agonists. (Wallukat et. al. 2021) The diversity of GPCR-fAABs identified, encompassing both agonist and antagonist activity on target receptors, strongly correlated with a range of post-COVID-19 symptoms, including tachycardia, bradycardia, alopecia, attention deficit, PoTS, neuropathies, and others.
The same study, referencing the autoantibodies predicted by Lyons-Weiler (2020) mentioned above, notes with obvious grave concern: ‘The Sars-CoV-2 spike protein is a potential epitopic target for biomimicry-induced autoimmunological processes [25]. Therefore, we feel it will be extremely important to investigate whether GPCR-fAABs will also become detectable after immunisation by vaccination against the virus.’
We have reviewed the evidence here that the spike protein of SARS-CoV-2 has extensive sequence homology with multiple endogenous human proteins and could prime the immune system toward development of both auto-inflammatory and autoimmune disease. This is particularly concerning given that the protein has been redesigned with two extra proline residues to potentially impede its clearance from the circulation through membrane fusion. These diseases could present acutely and over relatively short timespans such as with MIS-C or could potentially not manifest for months or years following exposure to the spike protein, whether via natural infection or via vaccination.
Many who test positive for COVID-19 express no symptoms. The number of asymptomatic, PCR-positive cases varies widely between studies, from a low of 1.6% to a high of 56.5% (Gao et. al., 2020). Those who are insensitive to COVID-19 probably have a very strong innate immune system.
The healthy mucosal barrier’s neutrophils and macrophages rapidly clear the viruses, often without the need for any antibodies to be produced by the adaptive system. However, the vaccine intentionally completely bypasses the mucosal immune system, both through its injection past the natural mucosal barriers and its artificial configuration as an RNA-containing nanoparticle. As noted in Carsetti (2020), those with a strong innate immune response almost universally experience either asymptomatic infection or only mild COVID-19 disease presentation. Nevertheless, they might face chronic autoimmune disease, as described previously, as a consequence of excessive antibody production in response to the vaccine, which was not necessary in the first place.
The Spleen, Platelets and Thrombocytopenia
Dr. Gregory Michael, an obstetrician in Miami Beach, died of a cerebral hemorrhage 16 days after receiving the first dose of the Pfizer/BioNTech COVID-19 vaccine. Within three days of the vaccine, he developed idiopathic thrombocytopenic purpura (ITP), an autoimmune disorder in which the immune cells attack and destroy the platelets. His platelet count dropped precipitously, and this caused an inability to stop internal bleeding, leading to the stroke, as described in an article in the New York Times (Grady and Mazzei, 2021). The New York Times followed up with a second article that discussed several other cases of ITP following SARS-CoV-2 vaccination (Grady, 2021), and several other incidences of precipitous drop of platelets and thrombocytopenia following SARS-CoV-2 vaccination have been reported in the Vaccine Adverse Event Reporting System (VAERS).’
SARS-CoV-2 may have effects on the human vascular system, including that of the brain. The primary function of the Spike protein is to allow the entry of the virus into a host cell via binding to the ACE2 receptor located in the cell membrane. ACE2 is a type I integral membrane protein that cleaves angiotensin II in angiotensin I, thus removing angiotensin II and lowering the blood pressure.”
Since that paper was published, much more has come to light about the pathogenesis of the SARS-CoV-2 Spike Protein. I’ll be reviewing those works in Part 2.
