Page 14 - Dr Stephanie Seneff - Reviewing Some Possible Unintended Consequences of the mRNA Vaccines Against COVID - 19

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 SARS-
CoV-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).

International Journal of Vaccine Theory, Practice, and Research 2(1), May 10, 2021 Page | 402