Autoimmunity, COVID-19, Immune Enhancement, implications for vaccines, Pathogenic priming, SARS-Cov-2
[Related: A Report on the U.S. Vaccine Adverse EventsReporting System (VAERS) of the COVID-1 9Messenger Ribonucleic Acid (mRNA) Biologicals.PDF by Dr. Jessica Rose. and this audio/visual presentation: Dr. Jessica Rose (PhD, MSc, BSc) – “A Study of the U.S. CVD-19 mRNA Biologicals” – Extensive Review. Dr. Rose believes that the best explanation for the increasing trend in vaccine induced injuries and deaths is ‘pathogenic priming,’ as described by James Lyons-Weiler.]
Hat tip: Zinnsgh0st
Source: Journal of Translational Autoimmunity, Volume 3, 2020, 100051
Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity
The Institute for Pure and Applied Knowledge, USA
Received 9 March 2020, Revised 31 March 2020, Accepted 2 April 2020, Available online 9 April 2020.
Under a Creative Commons license
•All SARS-CoV-2 immunogenic epitopes have similarity to human proteins except one.
•Roughly one-third of the potentially targeted human proteins (putative autoantigens) are key players in the adaptive immune system.
•The list of viral/human protein matches provides clues on which epitopes or parts of epitopes might be involved in the immunopathogenesis of COVID-19 disease from SARS-CoV-2 infection.
•It also indicates which epitopes might be responsible for autoimmunological pathogenic priming due to prior infection or following exposure to SARS-CoV-2 or relatives following vaccination.
•These epitopes should be excluded from vaccines under development to minimize autoimmunity due to risk of pathogenic priming.
Homology between human and viral proteins is an established factor in viral- or vaccine-induced autoimmunity. Failure of SARS and MERS vaccines in animal trials involved pathogenesis consistent with an immunological priming that could involve autoimmunity in lung tissues due to previous exposure to the SARS and MERS spike protein. Exposure pathogenesis to SARS-CoV-2 in COVID-19 likely will lead to similar outcomes. Immunogenic peptides in viruses or bacteria that match human proteins are good candidates for pathogenic priming peptides (similar to the more diffuse idea of “immune enhancement”). Here I provide an assessment of potential for human pathogenesis via autoimmunity via exposure, via infection or injection. SAR-CoV-2 spike proteins, and all other SARS-CoV-2 proteins, immunogenic epitopes in each SARS-CoV-2 protein were compared to human proteins in search of high local homologous matching. Only one immunogenic epitope in a SARS-CoV-2 had no homology to human proteins. If all of the parts of the epitopes that are homologous to human proteins are excluded from consideration due to risk of pathogenic priming, the remaining immunogenic parts of the epitopes may be still immunogenic and remain as potentially viable candidates for vaccine development. Mapping of the genes encoding human protein matches to pathways point to targets that could explain the observed presentation of symptoms in COVID-19 disease. It also strongly points to a large number of opportunities for expected disturbances in the immune system itself, targeting elements of MHC Class I and Class II antigen presentation, PD-1 signaling, cross-presentation of soluble exogenous antigens and the ER-Phagosome pathway. Translational consequences of these findings are explored.