Presented at the 13th International Congress on Autoimmunity in Athens, Greece

Speaker: Aristo Vojdani

Key Takeaways:

  • Molecular mimicry between SARS-CoV-2 spike proteins, nucleoproteins, and human autoantigens that contribute to ADs
  • The reaction of both animal and human monoclonal antibodies made against SARS-CoV-2 spike proteins and nucleoproteins with human autoantigens
  • The reaction of antibodies made against human autoantigens with SARS-CoV-2 spike proteins and nucleoproteins
  • Detection of autoantibodies made against human autoantigens known to cross-react with SARS-CoV-2 in the sera of COVID-19 patients
  • Similarities in lymphocyte map or lymphocyte subpopulation patterns between COVID-19 and ADs

Summary:

Vojdani’s lab tested blood specimens that had tested positive for SARS-CoV-2 for anti-nuclear antibody (ANA), anti-extractable nuclear antigen (ENA), anti-double-stranded DNA (dsDNA), actin antibody, mitochondrial antibody, rheumatoid factor (RF), and C1q immune complexes (all human autoantigens that contribute to ADs). They found that most of the specimens had significant elevations in ANA, ENA, actin, and mitochondrial antibodies which prompted them to investigate patterns of cross-reactivity between SARS-CoV-2 and autoimmune target proteins also known as “molecular mimicry.”

Next, they studied the reaction between the SARS-CoV-2 spike protein antibody and tissue proteins. They found significant reactivity against monoclonal antibodies against SARS-CoV-2 and nucleoproteins with about 40% of tested tissue antigens. This was a “strong indication of cross-reaction between SARS-CoV-2 proteins and a variety of tissue antigens beyond just pulmonary tissue, which could lead to autoimmunity against connective tissue and the cardiovascular, gastrointestinal, and nervous systems.” 

“This extensive immune cross-reactivity between SARS-CoV-2 antibodies and different antigen groups may play a role in the multi-system disease process of COVID-19, influence the severity of the disease, precipitate the onset of autoimmunity in susceptible subgroups, and potentially exacerbate autoimmunity in subjects that have pre-existing autoimmune diseases.” Vojdani’s lab has recently carried out a comprehensive assessment of autoantibodies known to be linked to diverse ADs in a cohort of 248 individuals (171 were COVID-19 patients – 74 mild, 65 moderate, and 32 severe disease). These results will be published upon acceptance of their paper.

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