Molecular and immunological evidence for SARS-CoV-2 being the autoimmune virus

Abstract

Cumulative evidence indicates that SARS-CoV-2 can induce hyper-stimulation of the immune system, leading to the synthesis of multiple autoantibodies. That is why the virus and the disease have been associated with various autoimmune disorders, including type 1 diabetes, Graves' disease, autoimmune hemolytic anemia, polyneuritis cranialis, postural orthostatic tachycardia syndrome, systemic lupus erythematosus, antiphospholipid syndrome, Guillain-Barré syndrome, rheumatoid arthritis, immune thrombocytopenic purpura, Miller-Fisher syndrome, NMDA receptor encephalitis, vasculitis, Kawasaki disease, and more. Because of this, and many other reasons, SARS-CoV-2 has been called the autoimmune virus. However, experimental evidence is needed to support the induction of autoimmunity by this virus. In this review article, the following molecular and immunological experimental evidence will be discussed to strengthen the connection between SARS-CoV-2 and many autoimmune diseases: 1. Identification of cross-reactive epitopes from SARS-CoV-2 that share homology with human proteomes that participate in autoimmune diseases 2. Reaction of both animal and human monoclonal antibodies to SARS-CoV-2 antigens with human tissue antigens 3. Reaction of antibodies made against human tissue with SARS-CoV-2 spike proteins and nucleoproteins 4. Detection of autoantibodies against human autoantigens in the sera of COVID-19 patients that cross-reacted with SARS-CoV-2 proteins This experimental evidence further supports that the title of autoimmune virus given to SARS-CoV-2 is very well deserved.