The molecular mimicry and COVID-19

Abstract

A significant part of the complications of COVID-19 and manifestations of post-COVID syndrome is associated with autoimmune reactions caused by SARS-CoV-2. The key mechanism for the implementation of autoimmunity in COVID-19 is molecular mimicry, which is involved in the development of a cytokine storm, systemic multiorgan hyperinflammation, endothelial dysfunction, and is also a trigger for the development of autoimmune diseases (autoimmune thrombocytopenia, autoimmune vasculitis, Guillain-Barr syndrome, Miller-Fisher syndrome, autoimmune neuropathy, autoimmune thyroiditis, rheumatoid arthritis and others) after COVID-19. In total, 59 common immune determinants were identified in 80 epitopes of the SARS-CoV-2 spike protein with 53 anti-inflammatory proteins, receptors that regulate cell proliferation, differentiation and apoptosis, as well as the immune response. It was found that among the 37 proteins of the virus, only 8 do not have immunogenic regions identical to human proteins. Cross-reactivity leads to the formation of more than 15 distinct types of autoantibodies, including antiphospholipid antibodies to cardiolipin and beta2-glycoprotein I, antibodies to the transmembrane adenosine receptor A2b, adiponectin, phosphatidylserine-prothrombin autoantibodies, antinuclear antibodies, antibodies to mitochondrial M2, autoantibodies against type I interferons, and other cytokines, chemokines, complement components and cell membrane proteins. Autoantibodies formed during COVID-19 react with antigens of cells of the thyroid gland, cardiac and skeletal muscles, lung, joints, liver, kidneys, brain and bone marrow, peripheral nervous system, skin and adipose tissue, gastrointestinal tract, testicles, eyes, and also with mitochondrial antigens, mediating the development of severe complications of the disease and the development of post-covid syndrome. The presence of 24 homologous pentapeptides with Bordetella pertussis, C. diphtheriae, C. tetani, H. influenzae and N. Meningitides provokes the risk of developing an ineffective immune response to vaccination against the background of an increased risk of autoimmune complications. It is imperative to take into account the phenomenon of molecular mimicry in the development of new approaches to the rehabilitation and treatment of COVID-19, as well as in the development and testing of vaccines against SARS-CoV-2.