Molecular mimicry, hyperactive immune system, and SARS-COV-2 are three prerequisites of the autoimmune disease triangle following COVID-19 infection

SARS-CoV-2 infection can produce a variety of clinical manifestations, which are either directly related to viral tissue damage or indirectly induced by the antiviral immune response. Molecular mimicry enables this virus to undermine self-tolerance in a host's immune system also immune system's attempts to eliminate SARS-COV-2 may trigger autoimmunity by hyper-activating the innate and adaptive immune systems. Auto immune dis-eases include Systemic lupus erythematosus, autoimmune thyroid diseases, Guillain-Barre syndrome, Immune thrombocytopenic purpura, and the detection of autoantibodies are the cues to the discovery of the potential of COVID-19 in inducing autoimmunity. As COVID-19 and autoimmune diseases share a common pathogenesis, autoimmune drugs may be an effective treatment option. Susceptible patients must be monitored for autoim-mune symptoms after contracting CVID-19. In light of the SARS-COV-2 virus' ability to induce autoimmunity in susceptible patients, will the various COVID-19 vaccines that are the only way to end the pandemic induce autoimmunity?

Automated summary

SARS-CoV-2 infection can lead to various clinical manifestations, either directly related to viral tissue damage or indirectly induced by the immune response. The virus's molecular mimicry can undermine the host's immune system and trigger autoimmunity. Autoimmune diseases like lupus and autoimmune thyroid disease have been linked to COVID-19, and monitoring for autoimmunity is important. Autoimmune drugs may be effective in treating COVID-19.