The impact of COVID-19 on autoimmune diseases.

Abstract

Various autoantibodies, such as antinuclear antibodies (ANA), anti-Ro/SSA, rheumatoid factor, lupus anticoagulant, and antibodies against interferon type I (IFN-I), have been frequently detected in COVID-19 patients, indicating a significant prevalence of autoimmune reactions following viral exposure. Additionally, the identification of human proteins with structural similarities to SARS-CoV-2 peptides as potential autoantigens underscores the complex interplay between the virus and the immune system in triggering autoimmunity. The chapter discusses probable pathways contributing to COVID-19-related autoimmunity, including bystander activation due to hyperinflammatory states, viral persistence, and the formation of neutrophil extracellular traps. These mechanisms illuminate a spectrum of autoimmune-related symptoms that can manifest, ranging from organ-specific to systemic autoimmune and inflammatory diseases. Importantly, there is emerging evidence of de novo autoimmunity arising after COVID-19 infection or vaccination, where new autoimmune conditions develop in previously healthy individuals. While various COVID-19 vaccines have received emergency use authorization, concerns regarding potential autoimmune side effects persist. Ongoing research is crucial to clarify these relationships and enhance our understanding of the risks associated with COVID-19 infections and vaccinations.