Viral infections such as COVID-19 are significant environmental triggers for autoimmune diseases [1]. After infection with COVID-19, many autoimmune disorders that can potentially impact diverse organ systems may emerge [2]. The processes underlying the onset of autoimmunity in post-COVID-19 patients are complex and varied. Recent research has proposed several plausible mechanisms and theories to elucidate the molecular basis of immune dysregulation associated with COVID-19. These include molecular mimicry by viral proteins, systemic manifestations and multiorgan involvement due to the extensive expression of the SARS-CoV-2 receptor ACE2, bystander activation of immune cells, the release of autoantigens from virus-damaged tissues, superantigen-mediated lymphocyte activation, and epitope spreading. Several host factors, including age, comorbidities, and genetic predispositions, may also play a role [3].
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