SARS-CoV-2 triggers development of new-onset IgG autoantibodies in hospitalized COVID-19 patients Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the causative agent for coronavirus disease 2019 (COVID-19), is associated with several clinical features common in autoimmune diseases as myalgias, arthralgias, fatigue, and rashes. COVID-19 patients also exhibit less common autoimmunity manifestations such as myositis, thrombosis, myocarditis, encephalitis, vasculitis, and arthritis. These observations, coupled with the increasing number of "recovered" long-COVID patients with post-COVID-19 symptoms, indicate that SARS-CoV-2-related inflammation promotes tissue damage. Prior research has shown that about 50% of hospitalized COVID-19 patients at an academic hospital in Greece had high serum levels of autoantibodies, often associated with thrombosis, rashes, and vasculitis. Also, serum anti-nuclear antibodies (ANAs) were detected in about one-third of the patients. Reports have also shown that autoantibodies can help the formation of clots in mouse models.