Presented at the 13th International Congress on Autoimmunity in Athens, Greece
Speaker: Gabriela Baiocchi
Speaker: Gabriela Baiocchi
Several studies have reported autoantibody production being induced by COVID-19 infection though we still do not understand their full spectrum. To better understand, Baiocchi and her team conducted a cross-sectional study of 246 patients, divided into mild, moderate, and severe covid disease, and controls. They used multiple data analysis techniques to assess commonalities and differences between the autoantibodies as well as between the different patient population groups.
The team found that dysregulated production of autoantibodies targeting GPCRs and RAS-related molecules in COVID-19 patients was accompanied by higher levels of some autoantibodies associated with classic autoimmune diseases when compared to healthy controls. Interestingly, they found no significant differences in antinuclear antibody (ANA) levels but found that the levels of rheumatoid factor (RF) and autoantibodies targeting double-stranded DNA (anti-dsDNA) were significantly increased according to COVID-19 severity.
This work reinforces the idea that a COVID-19 infection may trigger serious autoimmune disease, “suggesting that this occurs against multiple molecules with key functions in immune and vascular homeostasis such as GPCRs and RAS-related molecules.” “Furthermore, the hyperinflammatory reaction triggered by the virus results in tissue damage, causing systemic autoimmune-related manifestations that have been reported in patients with COVID-19.”