Post-acute cardiac sequelae, following
SARS-CoV-2 infection, are well recognized as complications of
COVID-19. We have previously shown the persistence of
autoantibodies against
antigens in skin, muscle, and heart in individuals following severe
COVID-19; the most common staining on skin tissue displayed an inter-cellular cement pattern consistent with
antibodies against desmosomal
proteins. Desmosomes play a critical role in maintaining the structural integrity of tissues. For this reason, we analyzed desmosomal
protein levels and the presence of anti-
desmoglein (DSG) 1, 2, and 3
antibodies in acute and convalescent sera from patients with
COVID-19 of differing clinical severity. We find increased levels of DSG2
protein in sera from acute
COVID-19 patients. Furthermore, we find that DSG2
autoantibody levels are increased significantly in convalescent sera following severe
COVID-19 but not in hospitalized patients recovering from
influenza infection or healthy controls. Levels of
autoantibody in sera from patients with severe
COVID-19 were comparable to levels in patients with non-COVID-19-associated
cardiac disease, potentially identifying DSG2
autoantibodies as a novel
biomarker for cardiac damage. To determine if there was any association between severe
COVID-19 and DSG2, we stained post-mortem cardiac tissue from patients who died from
COVID-19 infection. This confirmed DSG2
protein within the intercalated discs and disruption of the intercalated disc between cardiomyocytes in patients who died from
COVID-19. Our results reveal the potential for DSG2
protein and autoimmunity to DSG2 to contribute to unexpected pathologies associated with
COVID-19 infection.