ABSTRACT
Autoimmune blistering diseases have been associated with exposure to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In addition, oropharyngeal Pemphigus vulgaris appears to be associated with the coronavirus. In order to understand the molecular basis linking SARS-CoV-2 and Pemphigus vulgaris, this study explores the molecular mimicry hypothesis and analyzes the peptide sharing between the Pemphigus vulgaris autoantigen, i.e., Desmoglein 3 (Dsg-3), and the SARS-CoV-2 proteome. Results indicate a low molecular mimicry level, still immunologically significant, between SARS-CoV-2 and Dsg-3.
ABSTRACT
Although onset/exacerbation of bullous Pemphigoid (BP) has been reported to occur frequently following exposure to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the link, if any, between BP dermatoses and the viral infection remains obscure. Therefore, searching for possible molecular mechanisms, we hypothesise that molecular mimicry between BP antigens and the SARS-CoV-2 proteins might lead to autoimmune responses cross-reacting with the BP proteins, thus triggering the dermatosis pathologies. Using this research paradigm, we analyzed the Bullous Pemphigoid antigen 1 (BP230) and the SARS-CoV-2 proteome to share minimal immune determinants, i.e., pentapeptides. Results indicate a high level of molecular mimicry between BP230 and SARS-CoV-2, thus supporting the hypothesis of cross-reactivity as a possible major mechanism in the SARS-CoV-2-associated BP etiopathogenesis.