COVID 19 and Bullous Pemphigoid: a hypothesis for a causal link

Although onset/exacerbation of bullous Pemphigoid (BP) has been reported to occur frequently followingexposure to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the link, if any, betweenBP dermatoses and the viral infection remains obscure. Therefore, searching for possible molecularmechanisms, we hypothesise that molecular mimicry between BP antigens and the SARS-CoV-2 proteinsmight lead to autoimmune responses cross-reacting with the BP proteins, thus triggering the dermatosispathologies. Using this research paradigm, we analyzed the Bullous Pemphigoid antigen 1 (BP230) andthe SARS-CoV-2 proteome to share minimal immune determinants, i.e., pentapeptides. Results indicate ahigh level of molecular mimicry between BP230 and SARS-CoV-2, thus supporting the hypothesis of crossreactivityas a possible major mechanism in the SARS-CoV-2-associated BP etiopathogenesis.