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Bullous pemphigoid (BP) has been repeatedly reported to occur following exposure to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This study analyzes the molecular mimicry between the 180 kDa bullous pemphigoid antigen 2 (BP180) and the SARS-CoV-2 proteome to further our understanding of the molecular link between the BP and the SARS-CoV-2 infection. Results indicate a high degree of molecular mimicry between BP180, SARS-CoV-2, hCoV-229E and hCoV-NL63.

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.

The blistering disease Epidermolysis bullosa acquisita is a genetic/autoimmune disorder deriving from alterations of the human protein Collagen alpha-1(VII) chain (CO7A1). Exposure to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) promotes a wide variety of autoimmune diseases and might be a risk factor for Epidermolysis bullosa acquisita; in order to further our understanding of the link between this blistering disease and SARS-CoV-2, this study analyzes the peptide-sharing between CO7A1 and SARS-CoV-2 proteome. Results indicate a high level of molecular mimicry between CO7A1 and SARS-CoV-2 and hCoV-229E, and hCoV-NL63, thus suggesting a potential role of COVID-19 as a risk factor for Epidermolysis bullosa acquisita.

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.