The absence of extensive beta cell lysis and acute viral infection, even among donors examined near diagnosis or at the stage of multiple AAb positivity, and the presence of VP1+ cells in insulin-positive islets several years after diagnosis support the hypothesis of a low-grade, possibly persisting or recurrent enterovirus infection that could trigger IFN responses, leading to or contributing to the hyperexpression of HLA-I molecules. This evidence concerns the gene IFNA1 and enterovirus infectious disease.