Additionally, it has been proposed that HLAII–gp42 interactions in genetically predisposed individuals with SE-positive DRB1 alleles (DRB1*0401, *0404, *0405, *0408, *0409, *0101, *0102, *1001, and *1402) facilitate EBV entry and infection, which may ultimately result in uncontrolled EBV infection and, consequently, RA onset [23]. Here, HLA-DRB1 is linked to Epstein-Barr virus infection.