Based on the mechanisms involved in the glycosylation of HR of IgA1 (196, 200) and the familial epidemiology of EBV infection, it is plausible to speculate that EBV is also involved in the aberrant glycosylation of IgA1 in IgA vasculitis with nephritis. This evidence concerns the gene IGHA1 and Epstein-Barr virus infection.