“…5 Moreover, experimental studies, in vitro and in vivo animal models, revealed that CV-B4 may be involved in the pathogenesis of T1D through several mechanisms. 2,6,7,8 It has been shown that non-neutralizing anti-CV-B4 IgG obtained from serum of patients can increase the infection of peripheral blood mononuclear cells (PBMC) with CV-B4, which results in production of IFNa and other inflammatory cytokines. 9,10,11,12,13,14 The role of enhancing IgG levels in the outcome of CVB4 infections and other conditions such type 1 diabetes, cannot be ignored.…”