Epstein Barr virus infection and immune defense related to HLA‐DR15: consequences for multiple sclerosis

MS is a multifactorial disease in which a series of genetic and non‐genetic, environmental factors plays a role in its etiology. In particular, HLA class II alleles, mainly HLADRB1*15:01 (HLA‐DR15), increase the risk for this disease. Out of several environmental factors, and with regard to infections, EBV remains to be a strong candidate, and may synergize with HLA‐DR15 thus increasing the risk for MS. In this issue of the European Journal of Immunology, Zdimerova et al. present highly interesting experimental data using EBV infection in immune‐deficient mice engrafted with human immune cells, either HLA‐DR15(+) or HLA‐DRB1*04:01 (HLA DR4), here after denoted as HLA‐DR15(−). As a result of EBV infection, the viral load and CD8(+) cell expansion were conspicuously higher in mice engrafted with HLA‐DR15(+) compared to HLA‐DR15(−) mice; and myelin basic protein specific T cells emerged in mice engrafted with HLA‐DR15 bearing cells. This study sheds light on how EBV and the class II DR15 haplotype may jointly predispose and synergize in the etiology of MS.