Previous studies have shown EGF facilitates the cellular entry of EBV when infecting epithelial cells, which may increase the overall risk of EBV infection while also regulating viral activity and infected cell growth.45 Of the non-HLA genetic risks for MS, only rs2255214, near the CD86 gene, was significantly associated with EBV serology and was the only genetic association replicated from previous genetic EBV studies. This evidence concerns the gene CD86 and Epstein-Barr virus infection.