EBV infection also generates a large pool of antigen-presenting B cells, with latent EBV infection transforming B cells into potent antigen-presenters and inducing mutations in B cell receptors (BCRs) and co-stimulatory molecules, facilitating antigen uptake and presentation to CNS specific CD4+ T cells (344–346). This evidence concerns the gene CD4 and Epstein-Barr virus infection.