SH2D1A and Epstein-Barr virus infection: The reduced percentage of infected B cells with a GC phenotype, along with the increased percentage of infected naïve B cells in SAP-deficient mice, suggested that in contrast to what is proposed to happen following EBV infection of B cells [23], MHV68 may not play an active role in activating naïve B cells and driving them through the GC reaction.