Similar to the EBNA1-directed response, these results could be due to impaired Th1, (Th17), CTL, NK cell regulations, and acute phase responses against lytic EBV infection, besides a lack of the antiviral functions of TNFβ, yet with reasonable functioning macrophages producing IL12, IL18, and TNFα perhaps aiming (unsuccessfully) to induce IFNγ and thereby cell-mediated immunity and also to activate NK cells and mediate inflammation. Here, IFNG is linked to Epstein-Barr virus infection.