During the acute phase of EBV infection, oral mucosa cells and B-cells become infected, leading to a robust immunogenic response with both antibody and cellular upregulation (via specific CD8 and CD4-positive T-cells) [11]; by mechanisms of immune tolerance and by establishing itself in memory B-cells, the EBV becomes latent and remains dormant in the reticuloendothelial system for the rest of the host life [1,12]. The gene discussed is CD4; the disease is Epstein-Barr virus infection.