FIG 7.

Working model of EBV type 2 latency establishment and persistence based on our in vitro T-cell infection studies. Following primary exposure to EBV-2, CD8⁺ T cells, in addition to B cells, in the tonsil are infected, and the growth program is initiated, resulting in the activation and proliferation of the infected lymphocytes. At this time, EBV-2-infected CD8⁺ T cells could enhance the ability of the virus to establish latency in the B-cell compartment. EBV-2 may accomplish this by inducing alteration of T-cell cytokine production that could hamper the antiviral response, recruit additional target cells to the site of infection, enhance the activation and survival of lymphocytes, and/or induce expression of critical viral genes. Another, non-mutually exclusive possibility is that, in addition to memory B cells, T cells serve as a latency reservoir.