Immunity to latent viral infection: many skirmishes but few fatalities

During early childhood, herpes simplex virus type 1 (HSV-1) can establish a latent infection in sensory neurons, which then serves as a reservoir of the virus during recurrent disease. Accordingly, recurrent herpetic disease appears to result primarily from the reactivation of latent virus and its transport down nerve axons to the periphery, rather than from exogenous re-infection. Eradicating latent HSV-1 from sensory neurons is not currently feasible but recent findings implicating host immunity in maintaining HSV-1 in a latent state provide promise for immunological intervention in recurrent herpetic disease. We propose, and provide supporting evidence, for the concept that CD8+ T cells regulate HSV-1 gene expression during latency.