Herpes simplex virus type 1 (HSV-1) persists within the host in the presence of concomitant immunity by establishing a latent infection within sensory neurons. HSV-1 latency is widely viewed as a neuron-enforced quiescent state of the virus, in which a lack of viral protein synthesis prevents recognition of the infected neuron by the host immune system. On the basis of recent findings, however, we propose a more dynamic view of HSV-1 latency characterized by persistent or intermittent low-level viral gene expression in some latently infected neurons. We further propose that HSV-1-specific memory/effector CD8(+) T lymphocytes that are retained in the ganglion in close apposition to the neurons prevent full reactivation and virion formation through IFN-gamma production and an additional undefined mechanism(s).