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Figure 2: A model of CD8+ T-cell monitoring of HSV-1 latency in sensory ganglia. (a) During a primary infection (affecting the cornea of the eye), HSV-1 invades the termini of sensory neurons, the nucleocapsid travels by retrograde axonal transport to the neuron cell bodies within the trigeminal ganglion (TG), viral DNA is inserted into the nucleus, and a brief period of virus replication ensues (b). An initial infiltration of macrophages and T cells gives rise to an infiltrate dominated by CD4+ and CD8+ T cells and macrophages that persists for the life of the animal (c). The CD8+ T cells associate closely with the neuron cell bodies and directly monitor viral gene expression in neurons by detecting epitopes of viral epitopes that are produced early in a reactivation event and presented on the surface of the neuron within MHC class I. The CD8+ T cells force the viral genome into a quiescent state through IFN-γ production (early in reactivation) or through the release of lytic granules (at later stages of reactivation). A similar model can be extrapolated to genital herpes infection with HSV-2.