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The herpesviruses are characterized by their ability to undergo a productive infection upon infection of the host organism and then spread to establish a latent infection where they persist in the host. Later, under conditions of stress or other environmental stimuli, they reactivate to undergo a productive infection and spread to new host organisms. Herpes simplex virus (HSV), in particular, undergoes a productive infection in the mucosal epithelium and spreads to sensory neurons where it undergoes a latent infection. Reactivation leads to virus shedding but can also lead to recurrent disease. Much of the herpetic disease occurs following reactivation from latent infection, and all of the available antivirals target lytic infection. Thus, an understanding of the mechanisms of establishment and reactivation of HSV from latent infection is important for devising approaches for controlling HSV establishment, maintenance, and reactivation from latent infection. In epithelial cells, the HSV genome is initially silenced by host epigenetic mechanisms, but the virion protein 16 (VP16) and immediate early (IE) infected cell protein 0 reverse the heterochromatin modifications and promote euchromatin modifications on viral chromatin to promote lytic gene transcription, allowing lytic infection to proceed (1). In sensory neurons, VP16 cannot localize to the nucleus and/or assemble into nuclear complexes to activate IE gene expression, so the lytic cascade of gene expression is not initiated. Instead, a neuron-specific promoter in the viral genome drives the expression of the latency-associated transcript (LAT), which is processed into a stable lariat intron and microRNAs (miRNAs) (2). LAT is reported to enhance neuronal survival in several ways: (i) down-regulating lytic gene expression (3) by LAT sequences acting as a long noncoding RNA and promoting …

Clues to mechanisms of herpesviral latent infection and potential cures