Mechanisms of HSV gene regulation during latency and reactivation.

Abstract

Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) are prevalent human pathogens associated with many diseases. After productive (lytic) infection in peripheral tissues, HSV establishes lifelong latent infection in neurons of the peripheral nervous system. Periodic reactivation from latency, triggered by certain stimuli, can resume the lytic cycle. Lytic infection, latent infection and reactivation follow distinct viral gene expression patterns. The switch between the different infection programs is controlled by complicated regulatory mechanisms involving numerous viral and host molecules. Recent studies integrating cutting-edge technologies including neuronal culture techniques have greatly improved our understanding of the molecular details of latency and reactivation but many questions remain. This review summarizes the current knowledge about how HSV gene expression is regulated during latency and reactivation and discusses the important questions remaining to be addressed in future.