Influence of Herpes Simplex Virus Latency-Associated Transcript (LAT) on the Distribution of Latently Infected Neurons

Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are similar viruses with several notable differences. While both viruses establish latency in sensory ganglia and reactivate to cause recurrent disease, HSV-1 reactivates more efficiently from trigeminal ganglia to cause cold sores or keratitis and HSV-2 reactivates more efficiently from lumbosacral dorsal root ganglia (DRG) to cause genital herpes. Both viruses are capable of causing central nervous system (CNS) disease, but HSV-1 CNS infections typically manifest as severe necrotizing encephalitis while HSV-2 is more commonly associated with relatively benign meningitis. Potential mechanisms for type-specific differences between HSV-1 and HSV-2 have not been closely examined, although the latency associated transcript (LAT) of HSV plays a critical role in the establishment of latency and site-specific reactivation and may have regulatory influence over viral replication and spread