The neurotropic herpes viruses, as typified by herpes simplex virus type 1, are noted for their ability to form latent infections. The latent infection differs from the acute infection both in gene expression and the physical state of the viral genome. Latency can be divided into several stages - establishment, maintenance of reactivation - each of which are active areas of research. This review describes the molecular biology of HSV-1 latency and presents the current level of understanding of the molecular mechanism of HSV-1 latency.