Varicella zoster virus (VZV) is the herpesvirus which causes the childhood disease varicella, also known as chickenpox, and the adult disease herpes zoster, also known as shingles. These distinct diseases are separated by a lengthy period of latency, often lasting decades, in which the virus resides within the ganglia of the host. VZV latency and reactivation from it have, for the most part, been extraordinarily difficult to examine. This is due to the lack of a good animal model for the VZV latent state, the inability to experimentally reactivate VZV under any circumstances and the caveats and problems encountered in examining human ganglionic tissue. However, insights into features of the molecular events of VZV latency have been gleaned from its pathogenesis and from recent advances in molecular probing of human and animal ganglia. Evidence suggests that the latent VZV genome may express transcripts unlike those of closely related herpesviruses, and some evidence suggests an unusual site for the establishment of VZV latency. In this review, the current evidence for events occurring during the VZV latent state will be discussed, from a view of its pathogenesis as well as its molecular biology.