Varicella-zoster virus is a Herpesvirus responsible for three distinct clinical features : chicken pox (varicella), shingles (herpes zoster) and post-zosterian pain (post-herpetic neuralgia). Neurological aspects of these diseases such as complications of chicken pox, viral latency in sensory ganglia and reactivation as shingles with concurrent and at times subsequent prolonged pain, are the sequels of the invasion of the peripheral nervous system during primary infection. Prevention is achieved by vaccination with a live attenuated virus strain and therapy calls for specific antiviral agents. In many respects, VZV behaves differently from close relatives. In particular, viral latency in the nervous system is quite different from that of other Herpesviridae. The recent discovery of the expression and accumulation of some viral regulatory proteins during latency, although VZV latency had always been considered silent, as well as the demonstration that these proteins are immunogenic are opening new avenues to investigate the mechanisms of VZV latency and the immune control of VZV reactivation.