[Latency and reactivation of HSV: role of LAT and ICP0]

The virus herpes simplex type 1 (HSV1) is characterized by its ability to become latent within the nervous system after a primary infection that is almost always located into the oral mucosa. Several factors may trigger HSV1 reactivation, thus inducing recurrences, which are mostly located on the lips (cold sore), sometimes in the eye (most frequently into the cornea) and, exceptionally, in the central nervous system (meningitis and encephalitis). Considering the frequency of the HSV1 infection in the general population and the associated morbidity (approximately 15 % of people have relapsing cold sores, and 90,000 French people have an history of ocular herpes disease), many research projects are focused on the biologic patterns regulating the switch between viral latency and reactivation. In spite of the multitude of scientific publications, numerous points are still poorly understood. However, molecular biology allowed consequent progress. The putative roles of Latency Associated Transcripts (LAT), until recently considered as the only viral transcripts during viral latency, are now better identified. It is now obvious that LAT interact with other viral partners. The transcripts encoding ICP0, a viral protein which is known to have a key role in the reactivation process, could be involved in this phenomenon, since their properties are opposite to those of LAT. The couple LAT-ICP0 transcripts could thus represent the molecular aspect of the classic opposition between latency and reactivation of HSV1.