The survival strategy of herpes simplex virus centres on the establishment of latency in sensory neurons innervating the site of primary infection followed by periodic reactivation to facilitate transmission. This is a highly evolved and efficient survival mechanism, which despite being the subject of intense research, has proven remarkably difficult to dissect at a molecular level. This review will focus on data, emerging from both in vitro and in vivo model systems, which provide a framework for a mechanistic understanding of latency and the existence and possible significance of non-uniform latent states.