Herpes virus latency in sensory ganglia - a comparison with endogenous neuronal gene expression

Central to infection by a majority of DNA viruses is the expression of enco ded proteins that modify cell cycle. Viruses such as SV40 and Adenovirus vi ruses encode proteins that interact directly, or indirectly, with key cell cycle proteins such as CBP300 and the retinoblastoma gene product. However, neurons do not have a cell cycle as we generally describe it and this is a lso reflected in the difficulty in obtaining immortalised neuronal cultures . The replication strategies of viruses that infect post-mitotic cells such as neurons may be different from infection of other somatic cells. The lif e cycle for viral latency or slow infection of neurons appears to involve s ilencing or restricting expression of the viral genome until such times as dictated by the environment. These signals from the environment usually ref lect cell stress, otherwise the cell appears to tolerate the existence of t he virus genome. We will review the genomic structure of alphaherpesviruses in neurons and transcriptional control mechanisms that may regulate expres sion. Where appropriate we will contrast and compare virus and endogenous n euronal gene expression. (C) 1999 Elsevier Science Ltd. All rights reserved .