ICPO, a regulator of herpes simplex virus during lytic and latent infection

Cold sores produced by HSV-1 infection are an annoying but trivial recurren t problem for most of us, but the virus can also cause more serious disease . Episodes of active HSV-1 infection, in response to stress or sunlight, ar e possible because the virus establishes a latent infection in neurones whi ch can not be eliminated. Since vigorous transcription from the whole viral genome during lytic infection contrasts with almost complete quiescence du ring latency, the mechanisms controlling HSV-1 gene expression have come un der close scrutiny. These studies have demonstrated that the viral immediat e-early protein ICP0, a promiscuous activator of gene expression, is requir ed for efficient initiation of lytic infection and reactivation from latenc y. It is proposed that in the absence of functional ICP0, a cellular repres sion mechanism silences viral transcription. ICP0 appears to counteract thi s process by stimulating the degradation of a number of cellular proteins v ia the ubiquitin-proteasome pathway. (C) 2000 John Wiley & Sons, Inc.