HSV-Cellular Protein Interactions

Abstract

The herpes simplex virus (HSV) lytic cycle is dependent on a precise temporal pattern of viral gene expression with the initial expression of the immediate-early (IE) genes, followed by the early genes, and finally late gene expression (1). Although such a temporal cascade of viral gene expression involves the action of virally encoded regulatory proteins, such factors act, at least in part, by interacting with cellular transcription factors that are present in the uninfected cell. Thus, although the HSV virion protein Vmw65 is essential for transactivation of the viral IE genes in lytic infection by binding to the TAATGARAT sequences in the promoters (2), it can only achieve this by forming a complex with the cellular transcription factor Oct-1 (3,4) and other cellular factors (5). Similarly, the IE promoters contain binding sites for other cellular transcription factors such as Spl (6) and this is also observed in the promoters for viral genes of other kinetic classes, such as the early gene encoding thymidine kinase (7).