Herpesvirus lytic replication and the cell cycle: arresting new developments.

Flemington EK.

Department of Pathology, Tulane Health Sciences Center, New Orleans, LA 70112.

J Virol. 2001 May;75(10):4475-81.

Abstract
It has been clear for a number of years that small DNA tumor viruses such as SV40 and papilloma virus interact with cell cycle control pathways during lytic replication in a way that promotes entry into the S-phase of the cell cycle. Since these viruses do not code for their own DNA polymerase or other accessory factors that support DNA replication, this strategy is a means of subverting the cell cycle control machinery to support viral DNA replication. In contrast to these viruses, herpesviruses contain a much greater genetic complexity that encodes a viral DNA polymerase, as well as accessory factors involved in generating nucleotide pools, etc. Indeed, herpesviruses have evolved a distinct viral replication strategy and unlike SV40 and papilloma virus, herpesviruses do not require an S phase environment to support viral replication. Further, numerous studies from several different herpesviral systems have provided unifying evidence that these viruses encode factors that elicit a cell cycle block, thereby actively preventing entry into S phase. The conserved nature of this function across different members of the herpesvirus family suggests that it is an integral aspect of the herpesviral replication strategy. As discussed here, regulation of the cell cycle during herpesviral DNA replication has evolved as a complex series of interactions involving multiple viral factors, further implying an important role for this function in the life cycle of the virus.