Varicella Zoster Virus Transcriptional Regulation and the Roles of VZV IE Proteins
William T. Ruyechan
from: Alpha Herpesviruses: Molecular and Cellular Biology (Edited by: R. M. Sandri-Goldin). Caister Academic Press, U.K. (2006)
Abstract
Varicella zoster virus (VZV) is the causative agent of varicella (chickenpox) upon primary infection. The virus is spread from its initial sites of replication through T cell viremias to the internal organs and skin.VZV establishes latency in dorsal root ganglia and upon reactivation causes zoster (shingles). During productive infection the entire coding capacity of the VZV genome (some 69 unique open reading frames) is believed to be expressed. In contrast, during latent infection, a small number of lytic phase genes are expressed while the remainder of the genome is silent. Thus the biology of VZV infection indicates that control of expression of the viral genome is essential to the ability of the virus to replicate productively in a variety of cell types with minimal complications for the host, and to the establishment and maintenance of latency in neurons. In recent years, our understanding of some of the mechanisms of VZV gene expression and of the proteins which regulate those processes has significantly increased. This includes information on the roles of individual viral proteins and the involvement of ubiquitous cellular transcription factors read more ...
