%0 Journal Article
%T Tegument protein control of latent herpesvirus establishment and animation
%A Rhiannon R Penkert
%A Robert F Kalejta
%J Herpesviridae
%D 2011
%I BioMed Central
%R 10.1186/2042-4280-2-3
%X Herpesviruses are large double-stranded DNA viruses with a unique virion morphology consisting of a genome-containing capsid, a proteinaceous tegument, and a lipid envelope. Human herpesviruses are divided into three families (alpha, beta, and gamma) based on tissue tropism and sequence similarity [1]. The amplification of virus within an infected cell or host is accomplished by productive, lytic infection where, upon entry into a susceptible cell (Table 1), a specific cascade of viral gene expression is activated, the genome is replicated to high levels, and infectious progeny virions are assembled and released. The lytic cascade of herpesvirus gene expression initiates with the synthesis of the immediate early (IE) genes. Early and late gene expression follows [1]. Provocatively, unlike other large DNA viruses, many herpesvirus IE genes are not controlled by promoters that are efficient and constitutively active within the context of the viral genome. Rather, viral transactivator proteins incorporated into the virion tegument and released into the cell upon infection play critical roles in the activation of viral IE gene expression [2-5]. Such a mechanism permits a far greater level of regulation than a simple constitutive promoter would allow.The productive, lytic cycle is not the only possible outcome upon viral infection of an individual cell. In certain cell types (Table 1), herpesvirus infections establish the viral genomes in the nucleus but a productive round of replication is not completed in a timely manner. In such cells, a different, significantly smaller subset of viral genes is expressed. Importantly, because these infected cells maintain the potential to undergo productive replication at some later time after receiving the appropriate stimulus, this type of infection is described as latency. The resumption and completion of productive, lytic replication after a period of latency is called a reactivation event [1]. Both the restriction of substantial
%U http://www.herpesviridae.org/content/2/1/3