Varicella Zoster VirusA review of Varicella Zoster Virus and other alphaherpesviruses.
Varicella Zoster Virusfrom from Alphaherpesviruses: Molecular Virology edited by Sandra K. Weller (2011)
Varicella zoster virus (VZV) is a herpes viruses. It infects humans and other vertebrates. Varicella zoster virus has a smaller genome than herpes simplex virus. VZV induces a lifelong immunity that protects against clinical signs of exogenous re-infection read more ...
Varicella Zoster Virus Transcriptional Regulationfrom Jeffrey I. Cohen writing in Alphaherpesviruses: Molecular Virology:
Varicella-zoster virus (VZV) encodes three immediate-early proteins, IE4, IE62, and IE63; however, only IE62 has TAATGARAT-like sequences in its promoter which are present in the promoters of each of the herpes simplex virus immediate-early proteins. The TAATGARAT-like elements on the IE62 promoter bind to VZV ORF10 protein, Oct, and HCF-1. In addition, histone methyltransferases are recruited to the IE62 promoter to modify chromatin to a transcriptionally active form. VZV IE62, the major VZV transactivator binds to VZV IE4 and IE63, and Med25, part of the mediator complex which upregulates gene expression. VZV IE62, IE4, and IE63 are present in the viral tegument where they may help to regulate transcription early in infection. IE63 binds to several cellular proteins including ASF1 and RNA polymerase II. Two hypotheses have been proposed for regulation of VZV gene expression during latency. First, relocalization of HCF-1 from the cytoplasm to the nucleus of sensory ganglia in response to stimuli associated with reactivation may help to augment transcription of IE62 to reactivate VZV from latency. Second, promoters of latent genes are maintained in a euchromatic state allowing their transcription, while promoters of genes not associated with latency are in a heterochromatic state resulting in repression of transcription read more ...
Varicella-Zoster Virus Glycoproteinsfrom Charles Grose, Susan Vleck, Odd Andre Karlsen and Eduardo A. Montalvo writing in Alphaherpesviruses: Molecular Virology:
Varicella zoster virus has a smaller genome than herpes simplex virus and therefore encodes fewer glycoproteins. In a recent review nine VZV glycoproteins are profiled, including gE, gI, gC, gH, gL, gB, gK, gM, and gN. Although all VZV glycoproteins have HSV homologs, functions occasionally have greatly shifted. For example, VZV gE is the predominant VZV glycoprotein and exists as a monomer, dimer and trimer, as well as a gE/gI complex. VZV gE is essential, unlike HSV gE. Even though essential, mutations in gE had been detected in wild type VZV strains that exhibit an accelerated cell-spread phenotype. The VZV gC glycoprotein differs from HSV gC in that both transcription and translation of VZV gC are remarkably delayed in cultured cells; often VZV gC protein is difficult to detect altogether. The VZV gH/gL complex resembles the HSV gH/gL complex is that both are critical for virus induced fusion. Fusion is a prominent feature of VZV infected cells. Neutralization antibody to VZV gH dramatically reduces the spread of virus and limits pathogenesis in the skin. The VZV gB glycoprotein is also involved in virus-induced fusion. Of interest, four VZV glycoproteins (gE, gI, gH and gB) have functional endocytosis motifs in their cytoplasmic tail. Thus, all four are internalized from the cell surface in clathrin coated vesicles. This pathway appears critical for the process of virion envelopment in the assembly compartment. Even though abundant amounts of most glycoproteins are produced in cell culture, assembly of fully enveloped and infectious VZV particles rarely occurs. The particle:plaque forming unit ratio remains an extremely high 40,000:1. Likewise, the aberrant assembly process severely limits any assessment of egress mechanisms read more ...
Immunity to Varicella Zoster Virusfrom Paul R. Kinchington and Allison Abendroth writing in Alphaherpesviruses: Molecular Virology:
Of three human alphaherpesviruses, only Varicella Zoster Virus (VZV) induces a lifelong immunity that protects against clinical signs of exogenous re-infection and, for most of the population, from any sign of reactivation from the latent state. The importance of VZV specific immunity is exemplified by its absence: severity and morbidity of the primary infection (varicella) and incidence of reactivated disease (zoster) are greatly increased in those with immune compromise, particularly those impaired in the cell mediated immune responses. The protection afforded by VZV specific immunity underlies successful live attenuated vaccines that have greatly impacted the incidence of varicella, and reduce the incidence, severity and complications of zoster. Consequently, the important components of VZV induced immunity and their contribution to the protective state has been well studied and is outlined in a recent review. Less is known of the strategies exploited by VZV to evade the innate and adaptive arms, but their activities are presumed to be critical to extend the life of the infected cell and to enhance viral production and dissemination. Evasion appears to include distinct strategies from those used by Herpes simplex viruses and includes expression of novel immune evasion proteins read more ...
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