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A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kennedy, Peter G. E. Rovnak, Joel Badani, Hussain Cohrs, Randall J.
Description	Country affiliation: United kingdom Author Affiliation: Kennedy PG ( 1Institute of Infection, Immunity and Inflammation, University of Glasgow, Garscube Campus, Glasgow G61 1QH, UK.); Rovnak J ( 2Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80521, USA.); Badani H ( 3Department of Neurology, University of Colorado Medical School, Aurora, CO 80045, USA.); Cohrs RJ ( 3Department of Neurology, University of Colorado Medical School, Aurora, CO 80045, USA 4Department of Microbiology, University of Colorado Medical School, Aurora, CO 80045, USA.)
Abstract	Herpes simplex virus type 1 (HSV-1; human herpesvirus 1) and varicella-zoster virus (VZV; human herpesvirus 3) are human neurotropic alphaherpesviruses that cause lifelong infections in ganglia. Following primary infection and establishment of latency, HSV-1 reactivation typically results in herpes labialis (cold sores), but can occur frequently elsewhere on the body at the site of primary infection (e.g. whitlow), particularly at the genitals. Rarely, HSV-1 reactivation can cause encephalitis; however, a third of the cases of HSV-1 encephalitis are associated with HSV-1 primary infection. Primary VZV infection causes varicella (chickenpox) following which latent virus may reactivate decades later to produce herpes zoster (shingles), as well as an increasingly recognized number of subacute, acute and chronic neurological conditions. Following primary infection, both viruses establish a latent infection in neuronal cells in human peripheral ganglia. However, the detailed mechanisms of viral latency and reactivation have yet to be unravelled. In both cases latent viral DNA exists in an 'end-less' state where the ends of the virus genome are joined to form structures consistent with unit length episomes and concatemers, from which viral gene transcription is restricted. In latently infected ganglia, the most abundantly detected HSV-1 RNAs are the spliced products originating from the primary latency associated transcript (LAT). This primary LAT is an 8.3 kb unstable transcript from which two stable (1.5 and 2.0 kb) introns are spliced. Transcripts mapping to 12 VZV genes have been detected in human ganglia removed at autopsy; however, it is difficult to ascribe these as transcripts present during latent infection as early-stage virus reactivation may have transpired in the post-mortem time period in the ganglia. Nonetheless, low-level transcription of VZV ORF63 has been repeatedly detected in multiple ganglia removed as close to death as possible. There is increasing evidence that HSV-1 and VZV latency is epigenetically regulated. In vitro models that permit pathway analysis and identification of both epigenetic modulations and global transcriptional mechanisms of HSV-1 and VZV latency hold much promise for our future understanding in this complex area. This review summarizes the molecular biology of HSV-1 and VZV latency and reactivation, and also presents future directions for study.
File Format	HTM / HTML
ISSN	00221317
e-ISSN	14652099
DOI	10.1099/vir.0.000128
Journal	Journal of General Virology
Issue Number	Pt 7
Volume Number	96
Language	English
Publisher	Microbiology Society
Publisher Date	2015-07-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Comparative Study Discipline Virology Virus Latency Neurons Epigenesis, Genetic Herpesvirus 3, Human Ganglia Herpesvirus 1, Human Virology Gene Expression Regulation, Viral Transcription, Genetic Physiology Virus Activation
Content Type	Text
Resource Type	Article
Subject	Virology

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A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation

Distribution of Latent Herpes Simplex Virus Type-1 and Varicella Zoster Virus DNA in Human Trigeminal Ganglia

Neuronal expression of herpes simplex virus-1 VP16 protein induces pseudorabies virus escape from silencing and reactivation.

Broadening the repertoire of functional herpes simplex virus type 1-specific CD8+ T cells reduces viral reactivation from latency in sensory ganglia.

Varicella Virus-Host Interactions During Latency and Reactivation: Lessons From Simian Varicella Virus

Patterns of gene expression and sites of latency in human nerve ganglia are different for varicella-zoster and herpes simplex viruses.

Modulation of reactivation of latent herpes simplex virus 1 in ganglionic organ cultures by p300/CBP and STAT3.

The herpes simplex virus type 1 ICP0 promoter is activated by viral reactivation stimuli in trigeminal ganglia neurons of transgenic mice

A historical analysis of herpes simplex virus promoter activation in vivo reveals distinct populations of latently infected neurones.

A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation.

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