A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation
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TLDR
There is increasing evidence that HSV-1 and VZV latency is epigenetically regulated, and in vitro models that permit pathway analysis and identification of both epigenetic modulations and global transcriptional mechanisms hold much promise for the future understanding in this complex area.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.read more
Citations
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Journal ArticleDOI
Clinical Features of Varicella-Zoster Virus Infection.
TL;DR: Varicella-zoster virus (VZV) is a pathogenic human herpes virus that causes varicella (chickenpox) as a primary infection, following which it becomes latent in peripheral ganglia and may reactivate either spontaneously or after a number of triggering factors to cause herpes zoster (shingles).
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The etiology of Bell’s palsy: a review
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Epigenetics and Genetics of Viral Latency.
TL;DR: Eradicating latent virus has become an important but elusive challenge and will require a more complete understanding of the mechanisms controlling these processes.
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Diagnosis, antiviral therapy, and prophylaxis of varicella-zoster virus infections
TL;DR: The present manuscript provides an overview about the basic knowledge of VZV infections, their laboratory diagnosis, antiviral therapy, and the prevention procedures, especially in Germany.
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Varicella-zoster virus infection: natural history, clinical manifestations, immunity and current and future vaccination strategies.
Giulia Freer,Mauro Pistello +1 more
TL;DR: The natural history and pathophysiology of VZV infection and its current epidemiology are described and an overview of current and future vaccine options to protect against varicella and/or zoster are provided.
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