Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway

Like all herpesviruses, herpes simplex virus 1 (HSV1) is able to produce lytic or latent infections depending on the host cell type. Lytic infections occur in a broad range of cells while latency is highly specific for neurons. Although latency suggests itself as an attractive target for novel anti-...

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Main Author: Jay C. Brown
Format: Article
Language:English
Published: Hindawi Limited 2017-01-01
Series:Advances in Virology
Online Access:http://dx.doi.org/10.1155/2017/7028194
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spelling doaj-4fad49a4f1034de9905ce72bb7fa89e52021-07-02T01:47:00ZengHindawi LimitedAdvances in Virology1687-86391687-86472017-01-01201710.1155/2017/70281947028194Herpes Simplex Virus Latency: The DNA Repair-Centered PathwayJay C. Brown0Department of Microbiology, Immunology, and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USALike all herpesviruses, herpes simplex virus 1 (HSV1) is able to produce lytic or latent infections depending on the host cell type. Lytic infections occur in a broad range of cells while latency is highly specific for neurons. Although latency suggests itself as an attractive target for novel anti-HSV1 therapies, progress in their development has been slowed due in part to a lack of agreement about the basic biochemical mechanisms involved. Among the possibilities being considered is a pathway in which DNA repair mechanisms play a central role. Repair is suggested to be involved in both HSV1 entry into latency and reactivation from it. Here I describe the basic features of the DNA repair-centered pathway and discuss some of the experimental evidence supporting it. The pathway is particularly attractive because it is able to account for important features of the latent response, including the specificity for neurons, the specificity for neurons of the peripheral compared to the central nervous system, the high rate of genetic recombination in HSV1-infected cells, and the genetic identity of infecting and reactivated virus.http://dx.doi.org/10.1155/2017/7028194
collection DOAJ
language English
format Article
sources DOAJ
author Jay C. Brown
spellingShingle Jay C. Brown
Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway
Advances in Virology
author_facet Jay C. Brown
author_sort Jay C. Brown
title Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway
title_short Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway
title_full Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway
title_fullStr Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway
title_full_unstemmed Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway
title_sort herpes simplex virus latency: the dna repair-centered pathway
publisher Hindawi Limited
series Advances in Virology
issn 1687-8639
1687-8647
publishDate 2017-01-01
description Like all herpesviruses, herpes simplex virus 1 (HSV1) is able to produce lytic or latent infections depending on the host cell type. Lytic infections occur in a broad range of cells while latency is highly specific for neurons. Although latency suggests itself as an attractive target for novel anti-HSV1 therapies, progress in their development has been slowed due in part to a lack of agreement about the basic biochemical mechanisms involved. Among the possibilities being considered is a pathway in which DNA repair mechanisms play a central role. Repair is suggested to be involved in both HSV1 entry into latency and reactivation from it. Here I describe the basic features of the DNA repair-centered pathway and discuss some of the experimental evidence supporting it. The pathway is particularly attractive because it is able to account for important features of the latent response, including the specificity for neurons, the specificity for neurons of the peripheral compared to the central nervous system, the high rate of genetic recombination in HSV1-infected cells, and the genetic identity of infecting and reactivated virus.
url http://dx.doi.org/10.1155/2017/7028194
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