ArticleProceedings of the National Academy of Sciences of the United States of America2010
Disruption of HDAC/CoREST/REST repressor by dnREST reduces genome silencing and increases virulence of herpes simplex virus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- Unraveling the layers of epigenetic control in respiratory antiviral defense.Journal of virology · 2026Review
- RNA-binding protein PTBP1 mediates HSV-1 attachment and infection through regulation of heparan sulfate 3-O-sulfotransferase gene expression.Cell & bioscience · 2025Article
- The immunogenetic basis of severe herpes simplex infections in neonates and children: a review.Pediatric research · 2025Review
- REST Is Restless in Neuronal and Non-Neuronal Virus Infections: An In Silico Analysis-Based Perspective.Viruses · 2025Review
- Establishing a Herpesvirus Quiescent Infection in Differentiated Human Dorsal Root Ganglion Neuronal Cell Line Mediated by Micro-RNA Overexpression.Pathogens (Basel, Switzerland) · 2022Article
- Histone modifiers at the crossroads of oncolytic and oncogenic viruses.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
- Review
- Cutaneous innate immune tolerance is mediated by epigenetic control of MAP2K3 by HDAC8/9.Science immunology · 2021Article
- Herpesvirus latency.The Journal of clinical investigation · 2020Review
- Pharmacological inhibition of LSD1 activity blocks REST-dependent medulloblastoma cell migration.Cell communication and signaling : CCS · 2018Article
- Epigenetics and Genetics of Viral Latency.Cell host & microbe · 2016Review
- Role of ND10 nuclear bodies in the chromatin repression of HSV-1.Virology journal · 2016Review
- miR-H28 and miR-H29 expressed late in productive infection are exported and restrict HSV-1 replication and spread in recipient cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation.The Journal of general virology · 2015Review
- KDM1 class flavin-dependent protein lysine demethylases.Biopolymers · 2015Review
- Dynamic modulation of HSV chromatin drives initiation of infection and provides targets for epigenetic therapies.Virology · 2015Review
- The 3 facets of regulation of herpes simplex virus gene expression: A critical inquiry.Virology · 2015Review
- Combining HDAC inhibitors with oncolytic virotherapy for cancer therapy.Oncolytic virotherapy · 2015Review
- Cells infected with herpes simplex virus 1 export to uninfected cells exosomes containing STING, viral mRNAs, and microRNAs.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In nonneuronal cells, herpes simplex virus 1 overcomes host defenses, replicates, and ultimately kills the infected cell. Among the host defenses suppressed by the virus is a repressor complex whose key components are histone deacetylase (HDAC) 1 or 2, RE-1 silencing transcription factor (REST), corepressor of REST (CoREST), and lysine-specific demethylase (LSD) 1. In neurons innervating cells at the portal of entry into the body, the virus establishes a "latent" infection in which viral DNA is silenced with the exception of a family of genes. The question posed here is whether the virus hijacks this repressor complex to silence itself in neurons during the latent state. To test this hypothesis, we inserted into the wild-type virus genome a wild-type REST [recombinant (R) 111], a dominant-negative REST (dnREST) lacking the N- and C-terminal repressor domains (R112), or an insertion control consisting of tandem repeats of stop codons (R113). The recombinant virus R112 carrying the dnREST replicated better and was more virulent than the wild-type parent or the other recombinant viruses when administered by the corneal or i.p. routes. Moreover, in contrast to other recombinants, corneal route inoculation by R112 recombinant virus resulted in higher DNA copy numbers, higher levels of infectious virus in eye, trigeminal ganglion, or brain, and virtually complete destruction of trigeminal ganglia in mice that may ultimately succumb to infection. These results support an earlier conclusion that the HDAC/CoREST/REST/LSD1 repressor complex is a significant component of the host innate immunity and are consistent with the hypothesis that HSV-1 hijacks the repressor to silence itself during latent infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.