ArticleProceedings of the National Academy of Sciences of the United States of America2013
HSV carrying WT REST establishes latency but reactivates only if the synthesis of REST is suppressed.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- REST Is Restless in Neuronal and Non-Neuronal Virus Infections: An In Silico Analysis-Based Perspective.Viruses · 2025Review
- Evolution of lysine-specific demethylase 1 and REST corepressor gene families and their molecular interaction.Communications biology · 2023Article
- Review
- The chromatin remodeler SRCAP promotes self-renewal of intestinal stem cells.The EMBO journal · 2020Article
- Disturbed Yin-Yang balance: stress increases the susceptibility to primary and recurrent infections of herpes simplex virus type 1.Acta pharmaceutica Sinica. B · 2020Review
- Article
- Differentially expressed genes during spontaneous lytic switch of Marek's disease virus in lymphoblastoid cell lines determined by global gene expression profiling.The Journal of general virology · 2017Article
- Silencing of Viral Elements: An Available Cure for Schizophrenia?Frontiers in psychiatry · 2017Article
- Intrinsic and Innate Defenses of Neurons: Détente with the Herpesviruses.Journal of virology · 2017Review
- 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
- Role of activating transcription factor 3 in the synthesis of latency-associated transcript and maintenance of herpes simplex virus 1 in latent state in ganglia.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Clues to mechanisms of herpesviral latent infection and potential cures.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- KDM1 class flavin-dependent protein lysine demethylases.Biopolymers · 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
- Review
- Modulation of reactivation of latent herpes simplex virus 1 in ganglionic organ cultures by p300/CBP and STAT3.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
HSVs transit from vigorous replication at the portal of entry into the body to a latent state in sensory neurons in which only noncoding (e.g., latency-associated transcript) and micro-RNAs are expressed. In productive infection, viral genes must be sequentially derepressed at two checkpoints. A leading role in the repression of viral genes is carried out by histone deacetylase (HDAC)/corepressor element-1 silencing transcription factor (CoREST)/lysinespecific demethylase1(LSD1)/RE1-silencing transcription factor (REST) repressor complex (HCLR). Previously, we reported that to define the role of the components of the HCLR complex in the establishment of latency, we constructed recombinant virus (R112) carrying a dominant-negative REST that bound response elements in DNA but could not recruit repressive proteins. This recombinant virus was unable to establish latency. In the current studies, we constructed a virus (R111) carrying WT REST with a WT genome. We report the following findings: (a) R111 readily established latent infection in trigeminal ganglia; however, although the amounts of viral DNAs in latently infected neurons were similar to those of WT virus, the levels of latency-associated transcript and micro-RNAs were 50- to 100-fold lower; (b) R111 did not spontaneously reactivate in ganglionic organ cultures; however, viral genes were expressed if the synthesis of REST was blocked by cycloheximide; and (c) histone deacetylase inhibitors reactivated the WT parent but not the R111 recombinant virus. The results suggest that REST plays a transient role in the establishment of latency but not in reactivation and suggest the existence of at least two phases at both establishment and reactivation.
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