ArticlePloS one2010
Changes to euchromatin on LAT and ICP4 following reactivation are more prevalent in an efficiently reactivating strain of HSV-1.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- Systematic identification and characterization of virus lncRNAs suggests extensive structural mimicry of host lncRNAs.Briefings in bioinformatics · 2025Article
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- Lytic promoter activity during herpes simplex virus latency is dependent on genome location.Journal of virology · 2024Article
- The HSV-1 encoded CCCTC-binding factor, CTRL2, impacts the nature of viral chromatin during HSV-1 lytic infection.PLoS pathogens · 2024Article
- The immunobiology of herpes simplex virus encephalitis and post-viral autoimmunity.Brain : a journal of neurology · 2024Review
- Article
- Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy.Antiviral research · 2021Review
- Cohesin subunit Rad21 binds to the HSV-1 genome near CTCF insulator sites during latencyJournal of virology · 2021Article
- Strength in diversity: Understanding the pathways to herpes simplex virus reactivation.Virology · 2018Review
- Article
- Depletion of the Insulator Protein CTCF Results in Herpes Simplex Virus 1 ReactivationJournal of virology · 2018Article
- Human CHAC1 Protein Degrades Glutathione, and mRNA Induction Is Regulated by the Transcription Factors ATF4 and ATF3 and a Bipartite ATF/CRE Regulatory Element.The Journal of biological chemistry · 2015Article
- Dynamic modulation of HSV chromatin drives initiation of infection and provides targets for epigenetic therapies.Virology · 2015Review
- Characterization of herpes simplex virus 2 primary microRNA Transcript regulation.Journal of virology · 2015Article
- Inhibition of LSD1 reduces herpesvirus infection, shedding, and recurrence by promoting epigenetic suppression of viral genomes.Science translational medicine · 2014Article
- Epigenetic repression of herpes simplex virus infection by the nucleosome remodeler CHD3.mBio · 2014Article
- Role of polycomb proteins in regulating HSV-1 latency.Viruses · 2013Review
- Article
- CTCF occupation of the herpes simplex virus 1 genome is disrupted at early times postreactivation in a transcription-dependent manner.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEpigenetic mechanisms, via post-translational histone modifications, have roles in the establishment and maintenance of latency of the HSV-1 genome in the sensory neurons. Considering that many post-translational histone marks are reversible in nature, epigenetic mechanisms may also play a critical role in the process of induced HSV-1 reactivation. METHODOLOGY/PRINCIPAL
findingsThis study utilized the rabbit ocular model of HSV-1 infection and reactivation, induced by the transcorneal iontophoresis of epinephrine (TCIE), to characterize changes to chromatin that occur between 0.5 and 4 h following the application of the reactivation stimulus. Our goal was to explore the hypothesis that chromatin remodeling is an early and essential step in the process of HSV-1 reactivation. Analysis of the HSV-1 latently infected rabbit trigeminal ganglia (TG) showed that enrichment of the euchromatic marker H3K4me2 significantly decreased in the LAT 5'exon region (∼2.5-fold) and significantly increased in the lytic ICP4 promoter region (∼3-fold) by 1 h post-TCIE in the highly efficient reactivating McKrae strain of HSV-1. In contrast, we observed no significant change in the euchromatic marks of H3K4me2 associated with LAT 5'exon or ICP4 promoter regions of the poorly reactivating KOS strain of HSV-1 following TCIE through 4 h. The implication that these observed epigenetic changes were linked to transcriptional activity was confirmed by qRT-PCR examining both LAT and lytic transcript abundance following TCIE. We found a significant decrease in the abundance of LAT RNA by 2 h post-iontophoresis of epinephrine coupled to an increase in the transcript abundance of ICP4 in the McKrae strain of HSV-1. By comparison, we observed no change in the LAT or ICP4 transcript abundance of the poor reactivator KOS following iontophoresis of epinephrine through 4 h. CONCLUSIONS/SIGNIFICANCE: Our results implicate that chromatin remodeling is an early and essential step involved in the process of in vivo HSV-1 reactivation.
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