ArticleJournal of virology2012
CTCF occupation of the herpes simplex virus 1 genome is disrupted at early times postreactivation in a transcription-dependent manner.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- Molecular Mimics: How Viral Genomes Dupe Their Host by Usurping CTCF to Establish Infection.Viruses · 2026Review
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- Multiple long-rangemBio · 2025Article
- Non-replicative herpes simplex virus genomic and amplicon vectors for gene therapy - an update.Gene therapy · 2025Review
- 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
- Host-encoded CTCF regulates human cytomegalovirus latency via chromatin looping.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC.Nucleic acids research · 2023Article
- Three-Dimensional Chromatin Structure of the EBV Genome: A Crucial Factor in Viral Infection.Viruses · 2023Review
- Dynamics of Viral and Host 3D Genome Structure upon Infection.Journal of microbiology and biotechnology · 2022Review
- Human Cytomegalovirus Utilizes Multiple Viral Proteins to Regulate the Basement Membrane Protein Nidogen 1.Journal of virology · 2022Article
- Article
- The three-dimensional structure of Epstein-Barr virus genome varies by latency type and is regulated by PARP1 enzymatic activity.Nature communications · 2022Article
- Recent Issues in Varicella-Zoster Virus Latency.Viruses · 2021Review
- Cohesin subunit Rad21 binds to the HSV-1 genome near CTCF insulator sites during latencyJournal of virology · 2021Article
- Chromatin dynamics and the transcriptional competence of HSV-1 genomes during lytic infections.PLoS pathogens · 2019Article
- The CCCTC Binding Factor, CTRL2, Modulates Heterochromatin Deposition and the Establishment of Herpes Simplex Virus 1 LatencyJournal of virology · 2019Article
- Strength in diversity: Understanding the pathways to herpes simplex virus reactivation.Virology · 2018Review
- Cellular Antisilencing Elements Support Transgene Expression from Herpes Simplex Virus Vectors in the Absence of Immediate Early Gene Expression.Journal of virology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In herpes simplex virus 1 (HSV-1), binding clusters enriched in CTCF during latency have been previously identified. We hypothesized that CTCF binding to CTCF clusters in HSV-1 would be disrupted in a reactivation event. To investigate, CTCF occupation of three CTCF binding clusters in HSV-1 was analyzed following sodium butyrate (NaB)- and explant-induced reactivation in the mouse. Our data show that the CTCF domains positioned within the HSV-1 genome, specifically around the latency-associated transcript (LAT) and ICP0 and ICP4 regions of the genome, lose CTCF occupancy following the application of reactivation stimuli in wild-type virus. We also found that CTCF binding clusters upstream of the ICP0 and ICP4 promoters both function as classical insulators capable of acting as enhancer blockers of the LAT enhancer. Finally, our results suggest that CTCF occupation of domains in HSV-1 may be differentially regulated both during latency and at early times following reactivation by the presence of lytic transcripts and further implicate epigenetic regulation of HSV-1 as a critical component of the latency-reactivation transition.
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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.