ReviewViruses2013
Chromatin dynamics during lytic infection with herpes simplex virus 1.
Review in Viruses, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
24 citing papers in PubMed, 40 citations in OpenAlex.
- Equine histones are mobilized within equid alphaherpesvirus 1 (EHV1) replication compartments.Journal of virology · 2025Article
- Epigenetic drugs against human DNA viruses and retroviruses.Antiviral research · 2025Review
- HSV-1 infection induces a downstream shift of the +1 nucleosome.Journal of virology · 2025Article
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- Histone H2A variant H2A.B is enriched in transcriptionally active and replicating HSV-1 lytic chromatin.Journal of virology · 2024Article
- Article
- Single-genome analysis reveals heterogeneous association of the Herpes Simplex Virus genome with H3K27me2 and the reader PHF20L1 following infection of human fibroblasts.bioRxiv : the preprint server for biology · 2023Article
- Human cytomegalovirus lytic infection inhibits replication-dependent histone synthesis and requires stem loop binding protein function.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy.Antiviral research · 2021Review
- Article
- Virus DNA Replication and the Host DNA Damage Response.Annual review of virology · 2018Review
- Characterization of Elements Regulating the Nuclear-to-Cytoplasmic Translocation of ICP0 in Late Herpes Simplex Virus 1 Infection.Journal of virology · 2018Article
- Timing Is Everything.mBio · 2018Article
- Importin α1 is required for nuclear import of herpes simplex virus proteins and capsid assembly in fibroblasts and neurons.PLoS pathogens · 2018Article
- Spatiotemporal dynamics of HSV genome nuclear entry and compaction state transitions using bioorthogonal chemistry and super-resolution microscopy.PLoS pathogens · 2017Article
- Herpes Simplex Virus Establishment, Maintenance, and Reactivation: In Vitro Modeling of Latency.Pathogens (Basel, Switzerland) · 2017Review
- An Essential Viral Transcription Activator Modulates Chromatin Dynamics.PLoS pathogens · 2016Article
- PML plays both inimical and beneficial roles in HSV-1 replication.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Cellular Transcriptional Coactivator RanBP10 and Herpes Simplex Virus 1 ICP0 Interact and Synergistically Promote Viral Gene Expression and Replication.Journal of virology · 2016Article
- Alterations of Nuclear Architecture and Epigenetic Signatures during African Swine Fever Virus Infection.Viruses · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Latent HSV-1 genomes are chromatinized with silencing marks. Since 2004, however, there has been an apparent inconsistency in the studies of the chromatinization of the HSV-1 genomes in lytically infected cells. Nuclease protection and chromatin immunoprecipitation assays suggested that the genomes were not regularly chromatinized, having only low histone occupancy. However, the chromatin modifications associated with transcribed and non-transcribed HSV-1 genes were those associated with active or repressed transcription, respectively. Moreover, the three critical HSV-1 transcriptional activators all had the capability to induce chromatin remodelling, and interacted with critical chromatin modifying enzymes. Depletion or overexpression of some, but not all, chromatin modifying proteins affected HSV-1 transcription, but often in unexpected manners. Since 2010, it has become clear that both cellular and HSV-1 chromatins are highly dynamic in infected cells. These dynamics reconcile the weak interactions between HSV-1 genomes and chromatin proteins, detected by nuclease protection and chromatin immunoprecipitation, with the proposed regulation of HSV-1 gene expression by chromatin, supported by the marks in the chromatin in the viral genomes and the abilities of the HSV-1 transcription activators to modulate chromatin. It also explains the sometimes unexpected results of interventions to modulate chromatin remodelling activities in infected cells.
Indexed as
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What OpenQuestion holds
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.