ArticleeLife2019
Herpes simplex viral nucleoprotein creates a competitive transcriptional environment facilitating robust viral transcription and host shut off.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 76 citations in OpenAlex.
- Targeted mutagenesis of the ICP4 transactivation domain generates a protective DIVA vaccine against duck plague.Poultry science · 2026Article
- Kaposi's Sarcoma-associated herpesvirus uses a novel protein fold to hijack RNA Polymerase II for viral late gene transcription.bioRxiv : the preprint server for biology · 2026Article
- Article
- Review
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Equine histones are mobilized within equid alphaherpesvirus 1 (EHV1) replication compartments.Journal of virology · 2025Article
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- ATRX Promotes Transcription Initiation of HSV-1 Immediate Early Genes During Early Lytic Infection.Viruses · 2025Article
- Daxx mediated histone H3.3 deposition on HSV-1 DNA restricts genome decompaction and the progression of immediate-early transcription.PLoS pathogens · 2025Article
- Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking.Nature communications · 2025Article
- The impact of fatty acid synthase on HSV-1 infection dynamics.PLoS pathogens · 2025Article
- 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
- Control of HSV-1 Infection: Directions for the Development of CRISPR/Cas-Based Therapeutics and Diagnostics.International journal of molecular sciences · 2024Review
- Fungal Apoptosis-Related Proteins.Microorganisms · 2024Review
- Review
- Herpes simplex virus 1 inhibits phosphorylation of RNA polymerase II CTD serine-7.Journal of virology · 2024Article
- Aberrant RNA polymerase initiation and processivity on the genome of a herpes simplex virus 1 mutant lacking ICP27.Journal of virology · 2024Article
- Review
- Histone H2A variant H2A.B is enriched in transcriptionally active and replicating HSV-1 lytic chromatin.Journal of virology · 2024Article
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
Herpes simplex virus-1 (HSV-1) replicates within the nucleus coopting the host's RNA Polymerase II (Pol II) machinery for production of viral mRNAs culminating in host transcriptional shut off. The mechanism behind this rapid reprogramming of the host transcriptional environment is largely unknown. We identified ICP4 as responsible for preferential recruitment of the Pol II machinery to the viral genome. ICP4 is a viral nucleoprotein which binds double-stranded DNA. We determined ICP4 discriminately binds the viral genome due to the absence of cellular nucleosomes and high density of cognate binding sites. We posit that ICP4's ability to recruit not just Pol II, but also more limiting essential components, such as TBP and Mediator, create a competitive transcriptional environment. These distinguishing characteristics ultimately result in a rapid and efficient reprogramming of the host's transcriptional machinery, which does not occur in the absence of ICP4.
Indexed as
Identifiers
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.