ArticleJournal of virology2023
HSV-1 Infection Induces a Downstream Shift of Promoter-Proximal Pausing for Host Genes.
Article in Journal of virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Analysis of host and viral nascent and steady-state RNA levels in a human neuronal model of herpes simplex virus 1 infection.PLoS pathogens · 2026Article
- Cell type differences in human cytomegalovirus transcription and epigenetic regulation with insights into major immediate-early enhancer-promoter control.PLoS pathogens · 2025Article
- HSV-1 infection induces a downstream shift of the +1 nucleosome.Journal of virology · 2025Article
- HSV-1 ICP22 condensates impair host transcription by depleting promoter RNAPII Ser-2P occupation.Frontiers in microbiology · 2025Article
- Aberrant RNA polymerase initiation and processivity on the genome of a herpes simplex virus 1 mutant lacking ICP27.Journal of virology · 2024Article
- A Revision of Herpes Simplex Virus Type 1 Transcription: First, Repress; Then, Express.Microorganisms · 2024Review
- RegCFinder: targeted discovery of genomic subregions with differential read density.Bioinformatics advances · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus 1 (HSV-1) infection exerts a profound shutoff of host gene expression at multiple levels. Recently, HSV-1 infection was reported to also impact promoter-proximal RNA polymerase II (Pol II) pausing, a key step in the eukaryotic transcription cycle, with decreased and increased Pol II pausing observed for activated and repressed genes, respectively. Here, we demonstrate that HSV-1 infection induces more complex alterations in promoter-proximal pausing than previously suspected for the vast majority of cellular genes. While pausing is generally retained, it is shifted to more downstream and less well-positioned sites for most host genes. The downstream shift of Pol II pausing was established between 1.5 and 3 h of infection, remained stable until at least 6 hours postinfection, and was observed in the absence of ICP22. The shift in Pol II pausing does not result from alternative
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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.