ArticleNature communications2023
The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 19 citations in OpenAlex.
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
- Integrated Analysis of Chromatin Accessibility and Transcriptional Dynamics of the Viral Genome Following Pseudorabies Virus Infection.International journal of molecular sciences · 2026Article
- Targeted mutagenesis of the ICP4 transactivation domain generates a protective DIVA vaccine against duck plague.Poultry science · 2026Article
- Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC.iScience · 2026Article
- Alpha-herpesvirus US1 interacts with cGAS to suppress type I IFN responses and antiviral defense.PLoS pathogens · 2025Article
- Multiple long-rangemBio · 2025Article
- Antitumor power of oncolytic HSV engineered with IL-12 and IL-15.Molecular therapy. Oncology · 2025Article
- Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking.Nature communications · 2025Article
- HSV-1 infection induces a downstream shift of the +1 nucleosome.Journal of virology · 2025Article
- IP6K2 mutations as a novel mechanism of resistance to oncolytic virus therapy.Journal of translational medicine · 2025Article
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
- Identification of Viral Variants from Functional Genomics Data.F1000Research · 2025Article
- HSV-1 ICP22 condensates impair host transcription by depleting promoter RNAPII Ser-2P occupation.Frontiers in microbiology · 2025Article
- Impact of the interaction between herpes simplex virus 1 ICP22 and FACT on viral gene expression and pathogenesis.Journal of virology · 2024Article
- A Revision of Herpes Simplex Virus Type 1 Transcription: First, Repress; Then, Express.Microorganisms · 2024Review
- HSV-1 Infection Induces a Downstream Shift of Promoter-Proximal Pausing for Host Genes.Journal of virology · 2023Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus 1 (HSV-1) infection and stress responses disrupt transcription termination by RNA Polymerase II (Pol II). In HSV-1 infection, but not upon salt or heat stress, this is accompanied by a dramatic increase in chromatin accessibility downstream of genes. Here, we show that the HSV-1 immediate-early protein ICP22 is both necessary and sufficient to induce downstream open chromatin regions (dOCRs) when transcription termination is disrupted by the viral ICP27 protein. This is accompanied by a marked ICP22-dependent loss of histones downstream of affected genes consistent with impaired histone repositioning in the wake of Pol II. Efficient knock-down of the ICP22-interacting histone chaperone FACT is not sufficient to induce dOCRs in ΔICP22 infection but increases dOCR induction in wild-type HSV-1 infection. Interestingly, this is accompanied by a marked increase in chromatin accessibility within gene bodies. We propose a model in which allosteric changes in Pol II composition downstream of genes and ICP22-mediated interference with FACT activity explain the differential impairment of histone repositioning downstream of genes in the wake of Pol II in HSV-1 infection.
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