ArticleNature communications2025
Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed.
- 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
- MEK/ERK-Mediated Transcriptional Repression of Metabolic Genes Confers Host Defense AgainstMicroorganisms · 2026Article
- Transcriptional transactivation turns human iPSC-derived macrophages into an adenovirus-producing cell state.Journal of virology · 2026Article
- Stable state of hepatocyte chromatin during hepatitis B virus infection.Scientific reports · 2026Article
- A framework for the exploration of subcellular compartmentalization of RNA-binding proteins.Nature communications · 2026Article
- Roles of the cGAS-STING signaling pathway in viral latency.Journal of virology · 2026Review
- Review
- Dynamic chromatin accessibility and transcriptional landscapes of porcine kidney cells during pseudorabies virus infection.Frontiers in immunology · 2026Article
- Nucleus softens during herpesvirus infection.PLoS pathogens · 2026Article
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- Camptothecin, a topoisomerase I inhibitor, impedes productive herpes simplex virus type 1 infection.Journal of virology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) remodels the host chromatin structure and induces a host-to-virus transcriptional switch during lytic infection. We combine super-resolution imaging and chromosome-capture technologies to identify the mechanism of remodeling. We show that the host chromatin undergoes massive condensation caused by the hijacking of RNA polymerase II (RNAP II) and topoisomerase I (TOP1). In addition, HSV-1 infection results in the rearrangement of topologically associating domains and loops, although the A/B compartments are maintained in the host. The position of viral genomes and their association with RNAP II and cohesin is determined nanometrically. We reveal specific host-HSV-1 genome interactions and enrichment of upregulated human genes in the most contacting regions. Finally, TOP1 inhibition fully blocks HSV-1 infection, suggesting possible antiviral strategies. This viral mechanism of host chromatin rewiring sheds light on the role of transcription in chromatin architecture.
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Registered trials
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