ArticleThe Journal of cell biology2023
HSV-1 exploits host heterochromatin for nuclear egress.
Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Nucleus softens during herpesvirus infection.PLoS pathogens · 2026Article
- The inner nuclear membrane protein LEMD3 organizes the 3D chromatin architecture to maintain vascular smooth muscle cell identity.Nature communications · 2025Article
- Human cytomegalovirus induces neuronal gene expression through IE1 for viral maturation.Nature communications · 2025Article
- Sequestration of ribosome biogenesis factors in HSV-1 nuclear aggregates revealed by spatially resolved thermal profiling.Science advances · 2025Article
- Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking.Nature communications · 2025Article
- Intracellular and extracellular dynamics of herpes simplex virus 1 DNA and infectious particles in epithelial and neuronal cells.bioRxiv : the preprint server for biology · 2025Article
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- Controlling Much? Viral Control of Host Chromatin Dynamics.Annual review of virology · 2024Review
- Nucleation and spreading maintain Polycomb domains every cell cycle.Cell reports · 2024Article
- 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
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Authors and funding
9 authors.
Funding
Abstract
Herpes simplex virus (HSV-1) progeny form in the nucleus and exit to successfully infect other cells. Newly formed capsids navigate complex chromatin architecture to reach the inner nuclear membrane (INM) and egress. Here, we demonstrate by transmission electron microscopy (TEM) that HSV-1 capsids traverse heterochromatin associated with trimethylation on histone H3 lysine 27 (H3K27me3) and the histone variant macroH2A1. Through chromatin profiling during infection, we revealed global redistribution of these marks whereby massive host genomic regions bound by macroH2A1 and H3K27me3 correlate with decreased host transcription in active compartments. We found that the loss of these markers resulted in significantly lower viral titers but did not impact viral genome or protein accumulation. Strikingly, we discovered that loss of macroH2A1 or H3K27me3 resulted in nuclear trapping of capsids. Finally, by live-capsid tracking, we quantified this decreased capsid movement. Thus, our work demonstrates that HSV-1 takes advantage of the dynamic nature of host heterochromatin formation during infection for efficient nuclear egress.
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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.