ArticleJournal of virology2009
Regulation of histone deposition on the herpes simplex virus type 1 genome during lytic infection.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 57 citations in OpenAlex.
- BAF chromatin remodeling complexes inhibit immediate-early and early, but not late, transcription of herpes simplex virus 1.bioRxiv : the preprint server for biology · 2026Article
- Equine histones are mobilized within equid alphaherpesvirus 1 (EHV1) replication compartments.Journal of virology · 2025Article
- 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
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- Models of Herpes Simplex Virus Latency.Viruses · 2024Review
- Histone H2A variant H2A.B is enriched in transcriptionally active and replicating HSV-1 lytic chromatin.Journal of virology · 2024Article
- Article
- c-Jun signaling during initial HSV-1 infection modulates latency to enhance later reactivation in addition to directly promoting the progression to full reactivation.Journal of virology · 2024Article
- 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
- c-Jun Signaling During Initial HSV-1 Infection Modulates Latency to Enhance Later Reactivation in addition to Directly Promoting the Progression to Full Reactivation.bioRxiv : the preprint server for biology · 2023Article
- DLK-Dependent Biphasic Reactivation of Herpes Simplex Virus Latency Established in the Absence of Antivirals.Journal of virology · 2022Article
- Human cytomegalovirus lytic infection inhibits replication-dependent histone synthesis and requires stem loop binding protein function.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- The HSV-1 ubiquitin ligase ICP0: Modifying the cellular proteome to promote infection.Virus research · 2020Review
- Chromatin dynamics and the transcriptional competence of HSV-1 genomes during lytic infections.PLoS pathogens · 2019Article
- The canonical Wnt/β-catenin signaling pathway stimulates herpes simplex virus 1 productive infection.Virus research · 2018Article
- Timing Is Everything.mBio · 2018Article
- Promoting Simultaneous Onset of Viral Gene Expression Among Cells Infected with Herpes Simplex Virus-1.Frontiers in microbiology · 2017Article
- Cellular Transcriptional Coactivator RanBP10 and Herpes Simplex Virus 1 ICP0 Interact and Synergistically Promote Viral Gene Expression and Replication.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
During lytic infection by herpes simplex virus type 1 (HSV-1), histones are present at relatively low levels on the viral genome. However, the mechanisms that account for such low levels--how histone deposition on the viral genome is blocked or how histones are removed from the genome--are not yet defined. In this study, we show that histone occupancy on the viral genome gradually increased with time when transcription of the viral immediate-early (IE) genes was inhibited either by deletion of the VP16 activation domain or by chemical inhibition of RNA polymerase II (RNAP II). Inhibition of IE protein synthesis by cycloheximide did not affect histone occupancy on most IE promoters and coding regions but did cause an increase at delayed-early and late gene promoters. IE gene transcription from HSV-1 genomes associated with high levels of histones was stimulated by superinfection with HSV-2 without altering histone occupancy or covalent histone modifications at IE gene promoters. Moreover, RNAP II and histones cooccupied the viral genome in this context, indicating that RNAP II does not preferentially associate with viral genomes that are devoid of histones. These results suggest that during lytic infection, VP16, RNAP II, and IE proteins may all contribute to the low levels of histones on the viral genome, and yet the dearth of histones is neither a prerequisite for nor a necessary result of VP16-dependent transcription of nucleosomal viral genomes.
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