ArticleJournal of virology2009
Transcription of the herpes simplex virus latency-associated transcript promotes the formation of facultative heterochromatin on lytic promoters.
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 173 papers.
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Who cites it
173 citing papers in PubMed, 236 citations in OpenAlex.
- HSV-1 reactivation as an emergent property of neuronal stress: implications for traumatic brain injury.Journal of neuroinflammation · 2026Review
- 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
- Triple Latency as a Driver of Chronic Inflammation: An Integrative View of HSV, EBV, and CMV Persistence in Immunocompetent Hosts.Clinics and practice · 2026Review
- EGR Proteins Mediate Interferon-Independent Anti-HSV-1 Responses Through Viral and Host Targets.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Revisiting giant virus-host dynamics in brown algae: old stories and new perspectives.The EMBO journal · 2026Review
- Counteracting FOX proteins epigenetically control the herpesvirus lytic-latent balance.Nature communications · 2026Article
- AACRNL evolved from virulence factor to epigenetic parasite driving genome expansion in free-living eukaryotes.Nature communications · 2026Article
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Interferon dependent immune memory during HSV-1 neuronal latency via increased H3K9me3 and restriction by ATRX.Nature communications · 2025Article
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- Multiple long-rangemBio · 2025Article
- Article
- Glucocorticoid receptor occupancy of key bovine alphaherpesvirus 1 (BoHV-1) promoters correlates with chromatin remodeling during reactivation from latency.Journal of virology · 2025Article
- In the Absence of Type-1 IFN, HSV-1 LAT Increases γ34.5 Expression and Enhances Mortality in Infected Mice.Viruses · 2025Article
- Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking.Nature communications · 2025Article
- Article
- Herpesviruses: overview of systematics, genomic complexity and life cycle.Virology journal · 2025Review
- Shedding dynamics of a DNA virus population during acute and long-term persistent infection.PLoS pathogens · 2025Article
- Immunological Control of Herpes Simplex Virus Type 1 Infection: A Non-Thermal Plasma-Based Approach.Viruses · 2025Review
- Phosphorylated-tau associates with HSV-1 chromatin and correlates with nuclear speckles decondensation in low-density host chromatin regions.Neurobiology of disease · 2025Article
113 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
An important question in virology is the mechanism(s) by which persistent viruses such as the herpesviruses and human immunodeficiency virus (HIV) establish a latent infection in specific types of cells. In the case of herpesviruses, herpes simplex virus (HSV) infection of epithelial cells results in a lytic infection, whereas latent infection is established in sensory neurons. Recent studies have shown the importance of chromatin structure in the regulation of latent infection for both HSV and HIV. For HSV, we have shown previously that the viral latency-associated transcript (LAT) promotes lytic gene silencing and the association of one heterochromatin marker, dimethylation of lysine 9 on histone H3 (H3K9me2), with viral lytic genes. In this study, we further defined the structure of latent viral chromatin by examining the heterochromatin markers on histones associated with the HSV latent genome. We detected the H3K9me2, H3K9me3, and H3K27me3 modifications, with H3K27me3, which is indicative of facultative heterochromatin, exhibiting the highest enrichment on all viral promoters tested. A modification associated with cellular centromeric heterochromatin, H4K20me3, was not detected. A mutant virus containing a 1.8-kbp deletion within the LAT region showed reduced levels of the facultative heterochromatin marker (H3K27me3) along with H3K9me3 during latency, whereas a viral mutant defective for the LAT promoter showed a specific reduction in H3K27me3. Cellular long, noncoding RNAs induce facultative heterochromatin, and this study shows that transcription of a viral noncoding RNA can also induce facultative heterochromatin to promote lytic gene silencing during latency.
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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.