ArticlePLoS pathogens2016
The HSV-1 Latency-Associated Transcript Functions to Repress Latent Phase Lytic Gene Expression and Suppress Virus Reactivation from Latently Infected Neurons.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
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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
81 citing papers in PubMed, 118 citations in OpenAlex.
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- Viral reprogramming of neuronal metabolism captured by label-free imaging in a 3D human brain tissue model.Neurophotonics · 2026Article
- Non-neuronal sites of latency for alphaherpesviruses.Journal of virology · 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
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- The cell-mediated adaptive immune response to herpes simplex virus type 1 encephalitis: mechanisms and clinical implications.Frontiers in immunology · 2026Review
- Systematic identification and characterization of virus lncRNAs suggests extensive structural mimicry of host lncRNAs.Briefings in bioinformatics · 2025Article
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- Circadian clock proteins BMAL1 and CLOCK regulate HSV-1 entry into nerve cells through NECTIN-1.Virology journal · 2025Article
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Article
- Review
- Immunological Control of Herpes Simplex Virus Type 1 Infection: A Non-Thermal Plasma-Based Approach.Viruses · 2025Review
- Tug of war: innate immunity and herpes simplex keratitis.Frontiers in immunology · 2025Review
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- Vistas in Signaling Pathways Implicated in HSV-1 Reactivation.International journal of molecular sciences · 2024Article
- CRISPR-Cas9-mediated genome editing delivered by a single AAV9 vector inhibits HSV-1 reactivation in a latent rabbit keratitis model.Molecular therapy. Methods & clinical development · 2024Article
- Immunological Considerations for the Development of an Effective Herpes Vaccine.Microorganisms · 2024Review
- Hemophagocytic Lymphohistiocytosis Triggered by Herpes Simplex Virus 1 and 2: A Narrative Review.Hematology reports · 2024Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus 1 (HSV-1) establishes life-long latent infection within sensory neurons, during which viral lytic gene expression is silenced. The only highly expressed viral gene product during latent infection is the latency-associated transcript (LAT), a non-protein coding RNA that has been strongly implicated in the epigenetic regulation of HSV-1 gene expression. We have investigated LAT-mediated control of latent gene expression using chromatin immunoprecipitation analyses and LAT-negative viruses engineered to express firefly luciferase or β-galactosidase from a heterologous lytic promoter. Whilst we were unable to determine a significant effect of LAT expression upon heterochromatin enrichment on latent HSV-1 genomes, we show that reporter gene expression from latent HSV-1 genomes occurs at a greater frequency in the absence of LAT. Furthermore, using luciferase reporter viruses we have observed that HSV-1 gene expression decreases during long-term latent infection, with a most marked effect during LAT-negative virus infection. Finally, using a fluorescent mouse model of infection to isolate and culture single latently infected neurons, we also show that reactivation occurs at a greater frequency from cultures harbouring LAT-negative HSV-1. Together, our data suggest that the HSV-1 LAT RNA represses HSV-1 gene expression in small populations of neurons within the mouse TG, a phenomenon that directly impacts upon the frequency of reactivation and the maintenance of the transcriptionally active latent reservoir.
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Registered trials
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.