ArticlePLoS pathogens2012
Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 167 citations in OpenAlex.
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
- Counteracting FOX proteins epigenetically control the herpesvirus lytic-latent balance.Nature communications · 2026Article
- Single-cell transcriptomic analyses of HSV-1 reactivation from latently infected tree shrew and mouse trigeminal ganglia reveal differing molecular and cellular processes.Virologica Sinica · 2026Article
- 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
- Viral and host network analysis of the human cytomegalovirus transcriptome in latency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Herpesviruses: overview of systematics, genomic complexity and life cycle.Virology journal · 2025Review
- Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.PLoS pathogens · 2025Article
- Co-option of mitochondrial nucleic acid-sensing pathways by HSV-1 UL12.5 for reactivation from latent infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- Lytic promoter activity during herpes simplex virus latency is dependent on genome location.Journal of virology · 2024Article
- Control of HSV-1 Infection: Directions for the Development of CRISPR/Cas-Based Therapeutics and Diagnostics.International journal of molecular sciences · 2024Review
- Physiological oxygen concentration during sympathetic primary neuron culture improves neuronal health and reduces HSV-1 reactivation.bioRxiv : the preprint server for biology · 2024Article
- Neuronal expression of herpes simplex virus-1 VP16 protein induces pseudorabies virus escape from silencing and reactivation.Journal of virology · 2024Article
- Co-option of mitochondrial nucleic acid sensing pathways by HSV-1 UL12.5 for reactivation from latent Infection.bioRxiv : the preprint server for biology · 2024Article
- The nucleic acid binding protein SFPQ represses EBV lytic reactivation by promoting histone H1 expression.Nature communications · 2024Article
- Models of Herpes Simplex Virus Latency.Viruses · 2024Review
- Neuronal miR-9 promotes HSV-1 epigenetic silencing and latency by repressing Oct-1 and Onecut family genes.Nature communications · 2024Article
- 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
- Intimate Relationship Between Stress and Human Alpha‑Herpes Virus 1 (HSV‑1) Reactivation from Latency.Current clinical microbiology reports · 2023Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus type-1 (HSV-1) establishes latency in peripheral neurons, creating a permanent source of recurrent infections. The latent genome is assembled into chromatin and lytic cycle genes are silenced. Processes that orchestrate reentry into productive replication (reactivation) remain poorly understood. We have used latently infected cultures of primary superior cervical ganglion (SCG) sympathetic neurons to profile viral gene expression following a defined reactivation stimulus. Lytic genes are transcribed in two distinct phases, differing in their reliance on protein synthesis, viral DNA replication and the essential initiator protein VP16. The first phase does not require viral proteins and has the appearance of a transient, widespread de-repression of the previously silent lytic genes. This allows synthesis of viral regulatory proteins including VP16, which accumulate in the cytoplasm of the host neuron. During the second phase, VP16 and its cellular cofactor HCF-1, which is also predominantly cytoplasmic, concentrate in the nucleus where they assemble an activator complex on viral promoters. The transactivation function supplied by VP16 promotes increased viral lytic gene transcription leading to the onset of genome amplification and the production of infectious viral particles. Thus regulated localization of de novo synthesized VP16 is likely to be a critical determinant of HSV-1 reactivation in sympathetic neurons.
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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.