ArticleProceedings of the National Academy of Sciences of the United States of America2013
Modulation of reactivation of latent herpes simplex virus 1 in ganglionic organ cultures by p300/CBP and STAT3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
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- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
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- Germinal center cytokine driven epigenetic control of Epstein-Barr virus latency gene expression.PLoS pathogens · 2024Article
- Histone modifiers at the crossroads of oncolytic and oncogenic viruses.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
- How an increase in the copy number of HSV-1 during latency can cause Alzheimer's disease: the viral and cellular dynamics according to the microcompetition model.Journal of neurovirology · 2021Article
- Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy.Antiviral research · 2021Review
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- Acyclovir-Loaded Solid Lipid Nanoparticles: Optimization, Characterization and Evaluation of Its Pharmacokinetic Profile.Nanomaterials (Basel, Switzerland) · 2020Article
- Role of Marek's Disease Virus (MDV)-Encoded UJournal of virology · 2020Article
- Herpes Simplex Virus 1-Specific CD8Journal of virology · 2020Article
- Antisense Transcripts and Antisense Protein: A New Perspective on Human Immunodeficiency Virus Type 1.Frontiers in microbiology · 2020Review
- Antagonizing the Glucocorticoid Receptor Impairs Explant-Induced Reactivation in Mice Latently Infected with Herpes Simplex Virus 1.Journal of virology · 2019Article
- C1Q/TNF-related protein 4 expression correlates with herpes simplex encephalitis progression.Annals of translational medicine · 2019Article
- STAT3 roles in viral infection: antiviral or proviral?Future virology · 2018Review
- Influence of an immunodominant herpes simplex virus type 1 CD8+ T cell epitope on the target hierarchy and function of subdominant CD8+ T cells.PLoS pathogens · 2017Article
- Signal transducer and activator of transcription 3 (Journal of leukocyte biology · 2017Article
- Differentially expressed genes during spontaneous lytic switch of Marek's disease virus in lymphoblastoid cell lines determined by global gene expression profiling.The Journal of general virology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A key property of herpes simplex viruses (HSVs) is their ability to establish latent infection in sensory or autonomic ganglia and to reactivate on physical, hormonal, or emotional stress. In latently infected ganglia, HSV expresses a long noncoding RNA and a set of microRNAs, but viral proteins are not expressed. The mechanism by which latent HSV reactivates is unknown. A key question is, what is the mechanism of reactivation in the absence of tegument proteins that enable gene expression in productive infection? Elsewhere we have reported the use of ganglionic organ cultures that enable rapid reactivation in medium containing antibody to NGF or delayed reactivation in medium containing NGF and EGF. We also reported that in the ganglionic organ cultures incubated in medium containing antibody to NGF, all viral genes are derepressed at once without requiring de novo protein synthesis within the time frame of a single replicative cycle. Here we report that latent HSV in ganglia immersed in medium containing NGF and EGF is reactivated by (i) broad spectrum as well as specific histone deacetylase 1 or histone deacetylase 4 inhibitors, (ii) activation of p300/CBP, and (iii) either STAT3 carrying the substitution of tyrosine 705 to phenylalanine or an inhibitor of STAT3. Conversely, reactivation of latent HSV was blocked by p300/CBP inhibitor in medium containing antibody to NGF. The results suggest that (i) STAT3 is required for the maintenance of the latent state and interference with its functions leads to reactivation and (ii) p300/CBP is essential for HSV reactivation.
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