ArticleJournal of virology2011
Reversal of heterochromatic silencing of quiescent herpes simplex virus type 1 by ICP0.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Therapeutic potentials of CRISPR-Cas genome editing technology in human viral infections.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- The State-of-the-Art of Gene Editing and its Application to Viral Infections and Diseases Including COVID-19.Frontiers in cellular and infection microbiology · 2022Review
- Review
- Review
- Screening Method for CRISPR/Cas9 Inhibition of a Human DNA Virus: Herpes Simplex Virus.Bio-protocol · 2020Article
- Anterograde Neuronal Circuit Tracers Derived from Herpes Simplex Virus 1: Development, Application, and Perspectives.International journal of molecular sciences · 2020Review
- Herpesviral lytic gene functions render the viral genome susceptible to novel editing by CRISPR/Cas9.eLife · 2019Article
- Chromatin dynamics and the transcriptional competence of HSV-1 genomes during lytic infections.PLoS pathogens · 2019Article
- [Mechanisms of herpes simplex virus latency and reactivation].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Review
- Cellular Antisilencing Elements Support Transgene Expression from Herpes Simplex Virus Vectors in the Absence of Immediate Early Gene Expression.Journal of virology · 2018Article
- Promyelocytic leukemia (PML) nuclear bodies (NBs) induce latent/quiescent HSV-1 genomes chromatinization through a PML NB/Histone H3.3/H3.3 Chaperone Axis.PLoS pathogens · 2018Article
- Engineered HSV vector achieves safe long-term transgene expression in the central nervous system.Scientific reports · 2017Article
- Article
- Herpes simplex virus and the lexicon of latency and reactivation: a call for defining terms and building an integrated collective framework.F1000Research · 2016Review
- Herpes simplex viral-vector design for efficient transduction of nonneuronal cells without cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Novel roles of cytoplasmic ICP0: proteasome-independent functions of the RING finger are required to block interferon-stimulated gene production but not to promote viral replication.Journal of virology · 2014Article
- Transcription of the herpes simplex virus 1 genome during productive and quiescent infection of neuronal and nonneuronal cells.Journal of virology · 2014Article
- Article
- A neuron-specific host microRNA targets herpes simplex virus-1 ICP0 expression and promotes latency.Cell host & microbe · 2014Article
- Nuclear interferon-inducible protein 16 promotes silencing of herpesviral and transfected DNA.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Persisting latent herpes simplex virus genomes are to some degree found in a heterochromatic state, and this contributes to reduced gene expression resulting in quiescence. We used a relatively long-term quiescent infection model in human fibroblasts, followed by provision of ICP0 in trans, to determine the effects of ICP0 on the viral chromatin state as gene expression is reactivated. Expression of ICP0, even at low levels, results in a reduction of higher-order chromatin structure and heterochromatin on quiescent viral genomes, and this effect precedes an increase in transcription. Concurrent with transcriptional activation, high levels of ICP0 expression result in the reduction of the heterochromatin mark trimethylated H3K9, removal of histones H3 and H4 from the quiescent genome, and hyperacetylation of the remaining histones. In contrast, low levels of ICP0 did not appreciably change the levels of histones on the viral genome. These results indicate that ICP0 activity ultimately affects chromatin structure of quiescent genomes at multiple levels, including higher-order chromatin structure, histone modifications, and histone association. Additionally, the level of ICP0 expression affected its ability to change chromatin structure but not to reactivate gene expression. While these observations suggest that some of the effects on chromatin structure are possibly not direct, they also suggest that ICP0 exerts its effects through multiple mechanisms.
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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.