ArticleJournal of virology2002
Explant-induced reactivation of herpes simplex virus occurs in neurons expressing nuclear cdk2 and cdk4.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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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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
22 citing papers in PubMed, 55 citations in OpenAlex.
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- BMS-265246, a Cyclin-Dependent Kinase Inhibitor, Inhibits the Infection of Herpes Simplex Virus Type 1.Viruses · 2023Article
- GC/MS Analysis, Cytotoxicity, and Antiviral Activities ofMolecules (Basel, Switzerland) · 2023Article
- Review
- When cyclin-dependent kinases meet viral infections, including SARS-CoV-2.Journal of medical virology · 2022Review
- Brassicasterol with Dual Anti-Infective Properties against HSV-1 andBiomedicines · 2020Article
- Timing Is Everything.mBio · 2018Article
- Cdk3-promoted epithelial-mesenchymal transition through activating AP-1 is involved in colorectal cancer metastasis.Oncotarget · 2016Article
- Potential of protein kinase inhibitors for treating herpesvirus-associated disease.Trends in microbiology · 2013Review
- C-terminal trans-activation sub-region of VP16 is uniquely required for forskolin-induced herpes simplex virus type 1 reactivation from quiescently infected-PC12 cells but not for replication in neuronally differentiated-PC12 cells.Journal of neurovirology · 2013Article
- Virus reactivation: a panoramic view in human infections.Future virology · 2011Article
- Role of a cdk5-associated protein, p35, in herpes simplex virus type 1 replication in vivo.Journal of neurovirology · 2010Article
- Heat-induced reactivation of HSV-1 in latent mice: upregulation in the TG of CD83 and other immune response genes and their LAT-ICP0 locus.Investigative ophthalmology & visual science · 2009Article
- Cyclin-dependent kinase 3-mediated activating transcription factor 1 phosphorylation enhances cell transformation.Cancer research · 2008Article
- Herpes simplex virus type 1 preferentially targets human colon carcinoma: role of extracellular matrix.Journal of virology · 2008Article
- Roscovitine inhibits activation of promoters in herpes simplex virus type 1 genomes independently of promoter-specific factors.Journal of virology · 2004Article
- Quantitative analysis of herpes simplex virus in cranial nerve ganglia.Journal of neurovirology · 2004Article
- Comparison of herpes simplex virus reactivation in ganglia in vivo and in explants demonstrates quantitative and qualitative differences.Journal of virology · 2004Article
- Roscovitine, a cyclin-dependent kinase inhibitor, prevents replication of varicella-zoster virus.Journal of virology · 2004Article
- Geldanamycin, a ligand of heat shock protein 90, inhibits the replication of herpes simplex virus type 1 in vitro.Antimicrobial agents and chemotherapy · 2004Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus (HSV) establishes productive (lytic) infections in nonneuronal cells and nonproductive (latent) infections in neurons. It has been proposed that HSV establishes latency because quiescent neurons lack cellular factors required for productive infection. It has been further proposed that these putative factors are induced following neuronal stress, as a requirement for HSV reactivation. To date, the identity of these putative cellular factors remains unknown. We have demonstrated that cyclin-dependent kinase (cdk) 1, 2, or 7 is required for HSV replication in nonneuronal cells. Interestingly, cdks 1 and 2 are not expressed in quiescent neurons but can be induced in stressed neurons. Thus, cdks may be among the cellular proteins required for HSV reactivation whose neuronal expression is differentially regulated during stress. Herein, we determined that neuronal expression of nuclear cdk2, cdk4, and cyclins E and D2 (which activate cdks 2 and 4, respectively) was induced following explant cultivation, a stressful stimulus that induces HSV reactivation. In contrast, neuronal expression of cdk7 and cytoplasmic cdk4 decreased during explant cultivation, whereas cdk3 was detected in the same small percentage of neurons before and after explant cultivation and cdks 1, 5, and 6 were not detected in neuronal cell bodies. HSV-1 reactivated specifically in neurons expressing nuclear cdk2 and cdk4, and an inhibitor specific for cdk2 inhibited HSV-1 reactivation. We conclude that neuronal levels of cdk2 are among the factors that determine the outcome of HSV infections of neurons.
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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.