ArticleJournal of virology2006
Varicella-zoster virus infection of human foreskin fibroblast cells results in atypical cyclin expression and cyclin-dependent kinase activity.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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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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
18 citing papers in PubMed, 35 citations in OpenAlex.
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- Serum/glucocorticoid-regulated kinase 1 contributes to the proliferation of varicella-zoster virus and induction of cyclin B1 expression.Archives of virology · 2024Article
- In Silico Design and Experimental Validation of Novel Oxazole Derivatives Against Varicella zoster virus.Molecular biotechnology · 2024Article
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- Human Tumor Antigens Yesterday, Today, and Tomorrow.Cancer immunology research · 2017Review
- Vaccines for cancer prevention: a practical and feasible approach to the cancer epidemic.Cancer immunology research · 2014Review
- Influenza virus infection elicits protective antibodies and T cells specific for host cell antigens also expressed as tumor-associated antigens: a new view of cancer immunosurveillance.Cancer immunology research · 2014Article
- Varicella-zoster virus ORF12 protein activates the phosphatidylinositol 3-kinase/Akt pathway to regulate cell cycle progression.Journal of virology · 2013Article
- Epidemiologic perspective on immune-surveillance in cancer.Current opinion in immunology · 2011Review
- Compounds that target host cell proteins prevent varicella-zoster virus replication in culture, ex vivo, and in SCID-Hu mice.Antiviral research · 2010Article
- Healthy individuals have T-cell and antibody responses to the tumor antigen cyclin B1 that when elicited in mice protect from cancer.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Regulation of the retinoblastoma proteins by the human herpesviruses.Cell division · 2009Article
- Cyclin-dependent kinase 1/cyclin B1 phosphorylates varicella-zoster virus IE62 and is incorporated into virions.Journal of virology · 2008Article
- The phosphorylation profile of protein kinase A substrates is modulated during Varicella-zoster virus infection.Medical microbiology and immunology · 2008Article
- Varicella-zoster virus infection of human fibroblast cells activates the c-Jun N-terminal kinase pathway.Journal of virology · 2007Article
- Personal history of infections and immunotherapy: Unexpected links and possible therapeutic opportunities.OncoimmunologyReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In its course of human infection, varicella-zoster virus (VZV) infects rarely dividing cells such as dermal fibroblasts, differentiated keratinocytes, mature T cells, and neurons, none of which are actively synthesizing DNA; however, VZV is able to productively infect them and use their machinery to replicate the viral genome. We hypothesized that VZV alters the intracellular environment to favor viral replication by dysregulating cell cycle proteins and kinases. Cyclin-dependent kinases (CDKs) and cyclins displayed a highly unusual profile in VZV-infected confluent fibroblasts: total amounts of CDK1, CDK2, cyclin B1, cyclin D3, and cyclin A protein increased, and kinase activities of CDK2, CDK4, and cyclin B1 were strongly and simultaneously induced. Cyclins B1 and D3 increased as early as 24 h after infection, concurrent with VZV protein synthesis. Confocal microscopy indicated that cyclin D3 overexpression was limited to areas of IE62 production, whereas cyclin B1 expression was irregular across the VZV plaque. Downstream substrates of CDKs, including pRb, p107, and GM130, did not show phosphorylation by immunoblotting, and p21 and p27 protein levels were increased following infection. Finally, although the complement of cyclin expression and high CDK activity indicated a progression through the S and G(2) phases of the cell cycle, DNA staining and flow cytometry indicated a possible G(1)/S blockade in infected cells. These data support earlier studies showing that pharmacological CDK inhibitors can inhibit VZV replication in cultured cells.
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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.