ArticleJournal of virology2011
Human herpesvirus 6 suppresses T cell proliferation through induction of cell cycle arrest in infected cells in the G2/M phase.
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 27 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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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Revitalizing T cells: breakthroughs and challenges in overcoming T cell exhaustion.Signal transduction and targeted therapy · 2026Review
- Mesenchymal Stromal Cell-Derived Small Extracellular Vesicles Modulate Apoptosis, TNF Alpha and Interferon Gamma Response Gene mRNA Expression in T Lymphocytes.International journal of molecular sciences · 2023Article
- Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases.Infectious agents and cancer · 2023Review
- Integrative systems immunology uncovers molecular networks of the cell cycle that stratify COVID-19 severity.Journal of medical virology · 2023Article
- Immune cells-derived exosomes function as a double-edged sword: role in disease progression and their therapeutic applications.Biomarker research · 2022Review
- Japanese Encephalitis Virus NS1' Protein Interacts with Host CDK1 Protein to Regulate Antiviral Response.Microbiology spectrum · 2021Article
- Spermidine Attenuates Oxidative Stress-Induced Apoptosis via Blocking CaInternational journal of molecular sciences · 2021Article
- Human herpesvirus 6A promotes glycolysis in infected T cells by activation of mTOR signaling.PLoS pathogens · 2020Article
- miR-181c-5p mediates simulated microgravity-induced impaired osteoblast proliferation by promoting cell cycle arrested in the GJournal of cellular and molecular medicine · 2019Article
- Cell Cycle Arrest in GJournal of virology · 2019Article
- Myalgic Encephalomyelitis/Chronic Fatigue Syndrome as a Hyper-Regulated Immune System Driven by an Interplay Between Regulatory T Cells and Chronic Human Herpesvirus Infections.Frontiers in immunology · 2019Article
- Porcine reproductive and respiratory syndrome virus inhibits MARC-145 proliferation via inducing apoptosis and G2/M arrest by activation of Chk/Cdc25C and p53/p21 pathway.Virology journal · 2018Article
- Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018Review
- Activation of ATR-Chk1 pathway facilitates EBV-mediated transformation of primary tonsillar B-cells.Oncotarget · 2017Article
- Transcriptome sequencing of neurologic diseases associated genes in HHV-6A infected human astrocyte.Oncotarget · 2016Article
- Human Herpesvirus-6 U14 Induces Cell-Cycle Arrest in G2/M Phase by Associating with a Cellular Protein, EDD.PloS one · 2015Article
- Immune response to HHV-6 and implications for immunotherapy.Current opinion in virology · 2014Review
- Human herpesvirus 6A infection in CD46 transgenic mice: viral persistence in the brain and increased production of proinflammatory chemokines via Toll-like receptor 9.Journal of virology · 2014Article
- Classification of HHV-6A and HHV-6B as distinct viruses.Archives of virology · 2014Review
- Cell cycle perturbations induced by human herpesvirus 6 infection and their effect on virus replication.Archives of virology · 2014Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human herpesvirus 6 (HHV-6) is an important immunosuppressive and immunomodulatory virus that primarily infects immune cells and strongly suppresses the proliferation of infected cells. However, the mechanisms responsible for the regulation and suppression mediated by HHV-6 are still unknown. In this study, we examined the ability of HHV-6A to manipulate cell cycle progression in infected cells and explored the potential molecular mechanisms. We demonstrated that infection with HHV-6A imposed a growth-inhibitory effect on HSB-2 cells by inducing cell cycle arrest at the G(2)/M phase. We then showed that the activity of the Cdc2-cyclin B1 complex was significantly decreased in HHV-6A-infected HSB-2 cells. Furthermore, we found that inactivation of Cdc2-cyclin B1 in HHV-6A-infected cells occurred through the inhibitory Tyr15 phosphorylation resulting from elevated Wee1 expression and inactivated Cdc25C. The reduction of Cdc2-cyclin B1 activity in HHV-6-infected cells was also partly due to the increased expression of the cell cycle-regulatory molecule p21 in a p53-dependent manner. In addition, HHV-6A infection activated the DNA damage checkpoint kinases Chk2 and Chk1. Our data suggest that HHV-6A infection induces G(2)/M arrest in infected T cells via various molecular regulatory mechanisms. These results further demonstrate the potential mechanisms involved in immune suppression and modulation mediated by HHV-6 infection, and they provide new insights relevant to the development of novel vaccines and immunotherapeutic approaches.
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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.