ArticleJournal of virology2012
Ataxia telangiectasia mutated kinase controls chronic gammaherpesvirus infection.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 46 citations in OpenAlex.
- Conserved gammaherpesvirus protein kinase counters myeloid cell-specific type I IFN receptor but not IRF-3 expression to promote the establishment of chronic latent infection in the spleen.Journal of virology · 2026Article
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment.Nature communications · 2025Article
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- Gene expression analysis in EBV-infected ataxia-telangiectasia cell lines by RNA-sequencing reveals protein synthesis defect and immune abnormalities.Orphanet journal of rare diseases · 2021Article
- Interferon Regulatory Factor 3 Supports the Establishment of Chronic Gammaherpesvirus Infection in a Route- and Dose-Dependent Manner.Journal of virology · 2021Article
- Epstein-Barr Virus (EBV)-Related Lymphoproliferative Disorders in Ataxia Telangiectasia: Does ATM Regulate EBV Life Cycle?Frontiers in immunology · 2018Review
- B Cell-Specific Expression of Ataxia-Telangiectasia Mutated Protein Kinase Promotes Chronic Gammaherpesvirus Infection.Journal of virology · 2017Article
- Fatal Lymphoproliferative Disease in Two Siblings Lacking Functional FAAP24.Journal of clinical immunology · 2016Article
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- Type I Interferon Counteracts Antiviral Effects of Statins in the Context of Gammaherpesvirus Infection.Journal of virology · 2016Article
- Murine Gammaherpesvirus 68 LANA and SOX Homologs Counteract ATM-Driven p53 Activity during Lytic Viral Replication.Journal of virology · 2015Article
- ATM facilitates mouse gammaherpesvirus reactivation from myeloid cells during chronic infection.Virology · 2015Article
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- Role of ATM in the formation of the replication compartment during lytic replication of Epstein-Barr virus in nasopharyngeal epithelial cells.Journal of virology · 2015Article
- The Rad6/18 ubiquitin complex interacts with the Epstein-Barr virus deubiquitinating enzyme, BPLF1, and contributes to virus infectivity.Journal of virology · 2014Article
- Interferon regulatory factor 1 restricts gammaherpesvirus replication in primary immune cells.Journal of virology · 2014Article
- Keeping it quiet: chromatin control of gammaherpesvirus latency.Nature reviews. Microbiology · 2013Review
- Mutations in components of antiviral or microbial defense as a basis for breast cancer.Functional & integrative genomics · 2013Review
- Testing for herpesvirus infection is essential in children with chromosomal-instability syndromes.Journal of virology · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gammaherpesviruses, such as Epstein-Barr virus (EBV), are ubiquitous cancer-associated pathogens that interact with DNA damage response, a tumor suppressor network. Chronic gammaherpesvirus infection and pathogenesis in a DNA damage response-insufficient host are poorly understood. Ataxia-telangiectasia (A-T) is associated with insufficiency of ataxia-telangiectasia mutated (ATM), a critical DNA damage response kinase. A-T patients display a pattern of anti-EBV antibodies suggestive of poorly controlled EBV replication; however, parameters of chronic EBV infection and pathogenesis in the A-T population remain unclear. Here we demonstrate that chronic gammaherpesvirus infection is poorly controlled in an animal model of A-T. Intriguingly, in spite of a global increase in T cell activation and numbers in wild-type (wt) and ATM-deficient mice in response to mouse gammaherpesvirus 68 (MHV68) infection, the generation of an MHV68-specific immune response was altered in the absence of ATM. Our finding that ATM expression is necessary for an optimal adaptive immune response against gammaherpesvirus unveils an important connection between DNA damage response and immune control of chronic gammaherpesvirus infection, a connection that is likely to impact viral pathogenesis in an ATM-insufficient host.
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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.