ArticleOncogenesis2017
Limited nucleotide pools restrict Epstein-Barr virus-mediated B-cell immortalization.
Article in Oncogenesis, 2017. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Withaferin A inhibits EBV-driven lymphomagenesis through multiple mechanisms, including EBNA1 degradation.Blood · 2026Article
- Integrative analysis of scRNA-seq and bulk RNA-seq with machine learning develops a nucleotide metabolism-based prognostic model for ccRCC and reveals the function of IFI30.Frontiers in oncology · 2026Article
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- Fatty acid desaturases link cell metabolism pathways to promote proliferation of Epstein-Barr virus-infected B cells.PLoS pathogens · 2025Article
- Epstein-Barr virus latent membrane protein 1 subverts IMPDH pathways to drive B-cell oncometabolism.PLoS pathogens · 2025Article
- Epstein-Barr virus replication within differentiated epithelia requires pRb sequestration of activator E2F transcription factors.Journal of virology · 2024Article
- The Research Progress on Immortalization of Human B Cells.Microorganisms · 2023Review
- Divergent structures of Mammalian and gammaherpesvirus uracil DNA glycosylases confer distinct DNA binding and substrate activity.DNA repair · 2023Article
- Targeting Metabolic Vulnerabilities in Epstein-Barr Virus-Driven Proliferative Diseases.Cancers · 2023Review
- Contribution of viral and bacterial infections to senescence and immunosenescence.Frontiers in cellular and infection microbiology · 2023Review
- Review
- Epstein-Barr virus oncoprotein-driven B cell metabolism remodeling.PLoS pathogens · 2022Review
- Immunosenescence in atherosclerosis: A role for chronic viral infections.Frontiers in immunology · 2022Review
- Oncogenic Viruses as Entropic Drivers of Cancer Evolution.Frontiers in virology (Lausanne, Switzerland) · 2021Article
- Roles of extracellular vesicles in the aging microenvironment and age-related diseases.Journal of extracellular vesicles · 2021Review
- Epstein-Barr Virus Induced Cytidine Metabolism Roles in Transformed B-Cell Growth and Survival.mBio · 2021Article
- Epstein-Barr virus nuclear antigen 3C (EBNA3C) interacts with the metabolism sensing C-terminal binding protein (CtBP) repressor to upregulate host genes.PLoS pathogens · 2021Article
- A multi-omics approach to Epstein-Barr virus immortalization of B-cells reveals EBNA1 chromatin pioneering activities targeting nucleotide metabolism.PLoS pathogens · 2021Article
- The Essential Co-Option of Uracil-DNA Glycosylases by Herpesviruses Invites Novel Antiviral Design.Microorganisms · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of cellular oncogenes as well as infection with tumor viruses can promote aberrant proliferation and activation of the host DNA damage response. Epstein-Barr virus (EBV) infection of primary human B cells induces a transient period of hyper-proliferation, but many of these infected cells succumb to an ataxia telangiectasia mutated/checkpoint kinase 2 (ATM/Chk2)-mediated senescence-like growth arrest. In this study, we assessed the role of DNA replicative stress and nucleotide pool levels in limiting EBV-infected B-cell outgrowth. We found that EBV triggered activation of the ataxia telangiectasia and Rad3-related (ATR) signaling pathway in the early rapidly proliferating cells, which were also significantly more sensitive to inhibition of the ATR pathway than late attenuated proliferating cells. Through nuclear halo assays, we determined that early EBV-infected cells displayed increased replicative stress and DNA damage relative to late proliferating cells. Finally, we found that early after infection, hyper-proliferating B cells exhibited limited deoxyribonucleotide triphosphate (dNTP) pools compared with late proliferating and EBV-immortalized lymphoblastoid cell lines with a specific loss of purine dNTPs. Importantly, supplementation with exogenous nucleosides before the period of hyper-proliferation markedly enhanced B-cell immortalization by EBV and rescued replicative stress. Together our results suggest that purine dNTP biosynthesis has a critical role in the early stages of EBV-mediated B-cell immortalization.
Identifiers
What OpenQuestion holds
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.