ArticleOncogene2016
Oxidative stress enables Epstein-Barr virus-induced B-cell transformation by posttranscriptional regulation of viral and cellular growth-promoting factors.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Epstein-Barr virus-transformed B-cells from a hypoxia model of the germinal center requires external unsaturated fatty acids.PLoS pathogens · 2025Article
- From infection to infertility: a review of the role of human papillomavirus-induced oxidative stress on reproductive health and infertility.European journal of medical research · 2025Review
- Germinal center cytokine driven epigenetic control of Epstein-Barr virus latency gene expression.PLoS pathogens · 2024Article
- Germinal Center Cytokines Driven Epigenetic Control of Epstein-Barr Virus Latency Gene Expression.bioRxiv : the preprint server for biology · 2024Article
- The Research Progress on Immortalization of Human B Cells.Microorganisms · 2023Review
- The master antioxidant defense is activated during EBV latent infection.Journal of virology · 2023Article
- The Impact of Co-Infections for Human Gammaherpesvirus Infection and Associated Pathologies.International journal of molecular sciences · 2023Review
- EBV and Lymphomagenesis.Cancers · 2023Review
- Article
- Stress-Induced Epstein-Barr Virus Reactivation.Biomolecules · 2021Review
- Targeting K-Ras and apoptosis-driven cellular transformation in cancer.Cell death discovery · 2021Review
- Antiviral Effects of Polyphenols from Marine Algae.Biomedicines · 2021Review
- Investigating the Thioredoxin and Glutathione Systems' Response in Lymphoma Cells after Treatment with [Au(d2pype)2]CL.Antioxidants (Basel, Switzerland) · 2021Article
- Nicotinamide adenine dinucleotide phosphate oxidase inhibitor induces apoptosis on Epstein-Barr virus positive B lymphoma cells.Anatomy & cell biology · 2020Article
- Review
- Marine Algal Antioxidants as Potential Vectors for Controlling Viral Diseases.Antioxidants (Basel, Switzerland) · 2020Article
- Article
- Quercetin Interrupts the Positive Feedback Loop Between STAT3 and IL-6, Promotes Autophagy, and Reduces ROS, Preventing EBV-Driven B Cell Immortalization.Biomolecules · 2019Article
- Marek's Disease Virus Disables the ATR-Chk1 Pathway by Activating STAT3.Journal of virology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of human B lymphocytes by Epstein-Barr virus (EBV) leads to the establishment of immortalized lymphoblastoid cell lines (LCLs) that are widely used as a model of viral oncogenesis. An early consequence of infection is the induction of DNA damage and activation of the DNA damage response, which limits the efficiency of growth transformation. The cause of the DNA damage remains poorly understood. We have addressed this question by comparing the response of B lymphocytes infected with EBV or stimulated with a potent B-cell mitogen. We found that although the two stimuli induce comparable proliferation during the first 10 days of culture, the EBV-infected blasts showed significantly higher levels of DNA damage, which correlated with stronger and sustained accumulation of reactive oxygen species (ROS). Treatment with ROS scavengers decreased DNA damage in both mitogen-stimulated and EBV-infected cells. However, while mitogen-induced proliferation was slightly improved, the proliferation of EBV-infected cells and the establishment of LCLs were severely impaired. Quenching of ROS did not affect the kinetics and magnitude of viral gene expression but was associated with selective downregulation of the viral LMP1 and phosphorylated cellular transcription factor STAT3 that have key roles in transformation. Analysis of the mechanism by which high levels of ROS support LMP1 expression revealed selective inhibition of viral microRNAs that target the LMP1 transcript. Our study provides novel insights into the role of EBV-induced oxidative stress in promoting B-cell immortalization and malignant transformation.
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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.