ArticleJournal of virology2014
B lymphocytes from patients with a hypomorphic mutation in STAT3 resist Epstein-Barr virus-driven cell proliferation.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- STAT3, MYC, and EBNA1 cooperate through a ZC3H18 transcriptional network to regulate survival and proliferation of EBV-positive lymphomas.PLoS pathogens · 2025Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.PLoS pathogens · 2024Article
- Polymerase theta is a synthetic lethal target for killing Epstein-Barr virus lymphomas.Journal of virology · 2024Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.bioRxiv : the preprint server for biology · 2024Article
- 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
- ATM, KAP1 and the Epstein-Barr virus polymerase processivity factor direct traffic at the intersection of transcription and replication.Nucleic acids research · 2023Article
- Viruses in colorectal cancer.Molecular oncology · 2022Review
- Stress-Induced Epstein-Barr Virus Reactivation.Biomolecules · 2021Review
- STAT3 plays an important role in DNA replication by turning on WDHD1.Cell & bioscience · 2021Article
- Review
- STAT3 imparts BRCAness by impairing homologous recombination repair in Epstein-Barr virus-transformed B lymphocytes.PLoS pathogens · 2020Article
- Epstein-Barr Virus (EBV) Tegument Protein BGLF2 Suppresses Type I Interferon Signaling To Promote EBV Reactivation.Journal of virology · 2020Article
- Novel replisome-associated proteins at cellular replication forks in EBV-transformed B lymphocytes.PLoS pathogens · 2019Article
- Quercetin Interrupts the Positive Feedback Loop Between STAT3 and IL-6, Promotes Autophagy, and Reduces ROS, Preventing EBV-Driven B Cell Immortalization.Biomolecules · 2019Article
- Calcium mobilization is responsible for Thapsigargin induced Epstein Barr virus lytic reactivation inHeliyon · 2018Article
- STAT3 roles in viral infection: antiviral or proviral?Future virology · 2018Review
- Cytokine receptor signaling is required for the survival of ALK- anaplastic large cell lymphoma, even in the presence of JAK1/STAT3 mutations.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Chloroquine triggers Epstein-Barr virus replication through phosphorylation of KAP1/TRIM28 in Burkitt lymphoma cells.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) oncogenes exert potent B cell proliferative effects. EBV infection gives rise to B cell lines that readily proliferate in culture. This ability of EBV represents a powerful tool to study cell proliferation. In efforts to delineate the contribution of signal transducer and activator of transcription 3 (STAT3) toward EBV-driven cell proliferation, we have discovered that B cells from patients with autosomal dominant hyper-IgE syndrome (AD-HIES) resist such EBV oncogene-driven outgrowth of cells. Patients with AD-HIES have a dominant negative mutation in their STAT3 gene which renders most of the protein nonfunctional. Exposure of healthy subject-derived B cells to EBV resulted in early activation of STAT3, rapidly followed by increased expression of its mRNA and protein. STAT3 upregulation preceded the expression of EBNA2, temporally one of the first viral oncogenes to be expressed. We found that STAT3 was necessary for subsequent survival and for proliferation of EBV-infected cells past the S phase of the cell cycle. Consequently, B cells from AD-HIES patients were prone to dying and accumulated in the S phase, thereby accounting for impaired cell outgrowth. Of importance, we have now identified a cohort of patients with a primary immunodeficiency disorder whose B cells oppose EBV-driven proliferative signals. These findings simultaneously reveal how EBV manipulates host STAT3 even before expression of viral oncogenes to facilitate cell survival and proliferation, processes fundamental to EBV lymphomagenesis.
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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.