ArticlePloS one2011
Latent Epstein-Barr virus can inhibit apoptosis in B cells by blocking the induction of NOXA expression.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Caspase cleavage of Kaposi sarcoma-associated herpesvirus proteins: a role for K5 in preventing caspase-mediated cell death during lytic replication.Journal of virology · 2025Article
- Review
- Tomentosin a Sesquiterpene Lactone Induces Antiproliferative and Proapoptotic Effects in Human Burkitt Lymphoma by Deregulation of Anti- and Pro-Apoptotic Genes.Life (Basel, Switzerland) · 2021Article
- Tampering of Viruses and Bacteria with Host DNA Repair: Implications for Cellular Transformation.Cancers · 2021Review
- LIMD1 is induced by and required for LMP1 signaling, and protects EBV-transformed cells from DNA damage-induced cell death.Oncotarget · 2018Article
- Extra-telomeric functions of telomerase in the pathogenesis of Epstein-Barr virus-driven B-cell malignancies and potential therapeutic implications.Infectious agents and cancer · 2018Review
- Review
- Regulation of Apoptosis during Flavivirus Infection.Viruses · 2017Review
- Status of Epstein-Barr Virus Coinfection withJournal of oncology · 2017Review
- Metabolic stress is a barrier to Epstein-Barr virus-mediated B-cell immortalization.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The expanding roles of endoplasmic reticulum stress in virus replication and pathogenesis.Critical reviews in microbiology · 2015Review
- Different patterns of Epstein-Barr virus latency in endemic Burkitt lymphoma (BL) lead to distinct variants within the BL-associated gene expression signature.Journal of virology · 2013Article
- Widespread evidence of viral miRNAs targeting host pathways.BMC bioinformatics · 2013Article
- BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV.Nucleic acids research · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Latent Epstein-Barr virus (EBV) has been shown to protect Burkitt's lymphoma-derived B cells from apoptosis induced by agents that cause damage to DNA, in the context of mutant p53. This protection requires expression of the latency-associated nuclear proteins EBNA3A and EBNA3C and correlates with their ability to cooperate in the repression of the gene encoding the pro-apoptotic, BH3-only protein BIM. Here we confirm that latent EBV in B cells also inhibits apoptosis induced by two other agents--ionomycin and staurosporine--and show that these act by a distinct pathway that involves a p53-independent increase in expression of another pro-apoptotic, BH3-only protein, NOXA. Analyses employing a variety of B cells infected with naturally occurring EBV or B95.8 EBV-BAC recombinant mutants indicated that the block to NOXA induction does not depend on the well-characterized viral latency-associated genes (EBNAs 1, 2, 3A, 3B, 3C, the LMPs or the EBERs) or expression of BIM. Regulation of NOXA was shown to be at least partly at the level of mRNA and the requirement for NOXA to induce cell death in this context was demonstrated by NOXA-specific shRNA-mediated depletion experiments. Although recombinant EBV with a deletion removing the BHRF1 locus--that encodes the BCL2-homologue BHRF1 and three microRNAs--partially abrogates protection against ionomycin and staurosporine, the deletion has no effect on the EBV-mediated block to NOXA accumulation.
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Registered trials
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