ArticlePLoS pathogens2007
ZEB1 regulates the latent-lytic switch in infection by Epstein-Barr virus.
Article in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 83 citations in OpenAlex.
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- Characterization of microRNA Expression Profiles of Murine Female Genital Tracts FollowingMicroorganisms · 2025Article
- Profiling miRNA changes in Epstein-Barr virus lytic infection identifies a function for BZLF1 in upregulating miRNAs from the DLK1-DIO3 locus.PLoS pathogens · 2025Article
- Epstein-Barr virus and spontaneous lymphoblastoid cell lines: establishment, molecular characteristics, immune modulation, and therapeutic insight.Clinical and experimental immunology · 2025Review
- Epstein-Barr virus replication within differentiated epithelia requires pRb sequestration of activator E2F transcription factors.Journal of virology · 2024Article
- Identifying the key regulators orchestrating Epstein-Barr virus reactivation.Frontiers in microbiology · 2024Review
- MicroRNAs in infectious diseases: potential diagnostic biomarkers and therapeutic targets.Clinical microbiology reviews · 2023Review
- The Dual Functions of Andrographolide in the Epstein-Barr Virus-Positive Head-and-Neck Cancer Cells: The Inhibition of Lytic Reactivation of the Epstein-Barr Virus and the Induction of Cell Death.International journal of molecular sciences · 2023Article
- Andrographolide Inhibits Lytic Reactivation of Epstein-Barr Virus by Modulating Transcription Factors in Gastric Cancer.Microorganisms · 2021Article
- Review
- Prazoles Targeting Tsg101 Inhibit Release of Epstein-Barr Virus following Reactivation from Latency.Journal of virology · 2021Article
- B Cell Receptor-Responsive miR-141 Enhances Epstein-Barr Virus Lytic Cycle via FOXO3 Inhibition.mSphere · 2021Article
- Nascent Transcriptomics Reveal Cellular Prolytic Factors Upregulated Upstream of the Latent-to-Lytic Switch Protein of Epstein-Barr Virus.Journal of virology · 2020Article
- Identification of ARKL1 as a Negative Regulator of Epstein-Barr Virus Reactivation.Journal of virology · 2019Article
- Control of viral infections by epigenetic-targeted therapy.Clinical epigenetics · 2019Review
- Extracellular Vesicles in Epstein-Barr Virus' Life Cycle and Pathogenesis.Microorganisms · 2019Review
- Impact of HVT Vaccination on Splenic miRNA Expression in Marek's Disease Virus Infections.Genes · 2019Article
- Herpes Simplex Virus 1 Deregulation of Host MicroRNAs.Non-coding RNA · 2018Review
- ZEB Proteins in Leukemia: Friends, Foes, or Friendly Foes?HemaSphere · 2018Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The immediate-early (IE) BZLF1 gene of Epstein-Barr virus (EBV) regulates the switch between latent and lytic infection by EBV. We previously showed that the cellular transcription factor ZEB1 binds to a sequence element, ZV, located at nt -17 to -12 relative to the transcription initiation site of the BZLF1 promoter, Zp, repressing transcription from Zp in a transient transfection assay. Here, we report the phenotype in the context of a whole EBV genome of a variant of EBV strain B95.8 containing a 2-bp substitution mutation in the ZV element of Zp that reduced, but did not eliminate, ZEB1 binding to Zp. Strikingly, epithelial 293 cells latently infected with the EBV ZV mutant spontaneously produced IE-, early-, and late-gene products and infectious virus, while wild-type (WT)-infected 293 cells did not and have never been reported to do so. Furthermore, treatment with the chemical inducers sodium butyrate and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) led to an additional order-of-magnitude production of infectious virus in the ZV mutant-infected 293 cells, but still no virus in the WT-infected 293 cells. Similarly, ZV mutant-infected Burkitt's lymphoma BJAB cells accumulated at least 10-fold more EBV IE mRNAs than did WT-infected BJAB cells, with TPA or sodium butyrate treatment leading to an additional 5- to 10-fold accumulation of EBV IE mRNAs in the ZV mutant-infected cells. Thus, we conclude that ZEB1 binding to Zp plays a central role in regulating the latent-lytic switch in EBV-infected epithelial and B cells, suggesting ZEB1 as a target for lytic-induction therapies in EBV-associated malignancies.
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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.