ArticleNature communications2017
Epstein-Barr virus particles induce centrosome amplification and chromosomal instability.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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Who cites it
61 citing papers in PubMed, 92 citations in OpenAlex.
- TLR2 and TLR9 in Brain Cancer Patients in Relation to EBV Status.International journal of molecular sciences · 2026Article
- EBV nuclear antigen 1 hijacks DDX5/BZLF1 axis to facilitate viral lytic replication.Virologica Sinica · 2026Article
- SFK Inhibition Suppresses EBV-Encoded BART miRNAs and Induces Apoptosis in EBV-Positive Gastric Epithelial Cells.Cancers · 2026Article
- Human oncogenic herpesvirus latency proteins activate NEK2 to promote chromosomal instability and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Epstein-Barr virus-associated tumors: commonalities in pathogenesis and the tumor immune microenvironment.Frontiers in immunology · 2026Review
- Immunofluorescent microscopy to quantify and characterize chromosomal instability (CIN).Methods in cell biology · 2026Article
- Epstein-barr virus (EBV) in cervical carcinoma detected by in situ hybridization targeting ebers and the viral genome.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025Article
- Genome-wide mapping of EBV-induced genomic variations identifies the role of MUC19 in EBV latency.mBio · 2025Article
- Article
- Genome integration of human DNA oncoviruses.Journal of virology · 2025Review
- Virus-human chromatin interactions reorganise 3D genome and hijack KDM5B for promoting metastasis in nasopharyngeal carcinoma.Nature communications · 2025Article
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- Neurotropic Viruses as Acute and Insidious Drivers of Aging.Biomolecules · 2025Review
- Article
- Carcinogenesis trajectories.Frontiers in cell and developmental biology · 2025Article
- Epstein-Barr virus lytic gene BNRF1 promotes B-cell lymphomagenesis via IFI27 upregulation.PLoS pathogens · 2024Article
- An Epstein-Barr virus protein interaction map reveals NLRP3 inflammasome evasion via MAVS UFMylation.Molecular cell · 2023Article
- TheProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Role of the gut microbiota in anticancer therapy: from molecular mechanisms to clinical applications.Signal transduction and targeted therapy · 2023Review
- Contribution of Epstein-Barr Virus Lytic Proteins to Cancer Hallmarks and Implications from Other Oncoviruses.Cancers · 2023Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infections with Epstein-Barr virus (EBV) are associated with cancer development, and EBV lytic replication (the process that generates virus progeny) is a strong risk factor for some cancer types. Here we report that EBV infection of B-lymphocytes (in vitro and in a mouse model) leads to an increased rate of centrosome amplification, associated with chromosomal instability. This effect can be reproduced with virus-like particles devoid of EBV DNA, but not with defective virus-like particles that cannot infect host cells. Viral protein BNRF1 induces centrosome amplification, and BNRF1-deficient viruses largely lose this property. These findings identify a new mechanism by which EBV particles can induce chromosomal instability without establishing a chronic infection, thereby conferring a risk for development of tumours that do not necessarily carry the viral genome.
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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.