Shumilov, A.* ; Tsai, M.H.* ; Schlosser, Y.T.* ; Kratz, A.S.* ; Bernhardt, K.* ; Fink, S.* ; Mizani, T.* ; Lin, X.* ; Jauch, A.* ; Mautner, J. ; Kopp-Schneider, A.* ; Feederle, R. ; Hoffmann, I.* ; Delecluse, H.J.*
Epstein-Barr virus particles induce centrosome amplification and chromosomal instability.
Nat. Commun. 8:14257 (2017)
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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Publication type
Article: Journal article
Document type
Scientific Article
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Editors
Keywords
Comparative Genomic Hybridization; Posttransplant Lymphoproliferative Disorders; Cell-cycle Checkpoints; Nasopharyngeal Carcinoma; Infectious-mononucleosis; Cytogenetic Characterization; Endosomal Compartment; Extra Centrosomes; Hodgkins-lymphoma; Dna-damage
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Language
english
Publication Year
2017
Prepublished in Year
318
HGF-reported in Year
2017
ISSN (print) / ISBN
2041-1723
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2041-1723
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Article Number: 14257
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Nature Publishing Group
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London
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Peer reviewed
POF-Topic(s)
30203 - Molecular Targets and Therapies
30201 - Metabolic Health
Research field(s)
Immune Response and Infection
Helmholtz Diabetes Center
PSP Element(s)
G-501500-001
G-502210-001
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Erfassungsdatum
2017-02-27