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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
Keywords
Comparative Genomic Hybridization; Posttransplant Lymphoproliferative Disorders; Cell-cycle Checkpoints; Nasopharyngeal Carcinoma; Infectious-mononucleosis; Cytogenetic Characterization; Endosomal Compartment; Extra Centrosomes; Hodgkins-lymphoma; Dna-damage
ISSN (print) / ISBN
2041-1723
e-ISSN
2041-1723
Journal
Nature Communications
Quellenangaben
Volume: 8,
Article Number: 14257
Publisher
Nature Publishing Group
Publishing Place
London
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Research Unit Gene Vector (AGV)
CF Monoclonal Antibodies (CF-MAB)
CF Monoclonal Antibodies (CF-MAB)