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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)
Verlagsversion Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
Zeitschrift Nature Communications
Quellenangaben Band: 8, Heft: , Seiten: , Artikelnummer: 14257 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Gene Vector (AGV)
Monoclonal Antibody (IDO-MAB)