Epstein-Barr virus particles induce centrosome amplification and chromosomal instability.
Fiche publication
Date publication
février 2017
Journal
Nature communications
Auteurs
Membres identifiés du Cancéropôle Est :
Pr DELECLUSE Henri-Jacques
Tous les auteurs :
Shumilov A, Tsai MH, Schlosser YT, Kratz AS, Bernhardt K, Fink S, Mizani T, Lin X, Jauch A, Mautner J, Kopp-Schneider A, Feederle R, Hoffmann I, Delecluse HJ
Lien Pubmed
Résumé
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.
Mots clés
Animals, B-Lymphocytes, metabolism, Cell Line, Cell Line, Tumor, Cell Transformation, Neoplastic, Centrosome, metabolism, Chromosomal Instability, Epstein-Barr Virus Infections, genetics, HEK293 Cells, HeLa Cells, Herpesvirus 4, Human, genetics, Humans, Mice, Inbred NOD, Mice, Knockout, Mice, SCID, Viral Envelope Proteins, genetics, Virion, genetics
Référence
Nat Commun. 2017 Feb;8:14257