Epstein-Barr virus particles induce centrosome amplification and chromosomal instability
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 increase...
Gespeichert in:
| Hauptverfasser: | , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
10 Feb 2017
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| In: |
Nature Communications
Year: 2017, Jahrgang: 8 |
| ISSN: | 2041-1723 |
| DOI: | 10.1038/ncomms14257 |
| Online-Zugang: | Verlag, kostenfrei, Volltext: http://dx.doi.org/10.1038/ncomms14257 Verlag, kostenfrei, Volltext: https://www.nature.com/articles/ncomms14257 
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| Verfasserangaben: | Anatoliy Shumilov, Ming-Han Tsai, Yvonne T. Schlosser, Anne-Sophie Kratz, Katharina Bernhardt, Susanne Fink, Tuba Mizani, Xiaochen Lin, Anna Jauch, Josef Mautner, Annette Kopp-Schneider, Regina Feederle, Ingrid Hoffmann and Henri-Jacques Delecluse |
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| 520 | |a 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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