Epstein–Barr virus particles induce centrosome amplification and chromosomal instability

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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Anatoliy Shumilov: German Cancer Research Centre (DKFZ), Unit F100
Ming-Han Tsai: German Cancer Research Centre (DKFZ), Unit F100
Yvonne T. Schlosser: German Cancer Research Centre (DKFZ), Unit F045
Anne-Sophie Kratz: German Cancer Research Centre (DKFZ), Unit F045
Katharina Bernhardt: German Cancer Research Centre (DKFZ), Unit F100
Susanne Fink: German Cancer Research Centre (DKFZ), Unit F100
Tuba Mizani: German Cancer Research Centre (DKFZ), Unit F100
Xiaochen Lin: German Cancer Research Centre (DKFZ), Unit F100
Anna Jauch: Institute of Human Genetics University Hospital Heidelberg
Josef Mautner: Helmholtz Zentrum München, Research Unit Gene Vectors
Annette Kopp-Schneider: German Cancer Research Centre (DKFZ), Unit C060
Regina Feederle: German Cancer Research Centre (DKFZ), Unit F100
Ingrid Hoffmann: German Cancer Research Centre (DKFZ), Unit F045
Henri-Jacques Delecluse: German Cancer Research Centre (DKFZ), Unit F100

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract 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.

Date: 2017
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DOI: 10.1038/ncomms14257

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