Author
Listed:
- Anatoliy Shumilov
(German Cancer Research Centre (DKFZ), Unit F100
Inserm unit U1074, DKFZ
German Centre for Infection Research (DZIF))
- Ming-Han Tsai
(German Cancer Research Centre (DKFZ), Unit F100
Inserm unit U1074, DKFZ
German Centre for Infection Research (DZIF))
- 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
Inserm unit U1074, DKFZ
German Centre for Infection Research (DZIF))
- Susanne Fink
(German Cancer Research Centre (DKFZ), Unit F100
Inserm unit U1074, DKFZ
German Centre for Infection Research (DZIF))
- Tuba Mizani
(German Cancer Research Centre (DKFZ), Unit F100
Inserm unit U1074, DKFZ
German Centre for Infection Research (DZIF))
- Xiaochen Lin
(German Cancer Research Centre (DKFZ), Unit F100
Inserm unit U1074, DKFZ
German Centre for Infection Research (DZIF))
- Anna Jauch
(Institute of Human Genetics University Hospital Heidelberg)
- Josef Mautner
(Helmholtz Zentrum München, Research Unit Gene Vectors
Children’s Hospital Technische Universität München
German Center for Infection Research (DZIF))
- Annette Kopp-Schneider
(German Cancer Research Centre (DKFZ), Unit C060)
- Regina Feederle
(German Cancer Research Centre (DKFZ), Unit F100
Inserm unit U1074, DKFZ
Helmholtz Zentrum München, German Research Center for Environmental Health, Institute for Diabetes and Obesity, Core Facility Monoclonal Antibodies)
- Ingrid Hoffmann
(German Cancer Research Centre (DKFZ), Unit F045)
- Henri-Jacques Delecluse
(German Cancer Research Centre (DKFZ), Unit F100
Inserm unit U1074, DKFZ
German Centre for Infection Research (DZIF))
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.
Suggested Citation
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 & Re, 2017.
"Epstein–Barr virus particles induce centrosome amplification and chromosomal instability,"
Nature Communications, Nature, vol. 8(1), pages 1-15, April.
Handle:
RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14257
DOI: 10.1038/ncomms14257
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