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...

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Hauptverfasser: Shumilov, Anatoliy (VerfasserIn) , Tsai, Ming-Han (VerfasserIn) , Bernhardt, Katharina (VerfasserIn) , Delecluse, Susanne (VerfasserIn) , Mizani, Tuba (VerfasserIn) , Lin, Xiaochen (VerfasserIn) , Jauch, Anna (VerfasserIn) , Kopp-Schneider, Annette (VerfasserIn) , Feederle, Regina (VerfasserIn) , Hoffmann, Ingrid (VerfasserIn) , Delecluse, Henri-Jacques (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 10 Feb 2017
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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Zusammenfassung: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.
Beschreibung:Gesehen am 08.08.2018
Beschreibung:Online Resource
ISSN:2041-1723
DOI:10.1038/ncomms14257