TY - JOUR
T1 - Epstein-Barr virus particles induce centrosome amplification and chromosomal instability
AU - Shumilov, Anatoliy
AU - Tsai, Ming Han
AU - Schlosser, Yvonne T.
AU - Kratz, Anne Sophie
AU - Bernhardt, Katharina
AU - Fink, Susanne
AU - Mizani, Tuba
AU - Lin, Xiaochen
AU - Jauch, Anna
AU - Mautner, Josef
AU - Kopp-Schneider, Annette
AU - Feederle, Regina
AU - Hoffmann, Ingrid
AU - Delecluse, Henri Jacques
N1 - Publisher Copyright:
© The Author(s) 2017.
PY - 2017/2/10
Y1 - 2017/2/10
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85012173092&partnerID=8YFLogxK
U2 - 10.1038/ncomms14257
DO - 10.1038/ncomms14257
M3 - Article
C2 - 28186092
AN - SCOPUS:85012173092
SN - 2041-1723
VL - 8
JO - Nature Communications
JF - Nature Communications
M1 - 14257
ER -
