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@ARTICLE{Shumilov:119777,
author = {A. Shumilov$^*$ and M.-H. Tsai$^*$ and Y. Schlosser$^*$ and
A.-S. Kratz$^*$ and K. Bernhardt$^*$ and S. Fink$^*$ and T.
Mizani$^*$ and X. Lin$^*$ and A. Jauch and J. Mautner and A.
Kopp-Schneider$^*$ and R. Feederle$^*$ and I. Hoffmann$^*$
and H.-J. Delecluse$^*$},
title = {{E}pstein-{B}arr virus particles induce centrosome
amplification and chromosomal instability.060},
journal = {Nature Communications},
volume = {8},
issn = {2041-1723},
address = {London},
publisher = {Nature Publishing Group},
reportid = {DKFZ-2017-00404},
pages = {14257 -},
year = {2017},
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.},
cin = {F100 / F045 / C060},
ddc = {500},
cid = {I:(DE-He78)F100-20160331 / I:(DE-He78)F045-20160331 /
I:(DE-He78)C060-20160331},
pnm = {316 - Infections and cancer (POF3-316)},
pid = {G:(DE-HGF)POF3-316},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28186092},
pmc = {pmc:PMC5309802},
doi = {10.1038/ncomms14257},
url = {https://inrepo02.dkfz.de/record/119777},
}