期刊
CELL HOST & MICROBE
卷 23, 期 5, 页码 628-+出版社
CELL PRESS
DOI: 10.1016/j.chom.2018.04.005
关键词
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资金
- NIH Intramural Research Program
- San Paolo Company [CSP 2014]
- Italian Association for Cancer Research (AIRC) [IG 2012]
- Italian Foundation for Cancer Research (FIRC)
- National Science Foundation (NSF) Graduate Research Fellowship [00039202]
BK polyomavirus (BKV) frequently causes nephropathy (BKVN) in kidney transplant recipients (KTRs). BKV has also been implicated in the etiology of bladder and kidney cancers. We characterized BKV variants from two KTRs who developed BKVN followed by renal carcinoma. Both patients showed a swarm of BKV sequence variants encoding non-silent mutations in surface loops of the viral major capsid protein. The temporal appearance and disappearance of these mutations highlights the intrapatient evolution of BKV. Some of the observed mutations conferred resistance to antibody-mediated neutralization. The mutations also modified the spectrum of receptor glycans engaged by BKV during host cell entry. Intriguingly, all observed mutations were consistent with DNA damage caused by antiviral APOBEC3 cytosine deaminases. Moreover, APOBEC3 expression was evident upon immunohistochemical analysis of renal biopsies from KTRs. These results provide a snapshot of in-host BKV evolution and suggest that APOBEC3 may drive BKV mutagenesis in vivo.
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