The human polyomavirus BK: Potential role in cancer
Article first published online: 2 FEB 2005
Copyright © 2005 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 204, Issue 2, pages 402–406, August 2005
How to Cite
Fioriti, D., Videtta, M., Mischitelli, M., Degener, A.M., Russo, G., Giordano, A. and Pietropaolo, V. (2005), The human polyomavirus BK: Potential role in cancer. J. Cell. Physiol., 204: 402–406. doi: 10.1002/jcp.20300
- Issue published online: 26 MAY 2005
- Article first published online: 2 FEB 2005
- Manuscript Accepted: 10 NOV 2004
- Manuscript Received: 8 NOV 2004
- National programme on AIDS research
- MIUR (Italy)
In human cancer, a role has been suggested for the human polyomavirus BK, primarily associated with tubulointerstitial nephritis and ureteric stenosis in renal transplant recipients, and with hemorrhagic cystitis in bone marrow transplant (BMT) recipients. After the initial infection, primarily unapparent and without clinical signs, the virus disseminates and establishes a persistent infection in the urinary tract and lymphocytes. There is correlative evidence regarding potential role of polyomavirus BK in cancer. In fact, the BK virus (BKV) DNA (complete genome and/or subgenomic fragments containing the early region) is able to transform embryonic fibroblasts and cells cultured from kidney and brain of hamster, mouse, rat, rabbit, and monkey. Nevertheless, transformation of human cells by BKV is inefficient and often abortive. Evidence supporting a possible role for BKV in human cancer has accumulated slowly in recent years, after the advent of polymerase chain reaction (PCR). BKV is known to commonly establish persistent infections in people and to be excreted in the urine by individuals who are asymptomatic, complicating the evaluation of its potential role in development of human cancer. Therefore, there is no certain proof that human polyomavirus BK directly causes the cancer in humans or acts as a cofactor in the pathogenesis of some types of human cancer. © 2005 Wiley-Liss, Inc.