Evidence for Polyomavirus BK Role in Prostate Cancer

Prostate cancer is the leading cause of cancer morbidity and the third greatest cause of cancer death among men in developed countries. A major question in cancer research has been whether virus infection plays a role in cancers of the genitourinary tract. Now a team of Swiss investigators has new evidence suggesting human polyomavirus BK is involved in maintaining and enhancing an environment suitable for prostate cancer growth. The research, published in the August Journal of Virology, could lead to preventive and/or therapeutic prostate cancer vaccines.

The researchers found somewhat different immune responses against the virus' large tumor antigen between seropositive patients with prostate cancers, those seropositive patients with benign prostatic hyperplasia (the benign enlargement of the prostate that is common in older males), and those without prostate abnormalities. In prostate cancer patients, especially those expressing the large tumor antigen in tumor tissue, and showing evidence of recurrence following treatment, the researchers found that this viral antigen seems to influence immune responses in ways that encourage development of the tumor, says principal investigator Maurizio Provanzano of the University of Zurich, Switzerland.

Provenzano lists three major reasons why polyomavirus BK might play a causal role in genitourinary tract cancers: the virus resides asymptomatically in the genitourinary tract of nearly 80 percent of young individuals; it is expressed in inflammatory lesions at very early stages of prostate cancer onset; and it binds and sequesters the tumor suppressor protein p53 in its wild-type form in the cytoplasm of infected cells.

Provenzano says that although the current results are not yet strong enough to prove that polyomavirus BK can cause prostate cancer, some findings suggest ways of fighting the cancer. For example, the strong association between the detection of the virus in prostate cancer and disease recurrence suggests that boosting their immune systems might protect virus-positive individuals.

(G. Sais, S. Wyler, T. Hudolin, I. Banzola, C. Mengus, L. Bubendorf, P.J. Wild, H.H. Hirsch, T. Sulser, G.C. Spagnoli, and M. Provanzano, 2012. Differential patterns of large tumor antigen-specific immune responsiveness in patients with BK polyomavirus-positive prostate cancer or benign prostatic hyperplasia. J. Virol. 86:8461-8471.)