In contrast, Dr. Robert Silverman of the Cleveland Clinic and co-author of the first study linking prostate cancer to XMRV, talked about the RNASE-L mutation in his cohort. In one family of five sons, for instance, four had prostate cancer, along with the RNASE-L mutation. He also discussed the study he coauthored on macaques infected with XMRV. In these animals, he explained, the prostate epithelium is infected early on, followed by the seminal vesicles and epididymis, and finally the stromal fibroblasts. Prostate cancer is often preceded by inflammation and XMRV stimulates proinflammatory genes, so it’s conceivable, he said, that XMRV infection could cause inflammation and eventually prostate cancer. The enzyme APOBEC3G, a potent inhibitor of XMRV, mutated XMRV DNA in blood cells of the macaques. Silverman also said that androgen stimulates XMRV, and anti-androgens inhibit the retrovirus.
--Dr. Ila Singh of the University of Utah and co-author of a study linking XMRV to prostate cancer voiced that XMRV may become a marker for prostate cancer. It’s conceivable, she said, that XMRV status may eventually prove to be a better indicator than the current PSA test, and perhaps antiretroviral therapy will be effective in treating the disease. She explained that the XMRV gag (the basic physical infrastructure of the retrovirus) cross-reacts with Moloney mouse MLV. However, the envelop (the retroviral protein that makes up the outside of the retrovirus) reacts only to XMRV. Of 233 men with prostate cancer in her study, 27 percent were XMRV positive. Interestingly, the higher the Gleason score—which is used to determine the prostate-cancer prognosis and ranges from two to 10—the more likely the men were to be infected with XMRV.