Abstract
The Polyomavirus BK (BKV) has been proposed to be one of the possible co-factors in the genesis of prostate cancer (PCa) but, so far, the only convincing suggestion is the hypothesis of a "hit and run" carcinogenic mechanism induced by the virus at early stages of this disease. To support this hypothesis we conducted an updated systematic review on previous studies regarding the association between BKV and PCa, in order to interpret the contrasting results and to explore whether there might be a significant virus-disease link. This updated analysis provides evidence for a significant link between BKV expression and PCa development, particularly between the BKV infection and the cancer risk. Forthcoming scientific efforts that take cue from this study might overcome the atavistic and fruitless debate regarding the BKV-PCa association.
Highlights
Prostate cancer (PCa) is the third most common cause of morbidity and the fourth leading cause of cancer death in western countries [1], but it is becoming increasingly more relevant worldwide due to higher life expectancy and refinement of diagnostic procedures [2, 3]
The increase in rate and level of BKV replication might lead to severe diseases at the anatomical site of relevance, such as the hemorrhagic cystitis in bladder and/or the polyomavirus-associated nephropathy (PVAN) in kidney, which is the principal cause of the transplant rejection of the organ [18, 19]
Several oncogenic viruses have already been linked to human malignancies [21], such as papillomavirus (HPV) to cervical and anogenital cancer [22], Epstein-Barr virus (EBV) to Burkitt’s lymphoma [23] and nasopharyngeal carcinoma [24, 25], the confirmation of the effects of polyomaviruses in the genesis of human cancers, except for Merkel Cell polyomavirus and Merkel Cell carcinoma [26], has proven more difficult
Summary
Prostate cancer (PCa) is the third most common cause of morbidity and the fourth leading cause of cancer death in western countries [1], but it is becoming increasingly more relevant worldwide due to higher life expectancy and refinement of diagnostic procedures [2, 3]. With this updated analysis we were aiming at confirming the co-factorial activity of polyomavirus BK in prostate cancer by categorizing its expression in tumor lesions into marginal, moderate or substantial for risk of PCa development.
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