Abstract

Prostate cancer (PCa) is the most common malignancy and the second most leading cause of cancer death among men in the United States. More specifically, African American (AA) men are at 1.6 times higher risk of being diagnosed and 2 times higher risk of death from PCa, compared to European-American (EA) men or other ethnicities. BKV is an emerging opportunistic pathogen that infects 90% of the human population and is known to reactivate in immune-compromised hosts and has been implicated as a cofactor in early stages of PCa. Reactivated BKV may be a more virulent strain that emerges in the absence of host immune response. Therefore, it is plausible that BKV genetic diversity within immune-compromised cancer hosts may allow more virulent strains to reactivate to opportunistically cause disease.BKV replication is orchestrated by a regulatory protein large T antigen (LTag) which binds products of tumor suppressor genes (pRb family, p53) and interferes with the strategic checkpoints of the cell cycle of infected cells, thereby resulting in transformation and cancer progression. The association of viruses and their evolutionary dynamics in human disease is critical for advancement in tumor biology therapeutics and clinical diagnoses. This review article describes to better understand racially derived differences in PCa and a potential role for BKV as a cofactor in PCa progression..

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