The ability of host cells to activate apoptosis is perhaps the most potent weapon for helping cells eliminate viruses. Human papillomaviruses (HPV) activate several pathways, enabling the infected cells to avoid extrinsic and intrinsic apoptosis pathways. The incapacity of prostatic epithelial cells to induce apoptosis leads to the invasive development of prostate cancer. For the pathogenesis of prostate cancer, several risk factors have been reported; for example, some viruses and infectious diseases have been proposed as causative agents for their relation to prostate diseases. According to several studies, high-risk human papillomaviruses cause malignancy by interfering with the apoptotic and inflammatory pathways; these viruses, such as HPV16 and HPV18, block apoptotic pathways and result in prostate cancer. This review is dedicated to presenting a summary of oncogenes (E5, E6, and E7) HR-HPVs' functions on signaling pathways, inflammation in prostate tumorigenesis, and emphasizing the link between these oncogenes with apoptosis and prostate cancer.