Prostate cancer is the result of many factors, including geographical location, age, genetic mutations and viral infections [8, 9]. Over the past three decades, several studies have been conducted on the role of viral infections in the development and growth of cancer [10]. JC PYV and SV40 are considered to be one of the main infections linked to prostate cancer [11].
In Morocco, there is very little research on the prevalence of these two viruses, both in prostate cancer and in healthy men. The presence of JC PyV infections in blood samples from healthy and cancerous prostates has been reported previously, however, the frequency of this type of infection remains variable in patients with prostate cancer, and there is no absolute confirmation of the predisposing role of JC PyV infections in the development of prostate tumors [12]. Furthermore, only a small number of studies have examined JC PyV in relation to CPa and have produced conflicting data [13, 14, 15, 16].
Therefore, we conduct this study to investigate a possible causal link between JC PyV and CPa. The results of the present study, which focused on JC PyV, well-described as a high-risk genotype, reported 10 JC PyV infections (among 50 prostate cancer patients) in prostate cancer blood samples. And no SV40 infection was found in the same subset of subjects.
The correlation between tumor parameters and viral infections was studied and revealed a significant association between viral infections and age (P = 0.004), medical history (P = 0.034), alcohol (P = 0.035), and BMI (P = < 0.001). Most of the infected men had a score of 6. Depending on the pathology, a score of 6 or less describes cancer cells that show similarity to normal cells and indicates that the cancer is likely to grow slowly. In addition to these results, medical history, alcohol, and BMI were significantly deferential. This means that the JC PyV virus infection occurred at its variables, while the tumors were growing. We, therefore, concluded that there is a potential role of JC PyV genotypes in the early development of prostate tumors. This result should be interpreted with caution, however, as other data on tumor criteria, including pathological Gleason score, pathological T-stage, PSA ng / mL, surgical history, smoking status, pathological T-stage at diagnosis or treatment, were not significantly different between men infected with JC PyV and uninfected men (P = 0.172, P = 0.107, P = 1.00, P = 0.258, P = 0.884 respectively). Also, the Gleason pathological score, age, and surgical history were considered risk factors for the development of prostate cancer because the odds ratio value was greater than 1. Thus, the result of JC PyV infections in men who have undergone radical prostatectomy should be considered with specific attention to viral infections at clinical stages.
These results are in agreement with the data reported by Zambrano et al. In prostate tissue or urine samples, 50% of prostate cancer patients were detected by prostate cancer patients [17], Furthermore, no significant difference was observed in the two separate studies on JC PyV detection between cancerous samples and clear prostate tissue [18, 19]. In addition, Mexican researchers did not detect any JC PyV sequence [20] in prostate cancer biopsies. The differences observed between these studies may be explained by technical differences and the sample size of the virus detection method. In addition, due to the small number of samples taken in this study and the small number of previous samples, difficulties in obtaining new surgical structures limited the statistical significance of our data.
Research in 2015 also showed that the risk of prostate cancer infected by 58.3% of cancerous and clear prostate tissue samples was significantly increased. Haemophilic viruria and JC virus were observed in 62.5% and 8.3% of prostate cancer patients. In addition to BK virus, replication is evident in the urine pool. Therefore, in the prostate cancer patients included in this study, JC virus is more important than BK virus. Even with regard to the average number of BK virus genomes in the prostate sample, the average number of BK virus genomes is higher. JC virus (P = 0.002) [21].
In another study conducted in 2021, the prevalence of JCPyV/BKPyV DNA was significantly different between PCa and BPH tissues (27/76 [35.52%] and 2/30 [6.7%], respectively, p = 0.003). LT and VP1 proteins were identified in 27 (35.52%) and 29 (38.2%) PCa samples, respectively, compared to no protein in BPH samples (p < 0.001). PCa cells were more susceptible to JCPyV infection than BPH tissues [odds ratio (OR) 7.71, 95% CI: 1.71–34.09, p = 0.003]. Prostate cancer patients with elevated PSA levels and high Gleason scores were also estimated to have an elevated risk of viral infection (OR 1.1, 95% CI 1.000-1.003; p = 0.045 and OR 6.18, 95% CI 1.26–30.33, p = 0.025, respectively). Expressed LT protein associated with risk of prostate cancer was 2923.39-fold (95% CI 51.19-166963.62, p < 0.001) [22].
In previous studies that examined mRNA expression to identify disease severity, patients diagnosed with high-grade PCa (GS > 7) were shown to have high mRNA expression of specific genes [23, 24, 25, 26]. They demonstrated that when JCPyV attacks PCa cells, its oncoprotein LT may increase cellular mRNA expression of specific genes and may affect the GS score and PCa progression. However it remains to be studied whether the changes after the viral infection are related to the opinion [27].