JC virus urinary excretion and seroprevalence in natalizumab-treated multiple sclerosis patients.

The risk of developing progressive multifocal leukoencephalopathy (PML), as a consequence of infection/reactivation with JC virus (JCV), is consistent in natalizumab-treated multiple sclerosis (MS) patients, with 430 cases of PML reported so far. The risk of PML is higher in JCV seropositive patients, and it is recommended that only MS patients without JCV antibodies should be enrolled in the treatment postulating that they do not have JCV infection.We have studied forty-two natalizumab-treated MS patients, and urine and blood were collected monthly for up to 60 months. JCV and BK virus (BKV) DNA presence was verified using quantitative real-time PCR assays, and serum anti-JCV antibodies were measured with the Stratify and/or Stratify DxSelect tests.JCV and BKV DNA were not found in the blood samples, whereas they were found at least once in the urine of 21 of 42 (50 %) and of 25/42 (59.5 %) patients, respectively. JCV DNA urinary shedding increased up to month 24 of natalizumab treatment (45.2 %), and the effect of time was significant for JCV (p = 0.04), but not for BKV (p = 0.39). JCV viruria and seropositivity did not completely correlate, since three patients shedding JCV DNA in the urine were seronegative according to the serological tests.The results indicated that natalizumab therapy may increase the rate of JCV urinary shedding. Additionally, we confirmed that the identification of JCV carriers cannot solely rely on serological tests, but sensitive methods for viral DNA detection should be adopted to more precisely identify the truly JCV uninfected cases.

Evidence supporting the association of polyomavirus BK genome with prostate cancer.

Prostate cancer (PCA) is the most frequent cancer in men. Exposure to infectious agents has been reported to have a putative role in tumorigenesis. Among the infectious agents, convincing evidence has been accumulated about the human polyomavirus BK (BKV). Tissue fresh specimens, serum, and urine samples were collected from 124 consecutive patients, 56 with PCA and 68 with benign prostatic hyperplasia (BPH). Quantitative PCR assays were used to assess the presence of BKV and JC virus (JCV) genomes. BKV-positive tissue specimens were found in 32.1 and 22.1 % of PCA and BPH patients, respectively; in PCA group the number of positive BKV specimens/patients was significantly higher than in BPH group (3.06 vs. 1.73, p = 0.02). JCV genome was found in the biopsies collected from 28.1 and 24.2 % of PCA and BPH patients, respectively, with no significant difference in the rate of JCV specimens/patients between PCA and BPH groups. Our results support the putative causal association between BKV genome and PCA. Further studies are required to demonstrate the direct pathogenetic role of BKV in the PCA occurrence and progression in order to clear the tempting way of vaccine prophylaxis.