JC virus (JCV) rarely causes kidney disease, whereas BK virus (BKV) is a known cause of viral nephropathy. Existing studies on prevalence of JCV in healthy and transplanted subjects have reported only qualitative detection of viral DNA. We used quantitative PCR (qPCR) to assess JC viral load in transplant recipients and non-immunosuppressed controls, and compared JCV loads to BKV loads. JC viruria was seen in 8/23 (34.7%) controls, 23/103 (22.3%) renal, and 10/44 (22.7%) liver transplant patients. No patient developed JC viremia. BK viruria was seen in 2/23 (8.7%) controls, 36/103 (34.9%) renal, and 7/44 (15.9%) liver transplant patients. BK viremia was seen only in the kidney (8/103 = 7.7%) patients. The mean BKV urinary load was higher in kidney compared to liver patients and controls (4.22E + 07 vs. 2.88E + 05 vs. 4.39E + 02 copies/ml), whereas JC viral load was similar for all three patient groups (1.55E + 06 vs. 2.66E + 06 vs. 2.13E + 06 copies/ml). JCV viral loads were surprisingly high in all patient categories studied, but did not result in viremia or viral nephropathy. Although both BKV and JCV are widely latent in patients accepted for transplantation, concurrent reactivation of both viruses was infrequent. BKV viremia was seen in kidney but not liver recipients. The mechanisms underlying these notable phenomena remain to be investigated.
(c) 2005 Wiley-Liss, Inc.