Inhibitory interactions between BK and JC virus among kidney transplant recipients

Xingxing S. Cheng, Daniel L. Bohl, Gregory A. Storch, Caroline Ryschkewitsch, Monique Gaudreault-Keener, Eugene O. Major, Parmjeet Randhawa, Karen L. Hardinger, Daniel C. Brennan

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


BK and JC polyomaviruses can reactivate after transplantation, causing renal dysfunction and graft loss. The incidence of JC reactivation after renal transplant is not well understood. Here, we characterized JC reactivation using samples collected during the first year after transplantation from 200 kidney recipients. We detected BK and JC viruses in the urine of 35 and 16% of transplant recipients, respectively. The median viral load in the urine was 400 times higher for BK virus than JC virus. The presence of BK viruria made concurrent JC viruria less likely: JC viruria was detected in 22% of non-BK viruric recipients compared with 4% of BK viruric recipients (P = 0.001). The codetection rate was 1.5%, which is less than the expected 5.6% if reactivation of each virus was independent (P = 0.001). We did not observe JC viremia, JC nephropathy, or progressive multifocal leukoencephalopathy. The onset of JC viruria was associated with donor, but not recipient, JC-specific antibody in a titer-dependent fashion and inversely associated with donor and recipient BK-specific antibody. Donor and recipient JC seropositivity did not predict BK viruria or viremia. In conclusion, among renal transplant recipients, infection with one polyomavirus inversely associates with infection with the other.

Original languageEnglish
Pages (from-to)825-831
Number of pages7
JournalJournal of the American Society of Nephrology
Issue number5
StatePublished - May 2011


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