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BK and JC Polyomavirus (PyV) in HIV-1 Infected Kidney Transplant Recipients (KTR)


Conference Paper

Hirsch, H.H.; Barin, B.; Kardas, P.; Stock, P.; Blumberg, E.A.

Interscience Conference on Antimicrobial Agents and Chemotherapy - ICAAC 2013

Denver, CO


Background: BKPyV causes graft dysfunction and nephropathy (PyVAN) with graft loss in 1-15% of KTR. JCPyV causes progressive multifocal encephalopathy, but rarely PyVAN. The role of either PyV in HIV+ KTR is unknown. Methods: We analyzed frozen serum samples on 137 KTR (5 kidney/liver) from the Multisite Solid Organ Transplantation in HIV study for significant BKPyV or JCPyV exposure 3, 6, 12 and 24 mos posttransplant (PTx). Significant virus exposure was defined as increase in BKPyV or JCPyV IgG levels >0.5 units from baseline or PTx, or detection of viremia. We evaluated associations with clinical factors and outcomes. Results:JCPyV exposure PTx was seen in 29%; JC viremia in 1(0.7%). BKPyV exposure was seen in 49%; BK viremia in 25%. BKPyV & JCPyV co-exposure occurred in 34(25%)pts. BK viremia began 119 days (median) PTx (IQR 95-230); BK exposure started median 213 days PTx (IQR 176-378). Biopsyproven PyVAN was seen in 9/137 with BK viremia in 8/8 with available serum. PyVAN was seen in 12%(8/67) of pts with active BK infection. All 9 PyVAN had immunosuppression reduction (IR); 1 received cidofovir, 4 lefl unomide, 2 cidofovir & lefl unomide. 3 patients lost grafts within 15 mos of IR; 1 remained viremic at last follow up. Univariate (UVM) and multivariate (MVM) proportional hazards models for development of BK exposure/viremia investigated age, sex, race, CD4 nadir/study enroll, HCV, anti IL2R induction, initial thymoglobulin use, initial CNI (cyclosporine vs. tacrolimus), OI history, donor source/age, ECD as baseline factors, and CD4 count and treated acute rejection (AR) as time-dependent covariates. In UVM and MVM, AR (HR: 2.0; 95% CI: 0.9-4.0; p=0.07) was the only factor marginally associated with increased risk of BK viremia; initial tacrolimus use (vs cyclosporine) was associated with decreased risk of BK exposure (HR: 0.6; 95% CI: 0.3-0.9; p=0.01). BK exposure (HR:2.0; p=0.09) or viremia (HR:1.5; p=0.36) was not associated with increased risk of subsequent AR. In UVM, BK exposure was associated with a lower eGFR up to year 3 PTx(p=0.01), but not in MVM adjusting for baseline eGFR, AR, recipient & donor age, and time PTx (p=0.51). Conclusions:/Similar to HIV uninfected KTR, significant BKPyV exposure is common in HIV-1 infected KTR but PyVAN is not increased and JC viremia is rare.

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