Richard Baker

Different patterns of BK and JC polyomavirus reactivation following renal transplantation

Aim Reactivation of latent BK polyomavirus (BKV) infection is relatively common following renal transplantation and BKV-associated nephropathy has emerged as a significant complication. JC polyomavirus (JCV) reactivation is less well studied. The aim of the study was to determine reactivation patterns for these polyomaviruses in renal transplant recipients using an in-house quantitative real-time multiplex PCR assay and IgG serological assays using recombinant BK and JC virus-like particles. Methods Retrospective analysis of urine and plasma samples collected from 30 renal transplant patients from February 2004 to May 2005 at Leeds Teaching Hospitals NHS Trust. Samples were collected at 5u2005days and thereafter at 1, 3, 6 and 12u2005months post-transplantation. Results Eight patients (26.7%) were positive for BK viruria; three of these patients submitted plasma samples and two had BK viraemia. Five patients (16.7%) were positive for JC viruria. A corresponding rise in BKV and JCV antibody titres was seen in association with high levels of viruria. Conclusions Different patterns of reactivation were observed: BK viruria was detected after 3–6u2005months, and JC viruria was observed as early as 5u2005days post-transplantation. One patient had biopsy-proven BKV nephropathy. No dual infections were seen. In order to ensure better graft survival, early diagnosis of these polyomaviruses is desirable.

Early BK Polyomavirus (BKV) Reactivation in Donor Kidney Is a Risk Factor for Development of BKV-Associated Nephropathy

The pathogenesis of BK polyomavirus (BKV) infection and associated nephropathy in renal transplant recipients is not clearly understood. To gain insight, urine and plasma samples were collected from 112 renal transplant recipients before and after transplantation and tested for the presence of BKV by polymerase chain reaction. Detection of BKV infection very early (ie, 5 days) after transplantation was identified as a risk factor for subsequent BKV viremia and BKV-associated nephropathy. Phylogenetic analysis of VP1 sequences with corresponding ethnicity data suggests that reactivation was of donor origin. Thus, early testing of urine samples from renal transplant recipients may identify those at risk for BKV-associated nephropathy.

Who should have pelvic vessel imaging prior to renal transplantation

Subesinghe M, Cherukuri A, Ecuyer C, Baker RJ. Who should have pelvic vessel imaging prior to renal transplantation?u2028Clin Transplant 2011: 25: 97–103.

A prospective study of renal transplant recipients reveals an absence of primary JC polyomavirus infections

BACKGROUNDnBoth JC polyomavirus (JCPyV) and BK polyomavirus (BKPyV) are acquired at an early age. JCPyV causes progressive multifocal leukoencephalopathy and has been described in association with nephropathy.nnnOBJECTIVESnUrine and plasma samples from renal transplant recipients (RTRs) were examined for JCPyV to determine its involvement in causing infection and disease.nnnSTUDY DESIGNnJCPyV testing was performed on 112 RTRs included in a randomised controlled study of steroid-sparing immunosuppressive regimens [1]. Urine and EDTA blood samples were collected pre- and post-transplantation and analysed for JCPyV using real-time PCR and sequencing to determine genotype and viral variation. Donor and recipient IgG antibody status to JCPyV was also determined.nnnRESULTSnOverall, 13.3% of RTRs were positive for JCPyV of which one patient developed viraemia without viruria. JCPyV DNA was detected early following transplantation (defined as five days post transplantation) from recipients with donors that were positive for JCPyV IgG antibodies. No dual cases of JCPyV and BKPyV were observed. One patient sample had sequence duplication in the non-coding control region.nnnCONCLUSIONSnLike BKPyV, JCPyV tends to occur early post transplantation but did not result in sustained viraemia. There was no deterioration of renal function in patients positive for JCPyV. As with other viruses, JCPyV donor serostatus was a risk factor for detection of JCPyV DNA. JCPyV appears to protect individuals from BKPyV infection, as recipients were twice as likely to develop BKPyV with a negative JCPyV donor.