BK virus (BKV) infection and associated BK tubulointerstitial nephropathy (BKVN) still represents a challenge in the renal transplant context (1). Regarding this, molecular tools to test for DNA-BKV are essential in early detection and further management of the kidney transplant recipients (KTR) (2). Although extensive data on this viral infection are now available, some relevant aspects in relation to its pathogenesis, such as donor implication, continue to remain unclear (3).
We present new data on BKV infection obtained by a quantitative polymerase chain reaction (PCR) method and a transcription control region (TCR)-BK polymorphism sequence analysis on a renal donor and their corresponding recipient pair. The purpose of the analysis was to determine both the viral genotype involved and the possible role of the renal donor in the origin of this viral infection.
Management of BK infection in KTR at the University Hospital La Fe is based on the Nickeleit scheme (4). Since July 2003, a total of 190 KTR have been monitored by protocol. Furthermore, between November 2004 and March 2006, a study was carried out on 58 renal donors and their recipients. This protocol permits us to follow the evolution of those recipient pairs with BK-positive donors that may be at risk of BKV infection.
DNA was extracted from pure urine and serum using a QIAamp DNA Virus purification kit for automatic extraction by the BioRobot EZ1 (Qiagen, Valencia, CA). The quantitative PCR method was performed using the SybrGreen QuantiTect PCR assay (Qiagen, Valencia, CA) in the SmartCycler thermocycler (Cepheid, Sunnyvale, CA) to amplify the Large T (LT) and the TCR regions (4). Subsequently, the TCR region was amplified by a cyclesequencing PCR reaction in an automatic sequencer ABI PRISM 3100 (Applied Biosystem, Warrington, UK) using both primers (sense and antisense) examining the polymorphic sites by means of the Basic Local Alignment Search Tool program (http://www.ncbi.nlm.nih.gov) (5).
BK infection in KTR could be derived from either the donor or from the transplant recipient (3). Regarding the first possibility, we have found the same JL (Gene Bank: AY628236) viral genotype in a renal donor and their two recipients, supporting an exact identity between the donor and their recipient pair (see Table 1). Thus, we hypothesize that a recipient pair with the same BK genotype might have a possible donor origin of the infection, as was recently reported (3). As Bohl et al., demonstrated, if BKV infection in the recipient originates from the donor kidney, the recipient pairs would be concordant for BKV infection more often than expected (3). In spite of this, Hirsch et al., reported data in favor of the transplant recipient origin of BK infection. They found that 85% of recipients with BKVN were pretransplant seropositive, suggesting that the high-risk group is not the seropositive donor and seronegative recipient transplant combination (6).
In our opinion, the finding of matching “molecular finger-prints” in both the donor and their recipient pair, supports the hypothesis that posttransplant BKV infection, at least in some cases, derives from the transplant donor kidneys, reinforcing the possible implication of the renal donor as a source of BK infection in KTR. However, larger studies of donors and their recipients are now necessary in order to confirm such observations.
Luis A. Rubio
Francisco J. Vera-Sempere
Service of Pathology
Laboratory of Molecular Pathology
University Hospital La Fe
University Medical School
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