Variable sources of Bk virus in renal allograft recipients

Abstract

BK virus is the causative agent of polyomavirus‐associated nephropathy, a major cause of kidney transplant failure affecting 1%‐10% of recipients. Previous studies that investigated the viral source on the kidney recipient pointed that the donor is implicated in the origin of human polyomavirus BK (BKPyV) infection in recipients, but giving the low genetic variability of BKPyV this subject is still controversial. The aim of this study was to determine if BKPyV replicating in kidney recipients after transplantation is always originated from the donor. Urine and blood samples from 68 pairs of living donors and kidney recipients who underwent renal transplantation from August 2010‐September 2011 were screened for BKPyV by real time polymerase chain reaction. Only three recipients presented viremia. When both donors and recipients were BKPyV positive, a larger fragment of VP1 region was obtained and sequenced to determine the level of similarity between them. A phylogenetic tree was built for the 12 pairs of sequences obtained from urine and high level of similarity among all sequences was observed, indicating that homology inferences for donor and recipient viruses must be cautiously interpreted. However, a close inspection on the donor‐recipient pairs sequences revealed that 3 of 12 pairs presented considerably different viruses and 4 of 12 presented mixed infection, indicating that the source of BKPyV infection is not exclusively derived from the donor. We report that about 60% of the renal recipients shed BKPyV genetically distinct from the donor, confronting the accepted concept that the donor is the main source of recipients’ infection.

Detection of BK polyomavirus genotypes to predict the development of BK polyomavirus‐associated complications in kidney transplant recipients: A retrospective analysis

“…6 More interesting, from a clinical point of view, are our findings relating clinical manifestations to the various genotypes of other studies have previously suggested. 8,[16][17][18][19][20] The BKPyV infection in the transplant recipient could be a mixture of the reactivation of their own genotype and infection by some new genotype from the donor. However, there is a study that showed that donor-derived viral transmission is a more important mode of BKPyV infection than reactivation of the recipient's own latent virus.…”

“…15 A donor origin of BKPyV in kidney recipients has been suggested, after demonstrating a correlation between the serostatus of the donor and BKPyV replication in the recipient. [16][17][18][19][20] Very few studies have investigated the distribution of BKPyV genotypes and the clinical implications of the various BKPyV genotypes. [20][21][22] The aim of this study was to investigate the epidemiology of BKPyV genotypes in kidney transplant recipients in Spain and the influence of the BKPyV genotypes on the virological and clinical characteristics of BKPyV infection in this population.…”

Beyond Cytomegalovirus and Epstein-Barr Virus: a Review of Viruses Composing the Blood Virome of Solid Organ Transplant and Hematopoietic Stem Cell Transplant Recipients

“…The highest incidences of BKPyV DNA detection and viral loads above 1E4 copies/ml are most commonly observed within 6 months posttransplantation, with a median detection time of 2 to 4 months (98,112,119,122). A recent study investigated the impact of pretransplantation seroreactivity of donor-recipient pairs on posttransplantation BKPyV viremia and BKPyVAN development (123), considering that BKPyV infection might originate from the kidney allograft (124) and that BKPyV seroreactivity correlates with BKPyV replication after transplantation (125). The pretransplantation donor BKPyV IgG level was associated with the recipient's BKPyV viremia and BKPyVAN development and was the strongest pretransplantation factor for viremia and BKPyVAN in multivariate analysis; the recipient's BKPyV seroreactivity was inversely associated with BKPyV viremia and BKPyVAN, but these results were nonsignificant (123).…”

Outcomes of Living Kidney Donor Candidates and Living Kidney Recipient Candidates with JC Polyomavirus and BK Polyomavirus Viruria

“…Conversely, 71.4% of de novo JCV viruric KT patients received a graft from a JCV viruric donor. Literature regarding sources of polyomavirus in renal allograft recipients are scarce and conflicting [23,25,26]. Notwithstanding, the tendency is to accept that polyomavirus urinary viral shedding may be transmitted by the allograft.…”