Abstract
The human polyomavirus type 1, also called BK virus (BKV), causes polyomavirus-associated nephropathy (PVAN) in 1-10% of renal transplant recipients, with graft loss in over 50% of cases. The risk factors for PVAN are not conclusively defined and likely involve complementing determinants of recipient, graft, and virus. A central element seems to be the failing balance between BKV replication and BKV-specific immune control, which can result from intense triple immunosuppression, HLA-mismatches, prior rejection and anti-rejection treatment, or BKV-seropositive donor/seronegative recipient pairs. Consistent with this general hypothesis, the timely reduction of immunosuppression in kidney transplant recipients reduced graft loss to less than 10% of cases. However, the BKV-specific humoral and cellular immune response is not well characterized. Recent work from several groups suggest that changes in antibody titers and BKV-specific CD4+ and CD8+ T cells may help to better define the risk and the course of PVAN in renal transplant patients.
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