Polyomavirus-associated nephropathy: update on BK virus-specific immunity

Transpl Infect Dis. 2006 Jun;8(2):86-94. doi: 10.1111/j.1399-3062.2006.00167.x.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • BK Virus / immunology*
  • Humans
  • Kidney Diseases / epidemiology
  • Kidney Diseases / immunology*
  • Kidney Diseases / virology
  • Kidney Transplantation
  • Polyomavirus Infections / epidemiology
  • Polyomavirus Infections / immunology*
  • Polyomavirus Infections / virology