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BK Virus
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Description
BK virus associated nephropathy has become increasingly recognized as the cause of renal dysfunction and loss of the transplanted kidney in transplant patients.1 The BK virus is a human polyomavirus. Polyomaviruses are members of the Papovaviridae family, which are small, nonenveloped viruses with a closed, circular double DNA-stranded genome. Polyomaviruses are distinguished from papillomaviruses by a smaller virion size and a different genome size and organization. Polyomaviruses are ubiquitous in nature and can be isolated from a number of species. The human polyomaviruses were first isolated in 1971. They are named BK and JC after the initials of the patients in which they were first discovered. The BK virus was isolated from the urine of a renal transplant patient who developed ureteral stenosis postoperatively. The JC virus was isolated from the brain tissue of a patient with progressive multifocal leukoencephalopathy (PML). BKV and JCV share 75% homology at the level of nucleotide sequence. The two are not cross-reactive serologically and serologic tests for antibodies are able to distinguish between BKV and JCV.2

Epidemiology & Pathogenesis
Approximately 80% of adults in the United States have antibodies to the BK & JC virus. Peak seroprevalence is in early childhood. By the age of 3 or 4 years, 50% of children have antibodies to BK virus and by age 10, 100% have seroconverted. The majority of primary infections are asymptomatic or minimally symptomatic. Common primary infection symptoms are fever and non-specific upper respiratory infection. After primary infection a latent infection is established in renal epithelial cells. BK virus can remain latent in other tissues besides the kidney, possibly even the brain. Transmission of the virus remains unclear, but is thought to occur by exposure of body fluids or transplacental passage.3

Clinical Manifestations
In states of relative or absolute immunodeficiency, the BK virus can reactivate and cause disease.2 BK viremia can be seen in patients with a wide variety of immunodeficiencies, but appears most frequently in renal and bone marrow transplant patients.2

Primary and reactivation infections have been seen in renal transplant recipients. The incidence of infection is approximately 5%.4 The majority of infections occur within the first 3 months after transplant; however, infections occurring greater than 2 years after transplantation have been reported.2 BK virus disease is associated with hemorrhagic and non-hemorrhagic cystitis, ureteric stenosis and tubulointerstitial nephritis, rise in serum creatinine and allograft function loss.1,4 Whenever an episode of renal dysfunction occurs, a polyomavirus infection such as BK should be ruled out as the cause.6

Diagnosis
The diagnosis of the BK virus has relied heavily on biopsy-based evidence.4 Atharva BioSciences provide a sensitive and quantitative PCR assay that can aid in the diagnostic and therapeutic management of BKV nephropathy. The new assay: BKV qPCR will open the door to a better understanding of BK virus nephropathy, especially in patients who are suspected to have BKV nephropathy on biopsy.

Treatment
Reducing the dose of immunosuppressive therapy has currently been the best approach in treating BK virus in transplant recipients.5 A recent study successfully treated BKV interstitial nephritis patients with a reduced dose of cidofovir (10-20% of the recommended dose).1 The study suggests that cidofovir may be useful in treating a subgroup of patients. In another recent study, IVIG was found to be a useful adjunct to the reduction in immunosuppression for the treatment of BK nephropathy.7 Another recent study found the administration of leflunomide at immunosuppressive doses as part of a moderate dose calcineurin-inhibitor-based immunosuppressive scheme is associated with the eradication of BKV and improvement in renal graft function.8



  1. Vats A, Shapiro R, Randhawa PS, Scantlebury V, Tuzuner A et al. Role of Quantitative Viral Load and Cidofovir Therapy in The Management of BK Virus Nephropathy. Transplantation. 2003;75:105-112.
  2. Demeter LM. JC, BK, and other polyomaviruses; progressive multifocal leukoencephalopathy. In Mandell GL, Bennett JE, Dolin, eds. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases, 4th edition, Vol. 2. New York, NY: Churchill Livingstone; 1995:1400-1406.
  3. Kwak EJ, Vilchez RA, Randhawa, P, et al. Pathogenesis And Management of Polyomavirus Infection in Transplant Recipients. Clinical Infectious Diseases. 2002; 35:1081-1087.
  4. Mylonakis E, Goes N, Rubin RH, Cosimi AB, Colvin RB et al. BK Virus in Solid Organ Transplant Recipients: An Emerging Syndrome. Transplantation. 2001;72:1586-1592.
  5. Nickeleit V, Hirsch HH, Zeiler M, Gudat F, Prince O et al. BK-virus nephropathy in renal transplants—tubular necrosis, MCH-class II expression and rejection in a puzzling game. Nephrol Dial Transplant. 2000;15:324-332.
  6. Harault de Ligny B, Etienne I, Francois A, Toupance O, Buchler M et al. Polyomavirus-Induced Acute Tubulo-Intersittial Nephritis in Renal Allograft Recipients. Transplantation Proceedings. 2000;32:2760-2761.
  7. Cibrik, DM, O’Toole JF, Norman SP, et al. IVIG For the Treatment of Transplant BK Nephropathy. American Transplant Congress 2003, Abstract #850.
  8. Foster PF, Wright F, Mclean D, et al. Leflunomide Admnistration As An Adjunct In Treatment Of BK-Polyoma Viral Disease In Kidney Allografts. American Transplant Congress 2003, Abstract # 1053.

PCR tests are performed pursuant to a license agreement with Roche Molecular Systems, Inc.

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