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Pathogenesis and Management of Polyomavirus Infection in Transplant Recipients

Eun Jeong Kwak, Regis A. Vilchez, Parmjeet Randhawa, Ron Shapiro, Janet S. Butel and Shimon Kusne
Clinical Infectious Diseases
Vol. 35, No. 9 (Nov. 1, 2002), pp. 1081-1087
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/4483268
Page Count: 7
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Pathogenesis and Management of Polyomavirus Infection in Transplant Recipients
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Abstract

Polyomaviruses (JC virus [JVC], BK virus [BKV], and simian virus 40 [SV40]) establish subclinical and persistent infections and share the capacity for reactivation from latency in their host under immunosuppression. JCV establishes latency mainly in the kidney, and its reactivation results in the development of progressive multifocal leukoencephalopathy. BKV causes infection in the kidney and the urinary tract, and its activation causes a number of disorders, including nephropathy and hemorrhagic cystitis. Recent studies have reported SV40 in the allografts of children who received renal transplants and in the urine, blood, and kidneys of adults with focal segmental glomerulosclerosis, which is a cause of end-stage renal disease and an indication for kidney transplantation. Clinical syndromes related to polyomavirus infection are summarized in the present review, and strategies for the management of patients who receive transplants are discussed.

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