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Human Polyomavirus Infections with JC Virus and BK Virus in Renal Transplant Patients

THOMAS F. HOGAN, M.D.; ERNEST C. BORDEN, M.D.; J. A. McBAIN, B.S.; B. L. PADGETT, Ph.D.; and D. L. WALKER, M.D.
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Grant support: research funds from the Veterans Administration, and grants T32-CA09075, CA20432, and AI11217, National Institutes of Health. Dr. Hogan is a clinical fellow of the American Cancer Society.

▸Requests for reprints should be addressed to Thomas F. Hogan, M.D.; Oncology Division, W. S. Middleton Memorial Veterans Administration Hospital, 2500 Overlook Terrace; Madison, WI 53705.


Madison, Wisconsin


© 1980 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1980;92(3):373-378. doi:10.7326/0003-4819-92-3-373
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Infection with the human polyomaviruses JC virus and BK virus was studied in 61 immunosuppressed renal transplant patients. Urine cytologic studies, indirect immunofluorescence microscopy, electron microscopy, and serologic studies were used to assess viral activity. Patients records were abstracted for events associated with polyomavirus infections. Polyomavirus excretion in urine was detected in 12 of 61 patients (20%). Eleven excreted JC virus and nine, BK virus. Fourfold hemagglutination-inhibition antibody titer rises occurred in 25 of 61 patients (41%). The serologic data suggested that most JC virus infections were primary, whereas most BK virus infections resulted from virus reactivation. During this 2-year study, 32 of 61 patients (52%) had evidence of active viral replication. Urinary tract excretion was associated with drug-requiring diabetes mellitus (P = 0.001), arterial occlusive disease (P = 0.03), and ureteral stricture with loss of renal function (P = 0.02). Antibody increases to BK virus were associated with a rising serum creatinine (P = 0.02) and need for transplant biopsy (P = 0.02). Polyomavirus replication was therefore associated with an increased frequency of transplant related complications.

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