Human polyomavirus BKV and renal disease.

Urinary shedding of BKV is increased in immunocomIn 1971, two human polyomaviruses were discovered, BK virus (BKV ) from the urine of a renal transplant promising conditions. BKV infection has been linked to occasional cases of cystitis in immunocompetent recipient (whose initials were B.K.) and JC virus (JCV ) from the brain of a patient (whose initials were J.C.) children, to glomerulonephritis in immunodeficient children, and to haemorrhagic cystitis in bone marrow with progressive multifocal leukoencephalopathy (PML). The polyomavirus subfamily of the papovatransplant recipients. While BKV infections and BK viruria have been frequently documented in renal virus family also includes viruses of monkeys (rhesus and cynomologus macaques, African green monkey, transplant recipients, conclusive evidence of significant BKV-related kidney pathology has been recognized baboon), cattle, rabbit, mouse, rat and parakeet [1]. The viruses have a 5 kb double-stranded, circular, only recently. Reports from several groups clearly define BKV nephropathy, a clinical condition in renal supercoiled, DNA genome. Polyomaviruses are highly species-specific and have probably co-evolved with transplant recipients, in which extensive BKV multiplication in the tubular epithelium results in loss of their natural hosts. Primary infections are essentially harmless but the viruses tend to persist indefinitely in allograft function [5–7]. The disease occurs in about 2–3% of renal transplant recipients [4,7] and is the infected individual. correlated with the shedding of a large number of virus-infected epithelial cells in the urine [7] and with BKV and JCV biology the presence of BKV DNA in the serum [2]. The disease may be, in part, a result of the introduction of new immunosuppressive drugs [6 ]. Reduction in the Primary BKV infections occur in early childhood and immunosuppressive therapy often leads to improved primary JCV infections in late childhood. Both viruses clinical outcome. remain latent in the kidney and in B lymphocytes after primary infection. Almost all illnesses attributable to BKV and JCV occur in the background of immunoRole of donor kidney deficiency, most often as a result of reactivation of the latent virus. JCV is the aetiologic agent of PML, a fatal, subacute, progressive demyelinating disease of BKV in donor kidney is a determinant of BKV infection in the recipient. Previous studies of paired serum the brain, which occurs as a complication of AIDS and other immunosuppressive conditions. In contrast specimens have shown that about a quarter of BKV infections (as determined by a 4-fold or greater rise in to the tropism of JCV for brain, BKV-related pathology is largely confined to the urinary tract. BKV antibody titer) in renal transplant recipients occur in individuals who have no detectable antibodies in Some simian polyomaviruses produce illnesses in their natural hosts which closely resemble human their first serum, i.e. they are primary infections [8]. This is in contrast to BKV infections in bone marrow illnesses caused by JCV and BKV. Simian virus 40, an indigenous polyomavirus infection of rhesus macaques, produces a PML-like neurological disease in animals Table 1. BKV infection in renal transplant recipients which are immunosuppressed by infection with simian immunodeficiency virus [2]. The renal pathology Donor/recipient Number Number (%) of caused by infection with the newly described cynomBKV antibody statusa,b recipients with BKV infectionc olgus polyomavirus [3] in animals undergoing experimental renal transplantation is very similar to the +/− 44 19 (43%) BKV-associated human disease described in a recent −/− 21 2 (10%) issue of this journal [4]. +/+ 229 50 (22%) −/+ 48 6 (13%)