Role of Polyomavirus (BK) in Urinary Tract Pathology

Copyright: © 2012 Alexiev BA. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Polyomavirus hominis 1, better known as BK virus (BKV), infects up to 90% of the general population [1]. Following a typically subclinical primary infection, BKV establishes a lifelong persistent infection in the kidney and urinary tract. The introduction during the past two decades of new more potent immunosuppressive regimens has led to a significant increase in BKV associated pathology, including but not limited to BKV allograft nephropathy (BKAN), ureteral stenosis, and hemorrhagic cystitis [2,3]. Approximately 40 years ago, Koss described polyomavirus inclusion bearing cells for the first time in urine specimens [4]. He coined the term “decoy cells” to alert pathologists not to misdiagnose viral inclusion bearing cells as malignant cancer cells [3]. The name decoy cell is a descriptive term for epithelial cells with intranuclear viral inclusion bodies that can have different phenotypes (types 1-4) depending upon the state of viral replication and maturation as well as the state of cellular preservation [3]. The shedding of decoy cells generally indicates the (re)activation of polyomavirus (BK) in the urothelium [3]. Although productive infections with cytomegalovirus, herpes simplex virus or human papillomavirus can show nuclear abnormalities including viral inclusion bodies, typical decoy cells are generally not found in the urine in these infections [3].