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Overview of JC polyomavirus, BK polyomavirus, and other polyomavirus infections

Hans H Hirsch, MD, MSc
Section Editor
Martin S Hirsch, MD
Deputy Editor
Anna R Thorner, MD


Polyomavirus infections have been detected in vertebrate hosts including rodents, cattle, birds, monkeys, and primates. Despite some common features with papillomaviruses, including an oncogenic potential, polyomaviruses are recognized as members of the separate genus Polyomavirus in the Polyomaviridae family of the ungrouped DNA viruses [1].

An overview of the disease associations, clinical manifestations, and diagnosis of polyomavirus infections will be provided here. The virology, epidemiology, and pathogenesis of infections with human polyomaviruses will be presented separately. Progressive multifocal leukoencephalopathy and BK polyomavirus-associated nephropathy and ureteral stenosis are also discussed in detail elsewhere. (See "Virology, epidemiology, and pathogenesis of JC polyomavirus, BK polyomavirus, and other human polyomaviruses" and "Progressive multifocal leukoencephalopathy: Epidemiology, clinical manifestations, and diagnosis" and "Natalizumab for relapsing-remitting multiple sclerosis in adults", section on 'Risk of PML' and "Progressive multifocal leukoencephalopathy: Treatment and prognosis" and "Clinical manifestations and diagnosis of BK virus-induced (polyomavirus-induced) nephropathy in kidney transplantation" and "Prevention and management of BK virus-induced (polyomavirus-induced) nephropathy in kidney transplantation" and "Ureteral stenosis due to BK virus infection among kidney transplant recipients".)


Most immunocompetent individuals with primary polyomavirus infections have a subclinical or nonspecific influenza-like course. In immunocompromised individuals, however, human polyomavirus (HPyV) replication can cause specific syndromes and lead to substantial morbidity. Some HPyV-associated diseases are more frequently encountered in specific patient populations, suggesting that the interaction of patient, organ, and virus determinants underlie the pathogenesis; the reasons for these associations are not fully understood [2].

BK polyomavirus – BK polyomavirus (BKPyV) may cause nephropathy and, less commonly, ureteric stenosis in kidney transplant recipients (and rarely in recipients of other types of transplants) [3,4]. BKPyV also causes hemorrhagic cystitis, primarily in allogeneic hematopoietic cell transplant recipients [2,5]. (See "Clinical manifestations and diagnosis of BK virus-induced (polyomavirus-induced) nephropathy in kidney transplantation" and "Prevention and management of BK virus-induced (polyomavirus-induced) nephropathy in kidney transplantation" and "Ureteral stenosis due to BK virus infection among kidney transplant recipients" and "Overview of infections following hematopoietic cell transplantation", section on 'Hemorrhagic cystitis'.)

JC polyomavirus – JC polyomavirus (JCPyV) may cause progressive multifocal leukoencephalopathy in immunocompromised patients, such as those with advanced HIV infection, hematologic malignancies, and those receiving lymphocyte-targeted therapies for autoimmune diseases (eg, natalizumab). It rarely causes JCPyV-associated nephropathy [6]. (See "Progressive multifocal leukoencephalopathy: Epidemiology, clinical manifestations, and diagnosis" and "Progressive multifocal leukoencephalopathy: Treatment and prognosis" and "Natalizumab for relapsing-remitting multiple sclerosis in adults", section on 'Risk of PML'.)

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Literature review current through: Nov 2017. | This topic last updated: Jun 12, 2017.
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