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Published on: July 13, 2019
Human polyoma viruses and disease with emphasis on clinical BK and JC
Raghavender Boothpur1, Daniel C Brennan
1Barnes-Jewish Hospital, St. Louis, MO, United States.
Abstract:
Polyoma viruses are ubiquitous infecting many different mammalian species including humans. There are five known human polyoma viruses. JC virus and BK virus are two polyoma viruses identified nearly three decades ago. Recently WU, KI and Merkel cell polyoma viruses have been isolated from humans. The exact role of these three newly discovered viruses in human disease is not known. Most human polyoma disease is caused by BK and JC viruses which are usually acquired in childhood. Approximately 50-80% of humans have seropositivity to these viruses. Clinically apparent diseases in immunocompetent hosts are extremely rare. These viruses remain latent possibly in the lymphoid organs, neuronal tissue, and kidney and under the circumstances of severe immunosuppression both these viruses reactivate. Neurotropic JC virus reaches the brain and causes progressive multifocal leukoencephalopathy, a demyelinating disease of the central nervous system with a high mortality rate. BK virus is urotheliotropic and its reactivation causes a form of interstitial nephritis, known as BK or polyoma virus associated nephropathy which is associated with high graft loss if not recognized early. There are no known effective antiviral agents for any of the polyoma viruses.
Insights
Human polyoma viruses like JC and BK are common and usually latent. Reactivation in immunocompromised individuals can cause severe diseases, including progressive multifocal leukoencephalopathy and BK virus-associated nephropathy.
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Polyoma viruses are widespread in mammals, with five known human types: JC virus (JCV), BK virus (BKV), WU polyomavirus (WUPyV), KI polyomavirus (KIPyV), and Merkel cell polyomavirus (MCPyV).
- JCV and BKV, identified decades ago, are the primary causes of human polyoma virus-associated diseases, with seroprevalence in 50-80% of the human population.
- While infections are typically acquired in childhood and asymptomatic in immunocompetent individuals, these viruses can establish lifelong latent infections.
Purpose of the Study:
- To review the clinical significance of human polyoma viruses, focusing on JCV and BKV.
- To elucidate the pathogenesis of diseases caused by polyoma virus reactivation under immunosuppression.
- To highlight the diagnostic and management challenges associated with these infections.
Main Methods:
- Review of existing literature on human polyoma viruses, their epidemiology, pathogenesis, and associated clinical manifestations.
- Analysis of case studies and clinical data related to JCV and BKV infections.
- Discussion of the impact of immunosuppression on viral reactivation and disease progression.
Main Results:
- Reactivation of latent JCV and BKV under severe immunosuppression can lead to severe, life-threatening conditions.
- Neurotropic JCV reactivation causes progressive multifocal leukoencephalopathy (PML), a fatal demyelinating CNS disease.
- Urotheliotropic BKV reactivation results in BK virus-associated nephropathy (BKVAN), a significant cause of graft loss in kidney transplant recipients.
Conclusions:
- Human polyoma viruses, particularly JCV and BKV, pose significant health risks upon reactivation in immunocompromised hosts.
- Early recognition of JCV and BKV-associated diseases is crucial for patient management and improving outcomes.
- Currently, no effective antiviral therapies exist for polyoma virus infections, emphasizing the need for further research and development.
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