Single-Cell Transcriptome Identifies the Renal Cell Type Tropism of Human BK Polyomavirus

Yang, Feng; Chen, Xutao; Zhang, Hui; Zhao, Guodong; Yang, Hui-Fei; Qiu, Jian; Meng, Siyan; Wu, Penghan; Tao, Liang; Wang, Qin; Huang, Gang

doi:10.3390/ijms24021330

Cited by 1 publication

(1 citation statement)

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“…The kidney tubules were found to be the most permissive to BKPyV replication. The tubules facilitate polyomavirus replication via increased glycolysis and constitutive the expression of transcription factors that steer cells into S phase [ 110 ]. Kidney tubules are also considered to be immune-privileged, allowing the virus to replicate freely undetected by the innate or adaptive immune system.…”

Section: How Is Jcpyv Transmitted?mentioning

confidence: 99%

Polyomavirus Wakes Up and Chooses Neurovirulence

Butic,

Spencer,

Shaheen

et al. 2023

Viruses

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JC polyomavirus (JCPyV) is a human-specific polyomavirus that establishes a silent lifelong infection in multiple peripheral organs, predominantly those of the urinary tract, of immunocompetent individuals. In immunocompromised settings, however, JCPyV can infiltrate the central nervous system (CNS), where it causes several encephalopathies of high morbidity and mortality. JCPyV-induced progressive multifocal leukoencephalopathy (PML), a devastating demyelinating brain disease, was an AIDS-defining illness before antiretroviral therapy that has “reemerged” as a complication of immunomodulating and chemotherapeutic agents. No effective anti-polyomavirus therapeutics are currently available. How depressed immune status sets the stage for JCPyV resurgence in the urinary tract, how the virus evades pre-existing antiviral antibodies to become viremic, and where/how it enters the CNS are incompletely understood. Addressing these questions requires a tractable animal model of JCPyV CNS infection. Although no animal model can replicate all aspects of any human disease, mouse polyomavirus (MuPyV) in mice and JCPyV in humans share key features of peripheral and CNS infection and antiviral immunity. In this review, we discuss the evidence suggesting how JCPyV migrates from the periphery to the CNS, innate and adaptive immune responses to polyomavirus infection, and how the MuPyV-mouse model provides insights into the pathogenesis of JCPyV CNS disease.

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Section: How Is Jcpyv Transmitted?mentioning

confidence: 99%