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Polyomavirus Wakes Up and Chooses Neurovirulence
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)...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10612099/ https://www.ncbi.nlm.nih.gov/pubmed/37896889 http://dx.doi.org/10.3390/v15102112 |
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author | Butic, Arrienne B. Spencer, Samantha A. Shaheen, Shareef K. Lukacher, Aron E. |
author_facet | Butic, Arrienne B. Spencer, Samantha A. Shaheen, Shareef K. Lukacher, Aron E. |
author_sort | Butic, Arrienne B. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-10612099 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-106120992023-10-29 Polyomavirus Wakes Up and Chooses Neurovirulence Butic, Arrienne B. Spencer, Samantha A. Shaheen, Shareef K. Lukacher, Aron E. Viruses Review 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. MDPI 2023-10-18 /pmc/articles/PMC10612099/ /pubmed/37896889 http://dx.doi.org/10.3390/v15102112 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Butic, Arrienne B. Spencer, Samantha A. Shaheen, Shareef K. Lukacher, Aron E. Polyomavirus Wakes Up and Chooses Neurovirulence |
title | Polyomavirus Wakes Up and Chooses Neurovirulence |
title_full | Polyomavirus Wakes Up and Chooses Neurovirulence |
title_fullStr | Polyomavirus Wakes Up and Chooses Neurovirulence |
title_full_unstemmed | Polyomavirus Wakes Up and Chooses Neurovirulence |
title_short | Polyomavirus Wakes Up and Chooses Neurovirulence |
title_sort | polyomavirus wakes up and chooses neurovirulence |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10612099/ https://www.ncbi.nlm.nih.gov/pubmed/37896889 http://dx.doi.org/10.3390/v15102112 |
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