ArticleJournal of extracellular biology2022
Biogenesis of JC polyomavirus associated extracellular vesicles.
Article in Journal of extracellular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- CRISPR and Myelin regeneration: a systematic review of applications in demyelinating CNS Disorders, with a focus on MS.Regenerative medicine · 2025Pooled it
- Merkel cell polyomavirus exploits extracellular vesicles for skin infection and host immune evasion through activated Wnt signaling.PLoS pathogens · 2026Article
- Remodeling of the cellular membrane architecture in response to BK polyomavirus infection.Virology journal · 2026Review
- Interactions between extracellular vesicles and viruses: lessons learned across species and kingdoms.FEMS microbiology reviews · 2026Review
- Establishment of a Stable BK Polyomavirus-Secreting Cell Line: Characterization of Viral Genome Integration and Replication Dynamics Through Comprehensive Analysis.International journal of molecular sciences · 2025Article
- Editorial: Viral infection pathogenesis and pathology in nervous system.Frontiers in cellular and infection microbiology · 2025Article
- Neutral sphingomyelinase 2: A promising drug target for CNS disease.Advances in pharmacology (San Diego, Calif.) · 2025Review
- Shedding Light on Viral Shedding: Novel Insights into Nuclear Assembly, Cytoplasmic Transformation and Extracellular Vesicle Release of the BK Virus.International journal of molecular sciences · 2024Article
- The Conserved YPXViruses · 2024Article
- John Cunningham Virus and Progressive Multifocal Leukoencephalopathy: A Falsely Played Diagnosis.Diseases (Basel, Switzerland) · 2024Review
- Exploring the role of brain-derived extracellular vesicles in viral infections: from pathological insights to biomarker potential.Frontiers in cellular and infection microbiology · 2024Review
- Lessons from Polyomavirus Immunofluorescence Staining of Urinary Decoy Cells.Life (Basel, Switzerland) · 2023Article
- An Elusive Target: Inhibitors of JC Polyomavirus Infection and Their Development as Therapeutics for the Treatment of Progressive Multifocal Leukoencephalopathy.International journal of molecular sciences · 2023Review
- Complexities of JC Polyomavirus Receptor-Dependent and -Independent Mechanisms of Infection.Viruses · 2022Review
- Biogenesis of JC polyomavirus associated extracellular vesicles.Journal of extracellular biology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
JC polyomavirus (JCPyV) is a small, non-enveloped virus that persists in the kidney in about half the adult population. In severely immune-compromised individuals JCPyV causes the neurodegenerative disease progressive multifocal leukoencephalopathy (PML) in the brain. JCPyV has been shown to infect cells by both direct and indirect mechanisms, the latter involving extracellular vesicle (EV) mediated infection. While direct mechanisms of infection are well studied indirect EV mediated mechanisms are poorly understood. Using a combination of chemical and genetic approaches we show that several overlapping intracellular pathways are responsible for the biogenesis of virus containing EV. Here we show that targeting neutral sphingomyelinase 2 (nSMase2) with the drug cambinol decreased the spread of JCPyV over several viral life cycles. Genetic depletion of nSMase2 by either shRNA or CRISPR/Cas9 reduced EV-mediated infection. Individual knockdown of seven ESCRT-related proteins including HGS, ALIX, TSG101, VPS25, VPS20, CHMP4A, and VPS4A did not significantly reduce JCPyV associated EV (JCPyV(+) EV) infectivity, whereas knockdown of the tetraspanins CD9 and CD81 or trafficking and/or secretory autophagy-related proteins RAB8A, RAB27A, and GRASP65 all significantly reduced the spread of JCPyV and decreased EV-mediated infection. These findings point to a role for exosomes and secretory autophagosomes in the biogenesis of JCPyV associated EVs with specific roles for nSMase2, CD9, CD81, RAB8A, RAB27A, and GRASP65 proteins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.