ArticleJournal of virology2002
Oligosaccharides as receptors for JC virus.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Systematic review of the published data on the worldwide prevalence of John Cunningham virus in patients with multiple sclerosis and neuromyelitis optica.Epidemiology and health · 2018Pooled it
- Article
- Carbohydrates: Binding Sites and Potential Drug Targets for Neural-Affecting Pathogens.Advances in neurobiology · 2023Article
- Complexities of JC Polyomavirus Receptor-Dependent and -Independent Mechanisms of Infection.Viruses · 2022Review
- Bioinspired and Biomimetic Nanomedicines for Targeted Cancer Therapy.Pharmaceutics · 2022Review
- Sending mixed signals: polyomavirus entry and trafficking.Current opinion in virology · 2021Review
- Taking the Scenic Route: Polyomaviruses Utilize Multiple Pathways to Reach the Same Destination.Viruses · 2020Review
- How non-enveloped viruses hijack host machineries to cause infection.Advances in virus research · 2019Article
- Human Polyomavirus JCPyV and Its Role in Progressive Multifocal Leukoencephalopathy and Oncogenesis.Frontiers in oncology · 2019Review
- Virus-Receptor Interactions: The Key to Cellular Invasion.Journal of molecular biology · 2018Review
- Susceptibility of Primary Human Choroid Plexus Epithelial Cells and Meningeal Cells to Infection by JC Virus.Journal of virology · 2018Article
- Gene therapy for human glioblastoma using neurotropic JC virus-like particles as a gene delivery vector.Scientific reports · 2018Article
- Infectious Entry and Neutralization of Pathogenic JC Polyomaviruses.Cell reports · 2017Article
- Diagnosis and Treatment of Progressive Multifocal Leukoencephalopathy Associated with Multiple Sclerosis Therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Review
- JC Polyomavirus Attachment and Entry: Potential Sites for PML Therapeutics.Current clinical microbiology reports · 2017Article
- Host cell virus entry mechanisms enhance anti-JCV-antibody switch in natalizumab-treated multiple sclerosis patients.Journal of neurovirology · 2016Observational
- Glycosphingolipid-Protein Interaction in Signal Transduction.International journal of molecular sciences · 2016Review
- JC polyomavirus attachment, entry, and trafficking: unlocking the keys to a fatal infection.Journal of neurovirology · 2015Review
- Human polyomavirus receptor distribution in brain parenchyma contrasts with receptor distribution in kidney and choroid plexus.The American journal of pathology · 2015Article
- The Greater Affinity of JC Polyomavirus Capsid for α2,6-Linked Lactoseries Tetrasaccharide c than for Other Sialylated Glycans Is a Major Determinant of Infectivity.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
JC virus (JCV) belongs to the polyomavirus family of double-stranded DNA viruses and in humans causes a demyelinating disease of the central nervous system, progressive multifocal leukoencephalopathy. Its hemagglutination activity and entry into host cells have been reported to depend on an N-linked glycoprotein containing sialic acid. In order to identify the receptors of JCV, we generated virus-like particles (VLP) consisting of major viral capsid protein VP1. We then developed an indirect VLP overlay assay to detect VLP binding to glycoproteins and a panel of glycolipids. We found that VLP bound to sialoglycoproteins, including alpha1-acid glycoprotein, fetuin, and transferrin receptor, and that this binding depended on alpha2-3-linked sialic acids and N-linked sugar chains. Neoglycoproteins were synthesized by using ovalbumin and conjugation with oligosaccharides containing the terminal alpha2-3- or alpha2-6-linked sialic acid or the branched alpha2-6-linked sialic acid. We show that the neoglycoprotein containing the terminal alpha2-6-linked sialic acid had the highest affinity for VLP, inhibited the hemagglutination activity of VLP and JCV, and inhibited the attachment of VLP to cells. We also demonstrate that VLP bound to specific glycolipids, such as lactosylceramide, and gangliosides, including GM3, GD2, GD3, GD1b, GT1b, and GQ1b, and that VLP bound weakly to GD1a but did not bind to GM1a, GM2, or galactocerebroside. Furthermore, the neoglycoprotein containing the terminal alpha2-6-linked sialic acid and the ganglioside GT1b inhibited JCV infection in the susceptible cell line IMR-32. These results suggest that the oligosaccharides of glycoproteins and glycolipids work as JCV receptors and may be feasible as anti-JCV agents.
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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.