ArticleThe Journal of infectious diseases2011
Progressive multifocal leukoencephalopathy (PML) development is associated with mutations in JC virus capsid protein VP1 that change its receptor specificity.
Article in The Journal of infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 158 citations in OpenAlex.
- Human glial chimeric mice reveal astrocytic dependence of JC virus infection.The Journal of clinical investigation · 2014Trial
- JC polyomavirus infection is strongly controlled by human leucocyte antigen class II variants.PLoS pathogens · 2014Trial
- Structural characterization of human neutralizing antibodies against JC and BK polyomaviruses.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- Genetic Diversity of the Polyomavirus JC and Implications for the Pathogenesis of Progressive Multifocal Leukoencephalopathy.Viruses · 2026Review
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Live long and persist: polyomavirus immune evasion in the brain and kidney.Future virology · 2025Article
- Recent advances in discovery and functional analysis of the small proteins and microRNA expressed by polyomaviruses.Virology · 2025Review
- The CD4 T cell-independent IgG response during persistent virus infection favors emergence of neutralization-escape variants.bioRxiv : the preprint server for biology · 2024Article
- Prevalence of JC polyomavirus among rheumatoid arthritis and systemic lupus erythematosus patients and its correlation with vitamin D levels.Iranian journal of microbiology · 2024Article
- Polyomavirus Wakes Up and Chooses Neurovirulence.Viruses · 2023Review
- Progressive Multifocal Leukoencephalopathy: Pathogenesis, Diagnostic Tools, and Potential Biomarkers of Response to Therapy.Neurology · 2023Review
- Revisiting JC virus and progressive multifocal leukoencephalopathy.Journal of neurovirology · 2023Review
- Time-dependent variations in BK polyomavirus genome from kidney transplant recipients with persistent viremia.Scientific reports · 2023Article
- A multivalent polyomavirus vaccine elicits durable neutralizing antibody responses in macaques.Vaccine · 2023Article
- Long-term outcome of progressive multifocal leukoencephalopathy with recombinant interleukin-2 treatment and an associated increase in the number of HPyV-2-specific T-cells: a case report.Therapeutic advances in hematology · 2023Article
- T cell deficiency precipitates antibody evasion and emergence of neurovirulent polyomavirus.eLife · 2022Article
- Understanding polyomavirus CNS disease - a perspective from mouse models.The FEBS journal · 2022Review
- Complexities of JC Polyomavirus Receptor-Dependent and -Independent Mechanisms of Infection.Viruses · 2022Review
- The oncogenic roles of JC polyomavirus in cancer.Frontiers in oncology · 2022Review
37 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease caused by JC virus (JCV) infection of oligodendrocytes, may develop in patients with immune disorders following reactivation of chronic benign infection. Mutations of JCV capsid viral protein 1 (VP1), the capsid protein involved in binding to sialic acid cell receptors, might favor PML onset. Cerebrospinal fluid sequences from 37/40 PML patients contained one of several JCV VP1 amino acid mutations, which were also present in paired plasma but not urine sequences despite the same viral genetic background. VP1-derived virus-like particles (VLPs) carrying these mutations lost hemagglutination ability, showed different ganglioside specificity, and abolished binding to different peripheral cell types compared with wild-type VLPs. However, mutants still bound brain-derived cells, and binding was not affected by sialic acid removal by neuraminidase. JCV VP1 substitutions are acquired intrapatient and might favor JCV brain invasion through abrogation of sialic acid binding with peripheral cells, while maintaining sialic acid-independent binding with brain cells.
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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.