ArticleeLife2020
Antibody escape by polyomavirus capsid mutation facilitates neurovirulence.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
13 citing papers in PubMed, 18 citations in OpenAlex.
- PD-1 regulates CD4Nature communications · 2026Article
- Immune Modulation by Microbiota and Its Possible Impact on Polyomavirus Infection.Pathogens (Basel, Switzerland) · 2025Review
- Live long and persist: polyomavirus immune evasion in the brain and kidney.Future virology · 2025Article
- CXCR4 and CXCR6 dually limit T cell entry into the polyomavirus-infected brain.Journal of neuroinflammation · 2025Article
- The CXCR6-CXCL16 axis mediates T cell control of polyomavirus infection in the kidney.PLoS pathogens · 2025Article
- The CD4 T cell-independent IgG response during persistent virus infection favors emergence of neutralization-escape variants.bioRxiv : the preprint server for biology · 2024Article
- Article
- Polyomavirus Wakes Up and Chooses Neurovirulence.Viruses · 2023Review
- 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
- A ribavirin-induced ORF2 single-nucleotide variant produces defective hepatitis E virus particles with immune decoy function.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- High-resolution asymmetric structure of a Fab-virus complex reveals overlap with the receptor binding site.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- JCPyV VP1 Mutations in Progressive MultifocalLeukoencephalopathy: Altering Tropismor Mediating Immune Evasion?Viruses · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
JCPyV polyomavirus, a member of the human virome, causes progressive multifocal leukoencephalopathy (PML), an oft-fatal demyelinating brain disease in individuals receiving immunomodulatory therapies. Mutations in the major viral capsid protein, VP1, are common in JCPyV from PML patients (JCPyV-PML) but whether they confer neurovirulence or escape from virus-neutralizing antibody (nAb) in vivo is unknown. A mouse polyomavirus (MuPyV) with a sequence-equivalent JCPyV-PML VP1 mutation replicated poorly in the kidney, a major reservoir for JCPyV persistence, but retained the CNS infectivity, cell tropism, and neuropathology of the parental virus. This mutation rendered MuPyV resistant to a monoclonal Ab (mAb), whose specificity overlapped the endogenous anti-VP1 response. Using cryo-EM and a custom sub-particle refinement approach, we resolved an MuPyV:Fab complex map to 3.2 Å resolution. The structure revealed the mechanism of mAb evasion. Our findings demonstrate convergence between nAb evasion and CNS neurovirulence in vivo by a frequent JCPyV-PML VP1 mutation.
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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.