ArticleeLife2022
T cell deficiency precipitates antibody evasion and emergence of neurovirulent polyomavirus.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- PD-1 regulates CD4Nature communications · 2026Article
- Review
- Brain Immune Cell Composition in Multiple Sclerosis and Progressive Multifocal Leukoencephalopathy After Natalizumab: An Immunohistochemical Cohort Study.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Article
- Annual 12-Week Dosing Gap of Natalizumab: Clinical Efficacy, Blood Biomarkers, and CSF Cell Composition.Annals of clinical and translational neurology · 2026Observational
- 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
- Molecular epidemiology of JC polyomavirus genotypes in PLWH from Turkey.Journal of neurovirology · 2025Article
- Shedding dynamics of a DNA virus population during acute and long-term persistent infection.PLoS pathogens · 2025Article
- Review
- 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
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
JC polyomavirus (JCPyV) causes progressive multifocal leukoencephalopathy (PML), a life-threatening brain disease in immunocompromised patients. Inherited and acquired T cell deficiencies are associated with PML. The incidence of PML is increasing with the introduction of new immunomodulatory agents, several of which target T cells or B cells. PML patients often carry mutations in the JCPyV VP1 capsid protein, which confer resistance to neutralizing VP1 antibodies (Ab). Polyomaviruses (PyV) are tightly species-specific; the absence of tractable animal models has handicapped understanding PyV pathogenesis. Using mouse polyomavirus (MuPyV), we found that T cell deficiency during persistent infection, in the setting of monospecific VP1 Ab, was required for outgrowth of VP1 Ab-escape viral variants. CD4 T cells were primarily responsible for limiting polyomavirus infection in the kidney, a major reservoir of persistent infection by both JCPyV and MuPyV, and checking emergence of these mutant viruses. T cells also provided a second line of defense by controlling the outgrowth of VP1 mutant viruses that evaded Ab neutralization. A virus with two capsid mutations, one conferring Ab-escape yet impaired infectivity and a second compensatory mutation, yielded a highly neurovirulent variant. These findings link T cell deficiency and evolution of Ab-escape polyomavirus VP1 variants with neuropathogenicity.
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Registered trials
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