ArticleThe Journal of clinical investigation2025
EV-D68 neurological disease: tipping the scales toward immunopathogenesis.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Rational Design of Broad-Spectrum Anti-Enteroviral Molecular Glues Targeting Enteroviral RNAi Suppressors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spinal Cord Injury in Enterovirus D68 Infection: Mechanisms and Pathophysiology in a Mouse Model.Viruses · 2025Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the last decade, there have been multiple outbreaks of enterovirus D68 (EV-D68) disease and associated cases of acute flaccid myelitis (AFM). The underlying cause of EV-D68-induced AFM is contentious; whether spinal cord motor neurons are damaged by direct viral infection, infiltration of immune cells, or a combination of both is not clear. In this issue of the JCI, Woods Acevedo and coworkers used a neonatal WT mouse model of EV-D68 infection to attribute paralytic disease to immune cell infiltration into the spinal cord. The results of their work in cytokine-knockout or immune cell-depleted animals effectively argue that immunopathogenesis plays an integral role in EV-D68-induced AFM.
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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.