EV-D68 neurological disease: tipping the scales toward immunopathogenesis.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 40759565.
- Also identified by DOI 10.1172/JCI195839 and PMC identifier 12321398.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Enterovirus D, Human
- Enterovirus Infections
- Myelitis
- Neuromuscular Diseases