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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.
Authors
Peter W. Krug
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