Key result
Contemporary enterovirus D68 strains exhibit enhanced neurotropism and neuropathogenicity vs historical strains in animal models.
Why the study?
A definitive causal link between EV-D68 infection and acute flaccid myelitis had not been unequivocally established despite accumulating clinical, immunological, and epidemiological evidence.
Basic science models provide biological plausibility that recently emerged EV-D68 strains are the primary causal agent of acute flaccid myelitis outbreaks in children.
In 2014, the United States (US) experienced an unprecedented epidemic of enterovirus D68 (EV-D68)-induced respiratory disease that was temporally associated with the emergence of acute flaccid myelitis (AFM), a paralytic disease occurring predominantly in children, that has a striking resemblance to poliomyelitis. Although a definitive causal link between EV-D68 infection and AFM has not been unequivocally established, rapidly accumulating clinical, immunological, and epidemiological evidence points to EV-D68 as the major causative agent of recent seasonal childhood AFM outbreaks in the US. This review summarizes evidence, gained from in vivo and in vitro models of EV-D68-induced disease, which demonstrates that contemporary EV-D68 strains isolated during and since the 2014 outbreak differ from historical EV-D68 in several factors influencing neurovirulence, including their genomic sequence, their receptor utilization, their ability to infect neurons, and their neuropathogenicity in mice. These findings provide biological plausibility that EV-D68 is a causal agent of AFM and provide important experimental models for studies of pathogenesis and treatment that are likely to be difficult or impossible in humans.
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Hixon et al. (2019) conducted a review in Enterovirus D68-Induced Acute Flaccid Myelitis. Enterovirus D68 vs. Historical EV-D68 strains was evaluated. Contemporary enterovirus D68 strains demonstrate enhanced neurotropism, altered receptor utilization, and neuropathogenicity in mouse models compared to historical strains, providing biological plausibility as the causal agent of acute flaccid myelitis.
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