Key result
Enterovirus D68 adhesion to exosomes identifies a novel viral entry route into motor neurons.
Why the study?
It remains unclear how enterovirus D68 gains entry into the central nervous system and what receptors enable it to infect motor neurons in acute flaccid myelitis.
May not alter EV-D68 management; leaves open whether exosome adhesion contributes to motor neuron infection.
Despite the strong causal link between enterovirus D68 (EV-D68) and acute flaccid myelitis (AFM), it remains unclear how EV-D68 gains entry into the central nervous system and what receptors enable it to infect motor neurons. We show that EV-D68 particles can adhere to exosomes, placing EV-D68 among a handful of other picornaviruses which are known to interact with extracellular vesicles. Uptake and infection of permissive cells by virally contaminated exosomes would have major implications in the search for the EV-D68 receptor, as well as providing a possible route for viral entry into motor neurons. This work identifies a novel cellular entry route for EV-D68 and may facilitate the identification of genetic risk factors for development of AFM.
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Rudy et al. (2022) studied Enterovirus D68 (EV-D68) and acute flaccid myelitis (AFM). Enterovirus D68 (EV-D68) was evaluated on Viral particle association with exosomes. Enterovirus D68 particles can adhere to exosomes, identifying a novel cellular entry route that may facilitate viral entry into motor neurons.
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