Mitophagosomes induced during EV-D68 infection promote viral nonlytic release.

Enterovirus-D68 (EV-D68) is a plus-strand RNA virus that primarily causes infant respiratory infections. In rare pediatric cases, infection with EV-D68 has been associated with acute flaccid myelitis, a polio-like paralytic disease. We have previously demonstrated that EV-D68 induces nonselective autophagy for its benefit.

Some assembly required: a single-RNA vaccine against enterovirus-D68.

A single-RNA-based vaccine against enterovirus-D68, a respiratory virus and causative agent of severe paralytic disease in children, by the Erasmus group shows great promise in generating broadly cross-neutralizing antibodies in mice and macaque models of infection.

Transcription factor EB (TFEB) interaction with RagC is disrupted during enterovirus D68 infection.

Unlabelled: Enterovirus D68 (EV-D68) is a picornavirus associated with severe respiratory illness and a paralytic disease called acute flaccid myelitis in infants. Currently, no protective vaccines or antivirals are available to combat this virus. Like other enteroviruses, EV-D68 uses components of the cellular autophagy pathway to rewire membranes for its replication.

Enterovirus D68 capsid formation and stability requires acidic compartments.

The respiratory picornavirus enterovirus D68 is a causative agent of acute flaccid myelitis, a childhood paralysis disease identified in the last decade. Poliovirus, another picornavirus associated with paralytic disease, is a fecal-oral virus that survives acidic environments when passing from host to host. Here, we follow up on our previous work showing a requirement for acidic intracellular compartments for maturation cleavage of poliovirus particles.

Enterovirus D68 capsid formation and stability requires acidic compartments.

Enterovirus D68 (EV-D68), a picornavirus traditionally associated with respiratory infections, has recently been linked to a polio-like paralytic condition known as acute flaccid myelitis (AFM). EV-D68 is understudied, and much of the field's understanding of this virus is based on studies of poliovirus. For poliovirus, we previously showed that low pH promotes virus capsid maturation, but here we show that, for EV-D68, inhibition of compartment acidification during a specific window of infection causes a defect in capsid formation and maintenance.