Abstract
Enterovirus-D68 (EV-D68) is a medically important respiratory plus-strand RNA virus of children which has been linked to acute flaccid myelitis. We have determined that EV-D68 induces autophagic signaling and membrane formation. Autophagy, a homeostatic degradative process that breaks down protein aggregates and damaged organelles, promotes replication of multiple plus-strand viruses. Induction of autophagic signals promotes EV-D68 replication, but the virus inhibits the downstream degradative steps of autophagy in multiple ways. EV-D68 proteases cleave a major autophagic cargo adaptor and the autophagic SNARE Snap29, which reportedly regulates fusion between autophagosome to amphisome/autolysosome. Although the virus inhibits autophagic degradation, Snap29 promotes virus replication early in infection. An orphan SNARE, Snap47, is shown to have a previously unknown role in autophagy, and Snap47 promotes the replication of EV-D68. Our study illuminates a new mechanism for subversion of autophagic flux, and redirection of the autophagic membranes to benefit EV-D68 replication.
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