| Summary: | 碩士 === 國立成功大學 === 微生物及免疫學研究所 === 104 === Enterovirus 71 (EV71) infection can cause deaths and severe neurological complications in young children, especially in the Asia-Pacific region including Taiwan. Currently, the lack of antiviral therapies and vaccines specific for EV71 stresses the need to study viral pathogenesis. Autophagy maintains homeostasis by recycling cytoplasmic materials. The complete autophagic flux contains three major steps: autophagosome formation, autophagosome-lysosome fusion, and lysosomal degradation. Several positive-stranded RNA viruses, including EV71, can take advantage of autophagy for their own benefits. Previous studies showed that EV71 infection induces complete autophagic flux. However, the importance of each autophagic step in EV71 RNA replication, protein synthesis, virus production, and egress has not been addressed. In the present study, we confirmed that EV71 infection induces autophagic flux in human cell lines. To elucidate whether autophagy is essential to EV71 replication, we inhibited three major autophagic steps: autophagosome formation, autophagosome-lysosome fusion, and lysosomal degradation. Our findings uncover how autophagy contributes to EV71 replication, and provide strategies for developing effective antiviral therapies.
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