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. 2019 Sep 3;10:2032. doi: 10.3389/fmicb.2019.02032

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Copyright © 2019 Sun, Wen, Wang, Mao, Cheng, Yang, Jia, Chen, Yang, Wu, Zhu, Liu, Zhao, Zhang, Wang, Xu, Chen, Zhu, Luo, Liu, Yu, Zhang and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The interaction between picornaviruses and the host autophagy pathway. Autophagy is a five-step preprocess, including induction, nucleation, expansion (elongation), fusion, and cargo degradation/metabolic recycling. Picornaviruses have been shown to subvert the host autophagy machinery for viral replication and non-lytic release. Some viruses, including PV, CVB3, EV71, HRV, FMDV, and EMCV have been reported to utilize the autophagy for optimal infection. Picornaviruses replicate on membranous replication organelles, which require a complex containing viral (2B and 3A), ACBD3, OSBP, and PI4KB (or PI4KA). The fusion of autophagosome with lysosomes is inhibited by picornaviruses. HAV, CVB3, PV, HRV, and EMCV can trigger autophagy and release virions in single-membrane vesicles.