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Enteroviruses Remodel Autophagic Trafficking through Regulation of Host SNARE Proteins to Promote Virus Replication and Cell Exit.
Cell Reports ( IF 7.5 ) Pub Date : 2018-03-20 , DOI: 10.1016/j.celrep.2018.03.003 Abigail K Corona 1 , Holly M Saulsbery 1 , Angel F Corona Velazquez 1 , William T Jackson 1
Cell Reports ( IF 7.5 ) Pub Date : 2018-03-20 , DOI: 10.1016/j.celrep.2018.03.003 Abigail K Corona 1 , Holly M Saulsbery 1 , Angel F Corona Velazquez 1 , William T Jackson 1
Affiliation
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Enterovirus D68 (EV-D68) is a medically important respiratory plus-strand RNA virus of children that 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 mechanism for subversion of autophagic flux and redirection of the autophagic membranes to benefit EV-D68 replication.
中文翻译：
肠病毒通过调节宿主SNARE蛋白来重塑自噬运输，以促进病毒复制和细胞退出。
肠道病毒D68（EV-D68）是儿童的医学上重要的呼吸道正链RNA病毒，与急性弛缓性脊髓炎有关。我们已经确定，EV-D68诱导自噬信号传导和膜形成。自噬是一种体内稳态的降解过程，可分解蛋白质聚集体和受损的细胞器，促进多种正链病毒的复制。自噬信号的诱导促进EV-D68复制，但病毒以多种方式抑制自噬的下游降解步骤。EV-D68蛋白酶切割主要的自噬货物衔接子和自噬SNARE SNAP29，据报道，SNARE SNAP29调节自噬小体与两亲/自溶体之间的融合。尽管该病毒抑制自噬降解，但SNAP29在感染初期可促进病毒复制。孤儿SNARE，SNAP47，SNAP47被证明在自噬中具有以前未知的作用，并且SNAP47促进EV-D68的复制。我们的研究阐明了自噬通量的颠覆和自噬膜改向有利于EV-D68复制的机制。
更新日期：2018-03-22
中文翻译：
肠病毒通过调节宿主SNARE蛋白来重塑自噬运输，以促进病毒复制和细胞退出。
肠道病毒D68（EV-D68）是儿童的医学上重要的呼吸道正链RNA病毒，与急性弛缓性脊髓炎有关。我们已经确定，EV-D68诱导自噬信号传导和膜形成。自噬是一种体内稳态的降解过程，可分解蛋白质聚集体和受损的细胞器，促进多种正链病毒的复制。自噬信号的诱导促进EV-D68复制，但病毒以多种方式抑制自噬的下游降解步骤。EV-D68蛋白酶切割主要的自噬货物衔接子和自噬SNARE SNAP29，据报道，SNARE SNAP29调节自噬小体与两亲/自溶体之间的融合。尽管该病毒抑制自噬降解，但SNAP29在感染初期可促进病毒复制。孤儿SNARE，SNAP47，SNAP47被证明在自噬中具有以前未知的作用，并且SNAP47促进EV-D68的复制。我们的研究阐明了自噬通量的颠覆和自噬膜改向有利于EV-D68复制的机制。
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