Echovirus 7 Entry into Polarized Caco-2 Intestinal Epithelial Cells Involves Core Components of the Autophagy Machinery
Echovirus 7 Entry into Polarized Caco-2 Intestinal Epithelial Cells Involves Core Components of the Autophagy Machinery
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DOI：
10.1128/jvi.02706-13
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发表时间：
2014-01-01
影响因子：
5.4
通讯作者：
Bergelson, Jeffrey M.
中科院分区：
文献类型：
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作者：
Kim, Chonsaeng;Bergelson, Jeffrey M.
Echo病毒7通过网状蛋白介导的内吞过程进入极化的Caco-2肠上皮细胞，然后穿过内体系统，然后将其基因组释放到细胞质中。我们研究了自噬机制的核心组件在病毒进入过程中的可能作用。我们发现，用特定的小干扰RNA去除Beclin-1、Atg12、Atg14、Atg16或LC3可以抑制ECHO病毒7在去涂层上游的感染，但对病毒附着在细胞表面的影响很小或没有影响。这些数据表明，在病毒与细胞表面的受体结合之后、RNA从病毒衣壳中释放之前发生的一个或多个事件中，多个自噬相关蛋白是重要的。虽然我们还没有确定每个蛋白质促进病毒进入的机制，但我们发现Atg16L1的稳定耗尽干扰了病毒从细胞表面的内化，而不是细胞内的运输。因此，自噬基因产物可能参与将病毒移入极化的Caco-2细胞的内吞过程。
Echovirus 7 enters polarized Caco-2 intestinal epithelial cells by a clathrin-mediated endocytic process and then moves through the endosomal system before releasing its genome into the cytoplasm. We examined the possible role in virus entry of core components of the autophagy machinery. We found that depletion of Beclin-1, Atg12, Atg14, Atg16, or LC3 with specific small interfering RNAs inhibited echovirus 7 infection upstream of uncoating but had little or no effect on virus attachment to the cell surface. These data indicate that multiple autophagy-related proteins are important for one or more events that occur after the virus has bound its receptor on the cell surface but before RNA is released from the virus capsid. Although we have not determined the mechanism by which each protein contributes to virus entry, we found that stable depletion of Atg16L1 interfered with virus internalization from the cell surface rather than with intracellular trafficking. Autophagy gene products may thus participate in the endocytic process that moves virus into polarized Caco-2 cells.