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The autophagy machinery is required to initiate hepatitis C virus replication

机译:需要自噬机制启动丙型肝炎病毒复制

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In addition to its cellular homeostasis function, autophagy is emerging as a central component of antimicrobial host defense against diverse infections. To counteract this mechanism, many pathogens have evolved to evade, subvert, or exploit autophagy. Here, we report that autophagy proteins (i.e., Beclin-1, Atg4B, Atg5, and Atg12) are proviral factors required for translation of incoming hepatitis C virus (HCV) RNA and, thereby, for initiation of HCV replication, but they are not required once infection is established. These results illustrate a previously unappreciated role for autophagy in the establishment of a viral infection and they suggest that different host factors regulate the translation of incoming viral genome and translation of progeny HCV RNA once replication is established.
机译:除了其细胞稳态功能外,自噬正在成为抗微生物宿主防御多种感染的重要组成部分。为了抵消这种机制,许多病原体已经进化为逃避,破坏或利用自噬。在这里,我们报道自噬蛋白(即Beclin-1,Atg4B,Atg5和Atg12)是传入的丙型肝炎病毒(HCV)RNA的翻译以及由此引发HCV复制所需的前病毒因子,但并非如此建立感染后需要。这些结果说明了自噬在病毒感染建立中从未发挥过的作用,并且它们表明一旦建立复制,不同的宿主因素会调节传入病毒基因组的翻译和子代HCV RNA的翻译。

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