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Mouse Norovirus infection promotes autophagy induction to facilitate replication but prevents final autophagosome maturation

机译:小鼠诺罗病毒感染促进自噬诱导,以促进复制,但防止最终的自噬成熟成熟

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摘要

Autophagy is a cellular process used to eliminate intracellular pathogens. Many viruses however are able to manipulate this cellular process for their own advantage. Here we demonstrate that Mouse Norovirus (MNV) infection induces autophagy but does not appear to utilise the autophagosomal membrane for establishment and formation of the viral replication complex. We have observed that MNV infection results in lipidation and recruitment of LC3 to the autophagosome membrane but prevents subsequent fusion of the autophagosomes with lysosomes, as SQSTM1 (an autophagy receptor) accumulates and Lysosome-Associated Membrane Protein1 is sequestered to the MNV replication complex (RC) rather than to autophagosomes. We have additionally observed that chemical modulation of autophagy differentially affects MNV replication. From this study we can conclude that MNV infection induces autophagy, however suppresses the final maturation step of this response, indicating that autophagy induction contributes to MNV replication independently of RC biogenesis. (C) 2016 Elsevier Inc. All rights reserved.
机译:自噬是一种用于消除细胞内病原体的细胞过程。然而,许多病毒能够操纵这种细胞过程以获得自己的优势。在这里,我们证明小鼠诺罗病毒(MNV)感染诱导自噬但似乎没有使用自噬体膜来建立和形成病毒复制复合物。我们已经观察到MnV感染导致LC3的脂质和募集到自噬体膜中,而是防止随后与溶酶体的自噬体融合,因为Sqstm1(自噬受体)积累和溶酶体相关的膜蛋白1被隔离为MNV复制复合物(RC )而不是自噬复印件。我们还观察到自噬的化学调制差异地影响MNV复制。从该研究开始,我们可以得出结论,MNV感染诱导自噬,但抑制了这种反应的最终成熟步骤,表明自噬诱导有助于独立于RC生物发生的MNV复制。 (c)2016 Elsevier Inc.保留所有权利。

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