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本文引用的文献

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mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells.mTOR 非依赖性自噬可抵抗单纯疱疹病毒 1 感染的 U251 神经胶质瘤细胞中的细胞凋亡。
Microbes Infect. 2013 Jul-Aug;15(8-9):615-24. doi: 10.1016/j.micinf.2013.04.012. Epub 2013 May 10.
2
Excretion of enterovirus 71 in persons infected with hand, foot and mouth disease.手足口病患者肠道病毒 71 型的排泄。
Virol J. 2013 Jan 23;10:31. doi: 10.1186/1743-422X-10-31.
3
Japanese encephalitis virus activates autophagy as a viral immune evasion strategy.日本脑炎病毒通过激活自噬作为一种病毒免疫逃避策略。
PLoS One. 2013;8(1):e52909. doi: 10.1371/journal.pone.0052909. Epub 2013 Jan 8.
4
Viral subversion of host functions for picornavirus translation and RNA replication.小核糖核酸病毒翻译和RNA复制过程中宿主功能的病毒颠覆作用
Future Virol. 2012 Feb;7(2):179-191. doi: 10.2217/fvl.12.2.
5
Intracellular vesicle acidification promotes maturation of infectious poliovirus particles.细胞内囊泡酸化促进传染性脊髓灰质炎病毒颗粒的成熟。
PLoS Pathog. 2012;8(11):e1003046. doi: 10.1371/journal.ppat.1003046. Epub 2012 Nov 29.
6
Autophagy hijacked through viroporin-activated calcium/calmodulin-dependent kinase kinase-β signaling is required for rotavirus replication.病毒孔蛋白激活钙/钙调蛋白依赖性激酶激酶-β信号通路介导的自噬流被劫持对于轮状病毒的复制是必需的。
Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):E3405-13. doi: 10.1073/pnas.1216539109. Epub 2012 Nov 26.
7
Inhibition of cellular autophagy deranges dengue virion maturation.细胞自噬的抑制会扰乱登革热病毒粒子的成熟。
J Virol. 2013 Feb;87(3):1312-21. doi: 10.1128/JVI.02177-12. Epub 2012 Nov 21.
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The Legionella effector RavZ inhibits host autophagy through irreversible Atg8 deconjugation.军团菌效应蛋白 RavZ 通过不可逆的 Atg8 去共轭作用抑制宿主自噬。
Science. 2012 Nov 23;338(6110):1072-6. doi: 10.1126/science.1227026. Epub 2012 Oct 25.
9
Sudden unexpected death related to enterovirus myocarditis: histopathology, immunohistochemistry and molecular pathology diagnosis at post-mortem.与肠病毒心肌炎相关的突发性意外死亡:尸检时的组织病理学、免疫组织化学和分子病理学诊断。
BMC Infect Dis. 2012 Sep 11;12:212. doi: 10.1186/1471-2334-12-212.
10
Guidelines for the use and interpretation of assays for monitoring autophagy.自噬监测分析方法的使用和解读指南
Autophagy. 2012 Apr;8(4):445-544. doi: 10.4161/auto.19496.

正链 RNA 病毒如何从自噬体成熟中获益。

How positive-strand RNA viruses benefit from autophagosome maturation.

机构信息

Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.

出版信息

J Virol. 2013 Sep;87(18):9966-72. doi: 10.1128/JVI.00460-13. Epub 2013 Jun 12.

DOI:10.1128/JVI.00460-13
PMID:23760248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3754026/
Abstract

The autophagic degradation pathway is a powerful tool in the host cell arsenal against cytosolic pathogens. Contents trapped inside cytosolic vesicles, termed autophagosomes, are delivered to the lysosome for degradation. In spite of the degradative nature of the pathway, some pathogens are able to subvert autophagy for their benefit. In many cases, these pathogens have developed strategies to induce the autophagic signaling pathway while inhibiting the associated degradation activity. One surprising finding from recent literature is that some viruses do not impede degradation but instead promote the generation of degradative autolysosomes, which are the endpoint compartments of autophagy. Dengue virus, poliovirus, and hepatitis C virus, all positive-strand RNA viruses, utilize the maturation of autophagosomes into acidic and ultimately degradative compartments to promote their replication. While the benefits that each virus reaps from autophagosome maturation are unique, the parallels between the viruses indicate a complex relationship between cytosolic viruses and host cell degradation vesicles.

摘要

自噬降解途径是宿主细胞对抗细胞溶质病原体的有力工具。被捕获在细胞溶质小泡(称为自噬体)内的内容物被递送到溶酶体进行降解。尽管该途径具有降解性质,但一些病原体能够为了自身利益而颠覆自噬。在许多情况下,这些病原体已经开发出策略来诱导自噬信号通路,同时抑制相关的降解活性。最近文献中的一个令人惊讶的发现是,一些病毒不会阻碍降解,而是促进产生降解性自噬溶酶体,这是自噬的终点隔室。登革热病毒、脊髓灰质炎病毒和丙型肝炎病毒都是正链 RNA 病毒,它们利用自噬体成熟为酸性最终降解隔室来促进自身复制。虽然每种病毒从自噬体成熟中获得的益处是独特的,但病毒之间的相似之处表明细胞溶质病毒和宿主细胞降解小泡之间存在复杂的关系。