Autophagy during viral infection - a double-edged sword

被引:593
|
作者
Choi, Younho [1 ]
Bowman, James W. [1 ]
Jung, Jae U. [1 ]
机构
[1] Univ Southern Calif, Keck Sch Med, Dept Mol Microbiol & Immunol, Zilkha Neurogenet Inst, Los Angeles, CA 90007 USA
基金
美国国家卫生研究院;
关键词
EPSTEIN-BARR-VIRUS; HERPES-SIMPLEX-VIRUS; REGULATES LIPID-METABOLISM; CLASS-I PATHWAY; DENGUE VIRUS; DENDRITIC CELLS; SELECTIVE AUTOPHAGY; CROSS-PRESENTATION; IMMUNE-RESPONSES; DNA SENSOR;
D O I
10.1038/s41579-018-0003-6
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Autophagy is a powerful tool that host cells use to defend against viral infection. Double-membrane vesicles, termed autophagosomes, deliver trapped viral cargo to the lysosome for degradation. Specifically, autophagy initiates an innate immune response by cooperating with pattern recognition receptor signalling to induce interferon production. It also selectively degrades immune components associated with viral particles. Following degradation, autophagy coordinates adaptive immunity by delivering virus-derived antigens for presentation to T lymphocytes. However, in an ongoing evolutionary arms race, viruses have acquired the potent ability to hijack and subvert autophagy for their benefit. In this Review, we focus on the key regulatory steps during viral infection in which autophagy is involved and discuss the specific molecular mechanisms that diverse viruses use to repurpose autophagy for their life cycle and pathogenesis.
引用
收藏
页码:340 / 353
页数:14
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