Dual role of autophagy in HIV-1 replication and pathogenesis

被引:52
|
作者
Killian, M. Scott [1 ]
机构
[1] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA
来源
AIDS RESEARCH AND THERAPY | 2012年 / 9卷
基金
美国国家卫生研究院;
关键词
HIV; Autophagy; Innate immunity; T cells; Antiretroviral therapy; Pathogenesis; IMMUNODEFICIENCY-VIRUS TYPE-1; ENDOPLASMIC-RETICULUM STRESS; PLASMACYTOID DENDRITIC CELL; SINGLE-STRANDED RNA; MONITORING AUTOPHAGY; PROTEASE INHIBITOR; TRIGGERS AUTOPHAGY; IFN-GAMMA; CLASS-I; INFECTION;
D O I
10.1186/1742-6405-9-16
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
Autophagy, the major mechanism for degrading long-lived intracellular proteins and organelles, is essential for eukaryotic cell homeostasis. Autophagy also defends the cell against invasion by microorganisms and has important roles in innate and adaptive immunity. Increasingly evident is that HIV-1 replication is dependent on select components of autophagy. Fittingly, HIV-1 proteins are able to modulate autophagy to maximize virus production. At the same time, HIV-1 proteins appear to disrupt autophagy in uninfected cells, thereby contributing to CD4+ cell death and HIV-1 pathogenesis. These observations allow for new approaches for the treatment and possibly the prevention of HIV-1 infection. This review focuses on the relationship between autophagy and HIV-1 infection. Discussed is how autophagy plays dual roles in HIV-1 replication and HIV-1 disease progression.
引用
收藏
页数:13
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