Adapting the Stress Response: Viral Subversion of the mTOR Signaling Pathway

被引:94
作者
Le Sage, Valerie [1 ]
Cinti, Alessandro [1 ,2 ]
Amorim, Raquel [1 ,2 ]
Mouland, Andrew J. [1 ,2 ]
机构
[1] Jewish Gen Hosp, Lady Davis Inst, HIV RNA Trafficking Lab 1, Montreal, PQ H3T 1E2, Canada
[2] McGill Univ, Dept Med, Montreal, PQ H3A 0G4, Canada
来源
VIRUSES-BASEL | 2016年 / 8卷 / 06期
基金
加拿大健康研究院;
关键词
PI3K; Akt; mTOR; virus; 4EBP1; autophagy; HEPATITIS-C VIRUS; INFLUENZA-A VIRUS; HUMAN CYTOMEGALOVIRUS-INFECTION; MIDDLE T-ANTIGEN; PHOSPHATIDYLINOSITOL 3-KINASE ACTIVATION; ENDOPLASMIC-RETICULUM STRESS; MESSENGER-RNA TRANSLATION; PROTEIN-COUPLED RECEPTOR; HUMAN EPITHELIAL-CELLS; AKT/PROTEIN KINASE-B;
D O I
10.3390/v8060152
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The mammalian target of rapamycin (mTOR) is a central regulator of gene expression, translation and various metabolic processes. Multiple extracellular (growth factors) and intracellular (energy status) molecular signals as well as a variety of stressors are integrated into the mTOR pathway. Viral infection is a significant stress that can activate, reduce or even suppress the mTOR signaling pathway. Consequently, viruses have evolved a plethora of different mechanisms to attack and co-opt the mTOR pathway in order to make the host cell a hospitable environment for replication. A more comprehensive knowledge of different viral interactions may provide fruitful targets for new antiviral drugs.
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页数:19
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