期刊
CELL REPORTS
卷 17, 期 2, 页码 413-424出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.09.023
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资金
- SBO CellCoVir grant from the agency for Innovation by Science and Technology (IWT) (Flanders, Belgium)
- HIV-STOP Interuniversity Attraction Poles program of Belgian Science Policy
- European Union [FP7 Health-2007-2.3.2-1]
- Ghent University [BOF11/GOA/013]
- HIVERA IRIFCURE
- Research Foundation Flanders (FWO)
- BOF program Ghent University
- ANRS
- SIDACTION
- AREVA Foundation
- FP7 program HIT HIDDEN HIV [Health-F3-2012-305762]
- Vaccine Research Institute [ANR-10-LABX-77]
- Institut Pasteur
- International Graduate School in Molecular Medicine, Ulm
- Deutsche Forschungsgemeinschaft
- FP7 HIT HIDDEN HIV
- ERC
Several pattern-recognition receptors sense HIV-1 replication products and induce type I interferon (IFN-I) production under specific experimental conditions. However, it is thought that viral sensing and IFN induction are virtually absent in the main target cells of HIV-1 in vivo. Here, we show that activated CD4(+) T cells sense HIV-1 infection through the cytosolic DNA sensor cGAS and mount a bioactive IFN-I response. Efficient induction of IFN-I by HIV-1 infection requires proviral integration and is regulated by newly expressed viral accessory proteins: Vpr potentiates, while Vpu suppresses cGAS-dependent IFN-I induction. Furthermore, Vpr also amplifies innate sensing of HIV-1 infection in Vpx-treated dendritic cells. Our results identify cGAS as mediator of an IFN-I response to HIV-1 infection in CD4(+) T cells and demonstrate that this response is modulated by the viral accessory proteins Vpr and Vpu. Thus, viral innate immune evasion is incomplete in the main target cells of HIV-1.
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