期刊
IMMUNITY
卷 39, 期 6, 页码 1132-1142出版社
CELL PRESS
DOI: 10.1016/j.immuni.2013.11.002
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类别
资金
- Institut Curie
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- ATIP-Avenir program
- Agence Nationale de Recherche sur le SIDA (ANRS)
- Ville de Paris Emergence program
- European FP7 Marie Curie Actions [268311]
- European Research Council [309848]
- LABEX VRI
- LABEX DCBIOL
- European Research Council (ERC) [309848] Funding Source: European Research Council (ERC)
HIV-2 is less pathogenic for humans than HIV-1 and might provide partial cross-protection from HIV-1-induced pathology. Although both viruses replicate in the T cells of infected patients, only HIV-2 replicates efficiently in dendritic cells (DCs) and activates innate immune pathways. How HIV is sensed in DC is unknown. Capsid-mutated HIV-2 revealed that sensing by the host requires viral cDNA synthesis, but not nuclear entry or genome integration. The HIV-1 capsid prevented viral cDNA sensing up to integration, allowing the virus to escape innate recognition. In contrast, DCs sensed capsid-mutated HIV-1 and enhanced stimulation of T cells in the absence of productive infection. Finally, we found that DC sensing of HIV-1 and HIV-2 required the DNA sensor cGAS. Thus, the HIV capsid is a determinant of innate sensing of the viral cDNA by cGAS in dendritic cells. This pathway might potentially be harnessed to develop effective vaccines against HIV-1.
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