期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-03762-3
关键词
-
资金
- NIH [R37 AI50529, R01 AI 120810, R01 AI 114266, R37 AI66998, R01 AI 120860]
- BEAT-HIV Delaney Consortium [UM1 AI 126620]
- DFG [CRC 1279, SPP 1923]
- Advanced ERC investigator grant
- Sidaction
- VRI (Creteil, France)
- Pasteur-Paris University PhD program
- French ANR [10-INSB-04-01]
- DFG RTG CEMMA
HIV-1 causes chronic inflammation and AIDS in humans, whereas related simian immunodeficiency viruses (SIVs) replicate efficiently in their natural hosts without causing disease. It is currently unknown to what extent virus-specific properties are responsible for these different clinical outcomes. Here, we incorporate two putative HIV-1 virulence determinants, i.e., a Vpu protein that antagonizes tetherin and blocks NF-kappa B activation and a Nef protein that fails to suppress T cell activation via downmodulation of CD3, into a non-pathogenic SIVagm strain and test their impact on viral replication and pathogenicity in African green monkeys. Despite sustained high-level viremia over more than 4 years, moderately increased immune activation and transcriptional signatures of inflammation, the HIV-1-like SIVagm does not cause immunodeficiency or any other disease. These data indicate that species-specific host factors rather than intrinsic viral virulence factors determine the pathogenicity of primate lentiviruses.
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