Journal
CELL HOST & MICROBE
Volume 16, Issue 5, Pages 639-650Publisher
CELL PRESS
DOI: 10.1016/j.chom.2014.10.002
Keywords
-
Categories
Funding
- NIH [R01 AI058715, R37 AI050529, R01 AI 111789]
- Deutsche Forschungsgemeinschaft [FA 378/11-1, US116/1-1]
- European FP7 HIT HIDDEN HIV [305762]
- Advanced ERC investigator grant
- DFG Excellence Cluster ImmunoSensation
Ask authors/readers for more resources
Most simian immunodeficiency viruses use their Nef protein to antagonize the host restriction factor tetherin. A deletion in human tetherin confers Nef resistance, representing a hurdle to successful zoonotic transmission. HIV-1 group M evolved to utilize the viral protein U (Vpu) to counteract tetherin. Although HIV-1 group O has spread epidemically in humans, it has not evolved a Vpu-based tetherin antagonism. Here we show that HIV-1 group O Nef targets a region adjacent to this deletion to inhibit transport of human tetherin to the cell surface, enhances virion release, and increases viral resistance to inhibition by interferon-alpha. The Nef protein of the inferred common ancestor of group O viruses is also active against human tetherin. Thus, Nef-mediated antagonism of human tetherin evolved prior to the spread of HIV-1 group O and likely facilitated secondary virus transmission. Our results may explain the epidemic spread of HIV-1 group O.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available