Coevolutionary dynamics between tribe Cercopithecini tetherins and their lentiviruses.
Junko S Takeuchi1, Fengrong Ren2, Rokusuke Yoshikawa1
1Laboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto 6068507, Japan.
Scientific Reports
|November 5, 2015
Summary
The study reveals that primate lentiviruses (PLVs) and their hosts, like Cercopithecini monkeys, engage in an evolutionary arms race. This co-evolutionary dynamic influences viral pathogenicity, impacting human immunodeficiency virus (HIV) evolution.
Area of Science:
- Virology
- Evolutionary Biology
- Immunology
Background:
- Human immunodeficiency virus (HIV), a primate lentivirus (PLV), causes AIDS in humans, but most PLVs are not pathogenic in monkeys.
- The co-evolutionary process between PLVs and their hosts is linked to viral pathogenicity, making virus-host co-evolution a key research area.
- Intrinsic antiviral proteins, such as tetherin, and viral antagonists are crucial in the interplay between viruses and their hosts.
Purpose of the Study:
- To investigate the co-evolutionary interplay between Cercopithecini tetherin and viral antagonists (Nef and Vpu) using an experimental-phylogenetic approach.
- To understand the evolutionary history and functional interactions shaping primate lentivirus pathogenicity.
Main Methods:
- Experimental-phylogenetic analysis of tribe Cercopithecini tetherin and viral antagonists.
- Reconstruction of ancestral sequences for tribe Cercopithecini tetherin.
- Functional assays to assess the antagonistic capabilities of Nef proteins against ancestral tetherin.
Main Results:
- Tribe Cercopithecini tetherins exhibit positive selection, potentially driven by ancient Nef-like factors.
- Ancestral sequences of Cercopithecini tetherin were reconstructed.
- All tested Nef proteins demonstrated the ability to antagonize ancestral Cercopithecini tetherin.
Conclusions:
- An evolutionary arms race exists between Cercopithecini monkeys and their associated PLVs.
- The interplay between tetherin and viral antagonists like Nef is a significant factor in shaping PLV pathogenicity and host adaptation.
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