Abstract
Human immunodeficiency virus, a primate lentivirus (PLV), causes AIDS in humans, whereas most PLVs are less or not pathogenic in monkeys. These notions suggest that the co-evolutionary process of PLVs and their hosts associates with viral pathogenicity, and therefore, that elucidating the history of virus-host co-evolution is one of the most intriguing topics in the field of virology. To address this, recent studies have focused on the interplay between intrinsic anti-viral proteins, such as tetherin, and viral antagonists. Through an experimental-phylogenetic approach, here we investigate the co-evolutionary interplay between tribe Cercopithecini tetherin and viral antagonists, Nef and Vpu. We reveal that tribe Cercopithecini tetherins are positively selected, possibly triggered by ancient Nef-like factor(s). We reconstruct the ancestral sequence of tribe Cercopithecini tetherin and demonstrate that all Nef proteins are capable of antagonizing ancestral Cercopithecini tetherin. Further, we consider the significance of evolutionary arms race between tribe Cercopithecini and their PLVs.
Highlights
Human immunodeficiency virus, a primate lentivirus (PLV), causes AIDS in humans, whereas most primate lentiviruses (PLVs) are less or not pathogenic in monkeys
We constructed the ancestral sequence of tribe Cercopithecini tetherin and demonstrated that the ancestral Cercopithecini tetherin has a robust ability to inhibit viral release
Since a previous paper has shown that the “artificial” tetherin, which artificially forms the same topology to tetherin, sufficiently confers anti-viral activity[36], it might not be so surprising that the ancestral Cercopithecini tetherin estimated in this study exhibited anti-viral ability
Summary
A primate lentivirus (PLV), causes AIDS in humans, whereas most PLVs are less or not pathogenic in monkeys. To elucidate the co-evolutionary relationship between SIVs and their hosts, recent investigations have experimentally addressed the evolutionary conflict between viral and host proteins[8,9,10] that stems from the “Red Queen hypothesis”[11] or “evolutionary arms race” concept Such an approach can be the way to explain the co-evolutionary history of SIVs and their host species. Vif, a common protein encoded by all PLVs, has a robust ability to counteract a cellular anti-PLV restriction factor, apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G12 Another anti-PLV restriction factor, SAM domain and HD domain 1 (SAMHD1), can be antagonized by the viral accessory proteins, Vpr or Vpx[13,14]. Anti-SAMHD1 ability has been transferred from an old gene (vpr) to a new gene (vpx) during the co-evolution of SIVs and their hosts
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