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Gene Loss and Adaptation to Hominids Underlie the Ancient Origin of HIV-1
HIV-1 resulted from cross-species transmission of SIVcpz, a simian immunodeficiency virus that naturally infects chimpanzees. SIVcpz, in turn, is a recombinant between two SIV lineages from Old World monkeys. Lentiviral interspecies transmissions are partly driven by the evolution and capacity of vi...
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Published in: | Cell host & microbe 2013-07, Vol.14 (1), p.85-92 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | HIV-1 resulted from cross-species transmission of SIVcpz, a simian immunodeficiency virus that naturally infects chimpanzees. SIVcpz, in turn, is a recombinant between two SIV lineages from Old World monkeys. Lentiviral interspecies transmissions are partly driven by the evolution and capacity of viral accessory genes, such as vpx, vpr, and vif, to antagonize host antiviral factors, such as SAMHD1 and the APOBEC3 proteins. We show that vpx, which in other lentiviruses antagonizes SAMHD1, was deleted during the creation of SIVcpz. This genomic deletion resulted in the reconstruction of the overlapping vif gene by “overprinting,” creating a unique vif that overlaps in its 3′ end with the vpr gene and can antagonize hominid APOBEC3s. Moreover, passage of SIVs through chimpanzees facilitated the subsequent adaptation of HIV-1 to humans. Thus, HIV-1 originated through a series of gene loss and adaptation events that generated its chimpanzee precursor and lowered the species barrier to human infection.
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•The entire SIVrcm vpx gene was lost upon the adaptation of SIV to chimpanzee•The loss of vpx led to the creation of a unique vif region/gene by overprinting•SIVcpz Vif adapted to counteract hominid APOBEC3 proteins•Adaptation of SIV to chimpanzees facilitated virus adaptation to human APOBEC3G |
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ISSN: | 1931-3128 1934-6069 |
DOI: | 10.1016/j.chom.2013.06.002 |