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Virology. 2014 Apr;454-455:291-8. doi: 10.1016/j.virol.2014.02.029. Epub 2014 Mar 21.

Positive selection of primate genes that promote HIV-1 replication.

Author information

1
Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, 2500 Speedway, Austin, TX 78712-1191, USA.
2
Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, 2500 Speedway, Austin, TX 78712-1191, USA; Regents School of Austin, 3230 Travis Country Circle, Austin, TX, USA.
3
Department of Veterinary Sciences, Michale E Keeling Center for Comparative Medicine and Research, University of Texas, MD Anderson Cancer Center, Bastrop, TX, USA.
4
Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, 2500 Speedway, Austin, TX 78712-1191, USA. Electronic address: saras@austin.utexas.edu.

Abstract

Evolutionary analyses have revealed that most host-encoded restriction factors against HIV have experienced virus-driven selection during primate evolution. However, HIV also depends on the function of many human proteins, called host factors, for its replication. It is not clear whether virus-driven selection shapes the evolution of host factor genes to the extent that it is known to shape restriction factor genes. We show that five out of 40 HIV host factor genes (13%) analyzed do bear strong signatures of positive selection. Some of these genes (CD4, NUP153, RANBP2/NUP358) have been characterized with respect to the HIV lifecycle, while others (ANKRD30A/NY-BR-1 and MAP4) remain relatively uncharacterized. One of these, ANKRD30A, shows the most rapid evolution within this set of genes and is induced by interferon stimulation. We discuss how evolutionary analysis can aid the study of host factors for viral replication, just as it has the study of host immunity systems.

KEYWORDS:

Arms race; Co-factors; Genetic conflict; Host factors; Paleovirology

PMID:
24725956
PMCID:
PMC4028154
DOI:
10.1016/j.virol.2014.02.029
[Indexed for MEDLINE]
Free PMC Article
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