Molecular characterization of Mexican HIV-1 Vif sequences
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The viral infectivity factor (Vif) is an HIV accessory protein that counteracts host antiviral proteins of the APOBEC3 family. Accumulating evidence highlights the pivotal role that accessory HIV proteins have on disease pathogenesis, a fact that has made them targets of interest for novel therapeutic and preventive strategies. Little is known about Vif sequence diversity outside of African or white populations. Mexico is home to Americas%27 third largest HIV-affected population and Mexican Hispanics represent an ever-increasing U.S. minority. This study provides a detailed analysis of the diversity seen in 77 Mexican Vif protein sequences. Phylogenetic analysis shows that most sequences cluster with HIV-1 subtype B, while less than 10%25 exhibit greater similarity to subtype D and A subtypes. Although most functional motifs are conserved among the Mexican sequences, substantial diversity was seen in some APOBEC binding sites, the nuclear localization inhibitory signal, and the CBFβ interaction sites. © Mary Ann Liebert, Inc. 2016.
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The viral infectivity factor (Vif) is an HIV accessory protein that counteracts host antiviral proteins of the APOBEC3 family. Accumulating evidence highlights the pivotal role that accessory HIV proteins have on disease pathogenesis, a fact that has made them targets of interest for novel therapeutic and preventive strategies. Little is known about Vif sequence diversity outside of African or white populations. Mexico is home to Americas' third largest HIV-affected population and Mexican Hispanics represent an ever-increasing U.S. minority. This study provides a detailed analysis of the diversity seen in 77 Mexican Vif protein sequences. Phylogenetic analysis shows that most sequences cluster with HIV-1 subtype B, while less than 10%25 exhibit greater similarity to subtype D and A subtypes. Although most functional motifs are conserved among the Mexican sequences, substantial diversity was seen in some APOBEC binding sites, the nuclear localization inhibitory signal, and the CBFβ interaction sites. © Mary Ann Liebert, Inc. 2016.
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apolipoprotein B messenger RNA editing enzyme catalytic polypeptide 3C; core binding factor beta; hydrolase; unclassified drug; viral infectivity factor; virus protein; Vif protein; vif protein, Human immunodeficiency virus 1; amino acid sequence; amino acid substitution; amino terminal sequence; Article; binding site; carboxy terminal sequence; human; Human immunodeficiency virus 1 infection; Human immunodeficiency virus type 1 subtype A; Human immunodeficiency virus type 1 subtype B; Human immunodeficiency virus type 1 subtype D; major clinical study; Mexican; nuclear localization signal; nucleotide sequence; phylogeny; priority journal; protein analysis; protein degradation; protein expression; protein function; protein interaction; protein motif; sequence analysis; virus characterization; virus isolation; classification; cluster analysis; genetic variation; genetics; genotype; HIV Infections; Human immunodeficiency virus 1; isolation and purification; Mexico; virology; Cluster Analysis; Genetic Variation; Genotype; HIV Infections; HIV-1; Humans; Mexico; Phylogeny; vif Gene Products, Human Immunodeficiency Virus
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