DNA was extracted from 200 μl of packed blood pellets from HIV+ patients and whole-blood samples from HIV− donors using the QIAamp 96 spin blood kit (QIAGEN, Valencia, CA). DNA concentrations were measured using Qubit® Fluorometer (Invitrogen, Carlsbad, CA). SNPs were genotyped using Illumina’s GoldenGate® genotyping assay system combined with VeraCode® Technology (Illumina Inc., San Diego, CA). Allelic discrimination was performed using a BeadXpress® Reader (Illumina) according to the manufacturer’s instructions.
The genotype data were uploaded and filtered using the GenomeStudio data analysis software v2011.1 (Illumina Inc., San Diego, CA). SNPs were filtered by genotype call frequency (<0.9, n = 1) and replicate errors (n = 2). Samples with genotype call frequency <0.9 were excluded (n = 4). Subsequently, SNPs were excluded from analysis if genotypic distribution among HIV− donors, stratified by race, deviated from the Hardy-Weinberg equilibrium (HWE) with a significant cutoff value of P ≤ 0.001 (n = 1). Thus, in the final analysis, 41 SNPs, as listed inSupplementary Table A , were examined in a total of 276 subjects (HIV+, n = 180; HIV−, n = 96).
The genotype data were uploaded and filtered using the GenomeStudio data analysis software v2011.1 (Illumina Inc., San Diego, CA). SNPs were filtered by genotype call frequency (<0.9, n = 1) and replicate errors (n = 2). Samples with genotype call frequency <0.9 were excluded (n = 4). Subsequently, SNPs were excluded from analysis if genotypic distribution among HIV− donors, stratified by race, deviated from the Hardy-Weinberg equilibrium (HWE) with a significant cutoff value of P ≤ 0.001 (n = 1). Thus, in the final analysis, 41 SNPs, as listed in