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By inoculating macaques with cocktails of multiple SHIV variants, we selected SHIVs that can replicate and cause AIDS-like disease in immunologically intact rhesus macaques without requiring animal-to-animal passage.
For pharmacogenomic variants, we selected rs4149056 and rs11045819 in the SLCO1B1 gene and rs2108622 in the CYP4F2 gene.
To assess within population group LD structure and the distributions of haplotypes harboring known disease variants, we selected published obesity and pharmacogenomic variants that were genotyped in our Biobank sample of African Americans, European Americans and Hispanic Americans.
Among those with alternative splice variants, we selected the longest variant for further analysis.
For genes containing multiple LoF variants, we selected the most upstream LoF variant for this analysis.
From the DIAGRAM consortium meta-analysis of common variants we selected for replication all common SNPs with a p < 0.05.
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For each RRA variant we selected a 100 bp region surrounding the locus and we calculated GC content and mappability.
To search for a functional variant, we selected 61 tag-SNPs in and around the ELP3 gene for fine-mapping studies in the study populations (Supplementary Material, Table S4).
Instead of focusing exclusively on the two previously associated variants [14], we selected tagging SNPs (tSNPs) to efficiently study common TLR1 gene variation in order to test whether additional gene variants associated with the expression of the clinical phenotype.
Secondly, for each type of disease variants, we randomly selected 1000 equal size control groups which share the same allele frequency distribution of disease variants.
To investigate how well each of the algorithms captures such variants, we randomly selected 600 SNPs that were monomorphic in one algorithm but had a minor allele frequency between 4×10−4 and 0.01 in at least another two.
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