Schematic summary of our methodology.

<p>The data from three databases are integrated to provide us with functional SNPs likely to be associated with changes in gene transcription in the tissue of interest. Using the SNAP Pairwise LD server, we only kept independent SNPs by removing superfluous SNPs that were in linkage disequilibrium (<i>r</i>² ≥ 0.2). Among those SNPs, associations with slow and non-progression towards AIDS are sought and replicated. Randomisations are carried out in order to evaluate the statistical robustness of our results. Finally, the genetic associations are used to link progression to AIDS and gene expression in candidate genes.</p

Statistical significance of our associations.

<p>Histogram of the number of SNPs that pass the significance criterion for this study using phenotype and SNP randomisations. These results provide us with a way to estimate the sensitivity of our study (diamond): it would be extremely unlikely for our eight independent findings to arise by chance alone (<i>p</i> = 0.001).</p

List of the significant associations (<i>p</i> ≤ 0.05) with slow and non-progression.

<p>(*) Note that rs3749971 is in linkage disequilibrium with rs3130350 and is therefore not considered an independent finding in our statistics (see text).</p><p>Alleles, allele frequencies (AF), positional data and genetic modes are provided with the results of the statistical inferences. Opposite signs for the β coefficients are required for an association to be replicated in the GRIV (non-progression) and ACS cohorts (time to AIDS93).</p

List of SNP/gene pairs associated with AIDS progression.

<p>(*) Note that rs3749971 is in linkage disequilibrium with rs3130350 and is therefore not considered an independent finding (see text).</p><p>The genetic association is linked back to its association with gene expression levels to provide an association between transcription levels (we use the word ‘regulation’ for convenience’s sake) and AIDS progression.</p