Similarly, GWAS of genetic resistance to HIV-1 infection [15] could not find any common variants (with the exception of CCR5-delta 32) which were protective, while GWAS of host control of HIV-1 viral load found a number of genome-wide significant loci associated with lower HIV-1 viral load set points and slower progression to AIDS [12], [39]. This evidence concerns the gene CCR5 and HIV-1 infection.