recent GWAS used the largest sample size to date (N = 13,851),[12] the vast majority of population controls are unlikely to have been exposed to HIV. Without exposure to the virus, such controls may be minimally informative for studying host genetics of HIV-1 acquisition, suggesting that even larger sample sizes will be required for sufficient statistical power. We assessed top GWAS signals and candidate genes reported in the prior GWAS,[6–12] but did not find any other evidence of replicable association between the previously implicated variants and HIV acquisition in the UHS cohort (P>0.05, see S2 Table). Prior suggestive findings may not be truly associated; we may remain underpowered to adequately test these associations; and/or the difference in types (sexual vs. drug injection) or degree of HIV exposure across studies may limit the field’s ability to replicate findings.
