Psoriasis patients are enriched for genetic variants that protect against HIV-1 disease.

We found that the association of rs67384697 with psoriasis was largely driven by HLA-C*06:02 , since conditioning on HLA-C*06:02 resulted in only a marginally significant p-value for rs67384697 (p = 0.044, OR = 1.12).

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We were intrigued by the observation that several of the most highly significant SNPs from psoriasis GWAS were identical to the top SNPs from GWAS of HIV-1 virologic control, a clinical phenotype whereby certain HIV-1 infected individuals, termed “HIV-1 controllers,” are able to maintain low levels of plasma HIV-1 RNA in the absence of antiretroviral therapy and who generally do not develop clinical symptoms [12] .

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