Influence of Human Leukocyte Antigen–B22 Alleles

has been associated with rapidly progressive disease in white patients with human immunodeficiency virus (HIV) infection. Subjects from 3 cohorts of men who have sex with men (), all of whom experiencedNp 671 HIV-1 seroconversion at roughly the same time, were molecularly typed at HLA-A,-B, and-C loci. Mean HIV RNA loads during early HIV infection were higher in B22-positive men than in B22-negative men (difference, 0.481 log10 HIV RNA copies/mL; 95 % confidence interval [CI], 0.156–0.806 log10 HIV RNA copies/mL; Pp). Independent of accepted markers of progression, time-to-AIDS was shorter in B22-positive seroconverters.004 (adjusted hazard ratio, 1.98; 95 % CI, 1.27–3.10;). White B22 serogroup alleles (B*55 and *56) appearPp.003 to predispose to unfavorable outcome of HIV infection as strongly as some or all B*35 and B*53 alleles. This finding may have greater implications for Asians, because the marker frequency for B22 is higher among Asians than among whites (∼10 % vs. ∼4%). Host genetic variation influences the outcome of hu-man immunodeficiency virus (HIV) type 1 infection [1–3]. The effect of HLA class I loci appears to be stronger than those of other known genetic influences on the disease process at the population level [4–7]. Homozygosity at HLA class I loci increases the likeli