Our review of the HCV-HLA literature identified only three studies of HLA alleles and HCV serostatus in high-risk populations16–18 and there were no consistent findings or strong associations. We therefore treated all of the analysis of HCV serostatus LY2157299 concentration and HLA alleles as exploratory, and all significant P-values were adjusted for multiple comparisons. Of the 64 HLA class I and II alleles with >5% prevalence in the 838 IDUs studied, B*5703 (P = 0.03), Cw*0304 (P = 0.04), and Cw*0701 (P = 0.01), were significantly associated with HCV infection (see Supporting Table 2), but these associations did not retain significance after adjustment for multiple comparisons

(P = 0.99, 1.0, and 0.64, respectively). There were no significant interactions by race/ethnicity or HIV serostatus/CD4+ T-cell count. We studied the relation of high-resolution HLA class I and II genotype with HCV viremia and with HCV serostatus in IDUs. Although there have been a number of prior studies of HLA alleles and HCV viremia, many of the findings to date have been conflicting. Part of this variability may relate to aspects of study design, including differences in sample size Palbociclib datasheet and whether an appropriate control group was used. Furthermore,

few studies examined HLA class I alleles, with only one having conducted high-resolution class I genotyping.12 There have also been very little data regarding HLA and the prevalence of HCV infection (i.e., seropositivity) in high-risk populations.16–18 To build on the existing data, therefore, we conducted high-resolution HLA class I and II genotyping in a large multiracial cohort of U.S. women with high prevalence of HCV and HIV Baricitinib infection. Several significant associations between HLA class I and II alleles and HCV viremia were observed. These included 6 of the 12 HLA alleles that we identified as having a high prior probability of association with HCV viremia based on a critical review of the literature. Because each of these associations represented discrete a priori hypotheses it is unlikely that they occurred by chance. Both B*5701 and B*5703, for example, were

significantly associated with an absence of HCV RNA. Two earlier studies of HLA class I had reported similar associations with the B*57 allele group; the first was conducted in a large multiracial, majority male population in the United States,12 whereas the second was conducted in a small, majority male population in West Africa.13 A third study conducted in Ireland also found an association between the B*57 allele group and HCV viremia, although the results did not attain statistical significance.14 In the current study the relation of the B*57 allele group with HCV viremia mainly reflected the combined effects of B*5701 and B*5703, but we caution that our dataset included too few women with other B*57 alleles (e.g., B*5702, B*5704) to study in detail.