A genetic polymorphism near

the IL28B gene, which encodes for INFλ3, has been closely linked to the response to IFN in individuals infected with the HCV genotype 1 [12-16]. Patients with a CC allele in rs12979860 have a mTOR inhibitor much higher SVR than those who have a T allele. IL28B polymorphism has also been shown to strongly influence the rate of spontaneous clearance of the virus after acute HCV infection [14, 17-20]. Several SNPs (rs8105790, rs12979860, rs11881222, rs8103142, rs28416813, rs4803219, rs8099917 and rs7248668) of IL28B have been studied [17-19]. These SNP-based studies found rs12979860 and rs8099917 to be the most important determinants of treatment response. Allele frequencies differ between populations [12, 13]. Thomas et al. [12] measured C-allele frequencies in many ethnic selleck screening library groups from all continents and found frequencies as low as 25–30% in Africa, and as high as 90–100% in East Asia. This variability may explain the differences observed previously in treatment response discrepancy between caucasians, African–Americans and Eastern Asians [20, 21]. The Israeli population has been greatly affected by mass immigration, with immigrants coming from all over the globe. It is thus ethnically heterogeneous, and hence genetic variability is anticipated. The allelic distribution

of IL28B in non-haemophilic Israeli population Adenosine triphosphate of diverse

ethnical origin has not yet been reported. Furthermore, to our knowledge, HCV-infected haemophiliacs have not been systematically evaluated for the genetic polymorphism of IL28B and its impact on the outcomes of HCV infection. Our aim was to determine the frequency of different alleles at rs12979860 and rs8099917 in haemophiliacs from diverse ethnic backgrounds and to evaluate the association of these genotypes with treatment-induced or spontaneous clearance of HCV infection. About 239 patients with haemophilia and other disorders of coagulation were born before 1986, therefore potentially exposed to non-virucidally treated concentrated clotting factors. All these patients were managed in one centre – the Israeli National Hemophilia Center (INHC). Of these patients, 179 (75%) tested positive for anti-HCV antibodies. The study population consisted of a cohort of 130 patients who were positive for HCV-antibodies and consented to IL28B genotyping. Fifty-one patients (11 HIV co-infected) with genotype 1 (and all genotypes in HCV/HIV co-infected group) were treated with PEG–IFN/RBV for 48 weeks. Genotypes 2 and 3 were treated in the same way, but for 24 weeks. Only patients who received at least 80% of the recommended PEG–IFN/RBV dose were considered assessable for their response to treatment.