Younger patients, male sex, baseline

HCV RNA levels <400,000 IU/mL, low pretreatment levels of AST, and RVR and EVR achievement were factors predictive of SVR in the univariate analysis (Table 2). According to the multivariate analysis, RVR achievement was the single predictor of SVR (Table 3), whereas neither rs8099917 nor rs10853728 offered significant predictive value for SVR in HCV-2 patients. The basic demographic, virological, and clinical features were similar between patients with the major find more homozygote (TT) or GT/GG genotypes of rs8099917, except that those with the TT genotype had significantly lower baseline levels of HCV RNA (5.32 ± 0.94 versus 5.59 ± 0.66 log IU/mL, P = 0.02; Table 4). Patients with the homozygous TT genotype had a significantly higher rate of RVR than

G allele carriers (GT/GG; 85.2% versus 72.0%, P = 0.017). The other treatment responses, including the rates of EVR (99.1% versus 98.0%, P = 0.48), EOTVR (97.2% versus 94.0%, P = 0.2), SVR (89.4% versus 86.0%, P = 0.47), and relapse (8.1% versus 8.5%, P = 0.78), were not different between patients with the TT or GT/GG genotypes. BAY 57-1293 concentration Between-groups analysis by stratification of RVR achievement demonstrated that the rates of EOTVR, relapse, and SVR were similar between patients with the TT or GT/GG genotypes of rs8099917, regardless of RVR achievement (Table 5). Further analysis by stepwise logistic regression revealed that factors associated with SVR in patients with RVR were HCV RNA levels < 400,000 IU/mL [odds ratio (OR) = 2.91, 95% confidence interval (CI) = 1.18-7.19, P = 0.02] and age (OR = 0.94, 95% CI = 0.90-0.99, P = 0.01), whereas the achievement of complete EVR was the sole factor predictive of SVR in non-RVR patients (OR = ∞, 95% CI = 0.00-∞, P < 0.0001). Apart from environmental and viral factors, genetic variations are probably involved in the efficacy of interferon-based therapies for next chronic hepatitis C.21 Interferon-λ induces

antiviral, antiproliferative, and immune responses.22 It has been mentioned in the context of HCV infection (i.e., suppression of its replication in vitro)23, 24 and has been applied in clinical HCV treatment.25 IL-28B, located on chromosome 19, encodes interferon-λ3 and has been reported to be involved in the suppression of HCV replication. The present study, to the best of our knowledge, presents the largest cohort for elucidating the influence of genetic polymorphisms near the IL-28B gene on the treatment of HCV-2 patients in a Chinese population residing in Taiwan. We have demonstrated that carriers with the TT genotype of rs8099917, located 8 kb upstream of IL-28B, are more likely to achieve RVR with HCV-2 infection.