Clinical utility of host genetic IL ‐28 B variants in hepatitis C virus genotype 1 A sian patients retreated with pegylated interferon plus ribavirin

Background and Aim Host interleukin‐28 B ( IL ‐28 B ) genetic variants determine a sustained virological response ( SVR ) in hepatitis C virus genotype 1 ( HCV ‐1) treatment‐naïve patients. Its impact on treatment‐experienced A sian patients with peginterferon/ribavirin in is to be elucidated. Methods IL ‐28 B rs8099917 genotype was determined in 70 HCV ‐1 treatment‐experienced patients retreated with 48‐week peginterferon/ribavirin. Results The SVR rate was 60.0% and was significantly higher in previous relapsers than in nonresponders (72.7% and 13.3%, P  < 0.001). Multivariate analysis revealed that the most important factor predictive of an SVR was previous relapse (Odds ratio [ OR ]/95% confidence interval [ CI ]: 14.76/2.72–80.06, P  = 0.002), followed by the carriage of rs8099917 TT genotype ( OR /95% C . I .: 7.67/1.27–46.49, P  = 0.03). Comparing to patients with TG / GG genotype, those with TT genotype had significantly higher rates of rapid virological response (29.3% vs 0%, P  = 0.03), end‐of‐treatment virological response (86.2% vs 50.0%, P  = 0.01), SVR (69.0% vs 16.7%, P  = 0.002), and lower relapse rate (22.0 % vs 66.7%, P  = 0.04). The SVR rate was similarly low between previous nonresponders with different rs8099917 genotypes (12.5% vs 14.3%, P  = 1). On the contrary, previous relapsers with rs8099917 TT genotype had a significantly higher SVR rate than those who carried rs8099917 TG / GG genotype (78.0 % vs 20.0%, P  = 0.02). Stepwise logistic regression analysis revealed that the only factor predictive of an SVR in previous relapsers was the carriage of rs809997 TT genotype ( OR /95% CI :18.50/1.82–188.39, P  = 0.014). Conclusions Host IL ‐28 B genetic variants played a role in A sian relapsers but not nonresponders retreated with peginterferon/ribavirin. Direct antiviral agents might be possibly avoidable in A sian relapsers with favorable IL ‐28 B genotype.