Nesis and liver-related morbidity and mortality if left untreated. Successful HCV treatment using antiviral therapy would prevent the consequences of HCV infection.[2,3] Recently, the introduction of direct antiviral agents (DAA) has greatly improved the sustained virological response (SVR) rate in patients with HCV genotype 1 (HCV-1) infection.[4] On the other hand,pegylated interferon (peginterferon)/ribavirin, which is the standard-of-care for HCV-2 patients, has provided satisfactory results with an SVR rate of 80?3 .[5?] As a consequence, only a minority of HCV-2 patients fail antiviral therapy and are prone to be neglected because of the excellent treatment efficacy toward HCV-2 infection. It is noteworthy that these patients are still at high risk for liver disease progression and hepatocarcinogenesis.[2,3,8] Therefore, the issue of retreatment of HCV-2 patients who have failed previous treatments is important. However, it hasHCV-2 Retreatmentrarely been addressed, which may reflect the limited number of patients in this specific scenario. Recent studies have provided solid evidence that host interleukin 28B (IL-28B) genetic polymorphisms are associated with treatment efficacy in HCV-1 patients treated with peginterferon/ ribavirin.[9?1] However, the application of DAAs seems to attenuate the role of host IL-28B genetic variants in HCV-1 infection.[12] On the other hand, results regarding the role of IL28B in HCV-2 patients seem contradictory. Furthermore, the impact on viral kinetics was also inconsistent across studies. [13?15] A recent meta-analysis showed that favorable IL-28B polymorphisms were associated with a higher sustained virological response rate (SVR), but the effect was too limited to justify a clinical treatment decision.[16] It is noteworthy that the impact of host Il-28B genetic variants on HCV-2 treatment experienced patients with has never been explored. The current study aimed to elucidate the efficacy of HCV-2 patients retreated with 24-week peginterferon/ribavirin combination therapy. We also assessed the potential impact of host IL-28B genetic variants on a wellcharacterized Asian patient cohort.was defined as seronegativity of HCV RNA throughout 24 weeks of the post-treatment follow-up period.IL-28B genotyping and statistical analysesRs8099917 was selected as the candidate single-nucleotide polymorphism 25331948 (SNP) in the current study. Genetic testing of IL28B rs8099917 was determined using methods that have been previously described.[10,13] The frequency was SPDB site compared between groups using the x2 test and a Yates correction or a Fisher exact test. Group means and standard deviations were compared using an analysis of variance test and the Student’s t test or the Mann-Whitney U test. Serum HCV RNA levels were expressed after logarithmic transformation of the original values. The aspartate aminotransferase (AST)-to-platelet ratio index (APRI) was calculated using the following equation: (AST level/ upper limit of normal range)/platelet counts (109/L)6100. The APRI was used to reflect the severity of liver fibrosis.[18] The frequency of the rare INCB039110 site allele (G) of the rs8099917 genotype was too low; thus, the rare homozygote (GG) and heterozygote (GT) genotypes were combined together when analyzing the SNP. To assess the relative contribution of the predictors of a RVR, a multivariable model was applied with 26001275 age, sex, body weight, baseline HCV RNA levels, APRI, previous treatment regimen (optimal or suboptimal), previo.Nesis and liver-related morbidity and mortality if left untreated. Successful HCV treatment using antiviral therapy would prevent the consequences of HCV infection.[2,3] Recently, the introduction of direct antiviral agents (DAA) has greatly improved the sustained virological response (SVR) rate in patients with HCV genotype 1 (HCV-1) infection.[4] On the other hand,pegylated interferon (peginterferon)/ribavirin, which is the standard-of-care for HCV-2 patients, has provided satisfactory results with an SVR rate of 80?3 .[5?] As a consequence, only a minority of HCV-2 patients fail antiviral therapy and are prone to be neglected because of the excellent treatment efficacy toward HCV-2 infection. It is noteworthy that these patients are still at high risk for liver disease progression and hepatocarcinogenesis.[2,3,8] Therefore, the issue of retreatment of HCV-2 patients who have failed previous treatments is important. However, it hasHCV-2 Retreatmentrarely been addressed, which may reflect the limited number of patients in this specific scenario. Recent studies have provided solid evidence that host interleukin 28B (IL-28B) genetic polymorphisms are associated with treatment efficacy in HCV-1 patients treated with peginterferon/ ribavirin.[9?1] However, the application of DAAs seems to attenuate the role of host IL-28B genetic variants in HCV-1 infection.[12] On the other hand, results regarding the role of IL28B in HCV-2 patients seem contradictory. Furthermore, the impact on viral kinetics was also inconsistent across studies. [13?15] A recent meta-analysis showed that favorable IL-28B polymorphisms were associated with a higher sustained virological response rate (SVR), but the effect was too limited to justify a clinical treatment decision.[16] It is noteworthy that the impact of host Il-28B genetic variants on HCV-2 treatment experienced patients with has never been explored. The current study aimed to elucidate the efficacy of HCV-2 patients retreated with 24-week peginterferon/ribavirin combination therapy. We also assessed the potential impact of host IL-28B genetic variants on a wellcharacterized Asian patient cohort.was defined as seronegativity of HCV RNA throughout 24 weeks of the post-treatment follow-up period.IL-28B genotyping and statistical analysesRs8099917 was selected as the candidate single-nucleotide polymorphism 25331948 (SNP) in the current study. Genetic testing of IL28B rs8099917 was determined using methods that have been previously described.[10,13] The frequency was compared between groups using the x2 test and a Yates correction or a Fisher exact test. Group means and standard deviations were compared using an analysis of variance test and the Student’s t test or the Mann-Whitney U test. Serum HCV RNA levels were expressed after logarithmic transformation of the original values. The aspartate aminotransferase (AST)-to-platelet ratio index (APRI) was calculated using the following equation: (AST level/ upper limit of normal range)/platelet counts (109/L)6100. The APRI was used to reflect the severity of liver fibrosis.[18] The frequency of the rare allele (G) of the rs8099917 genotype was too low; thus, the rare homozygote (GG) and heterozygote (GT) genotypes were combined together when analyzing the SNP. To assess the relative contribution of the predictors of a RVR, a multivariable model was applied with 26001275 age, sex, body weight, baseline HCV RNA levels, APRI, previous treatment regimen (optimal or suboptimal), previo.

Nesis and liver-related morbidity and mortality if left untreated. Successful HCV

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