Table 1.
Comparison of IL28B genotype and outcome of HCV treatment with pegylated interferon-α and ribavirina
SNP Study | Overall SVRb(%) |
SVR in persons with indicated genotype (%) |
% of SVR explained by the favorable genotype | |
---|---|---|---|---|
Homozygous favorable allele | Heterozygous or homozygous unfavorable allele | |||
rs12979860 | ||||
Ge et al. (USA)c,d | 56 | 82 | 40 | 56 |
rs8099917 | ||||
Suppiah et al. (Australia)d | 46 | 56 | 36 | 63 |
Tanaka et al. (Japan)d,e | NA | NA | NA | NA |
Rauch et al. (Switzerland)d | 64 | 74 | 50 | 68 |
SVR rates for the indicated SNPs, selected as the most predictive polymorphisms in the respective studies, were calculated using published outcome data.10,12–14 As a clinical predictor, IL28B is similar to other determinants of HCV treatment outcome, such as race, HCV RNA level, and HCV genotype.
The proportion of persons with SVR included in the study.
While the full cohort included persons of European, African, and Hispanic descent, SVR rates are given here for Caucasians. For African Americans, the SVR rates were 53% and 18% in the protective and risk genotypes, respectively.
SVR rates are presented for HCV genotype 1 infections except for Rauch et al., which included persons infected with HCV genotypes 1/2/3/4.
Tanaka et al. was a case-control study, and therefore these percentages are not relevant.