GWAS | SNP (linked to IFNλ3) | Position in relation to IFNλ3, + (upstream), − (downstream) | Wild type/risk allele | Population studied (frequency risk allele) | OR of spontaneous clearance | OR of treatment outcome (95% CI) | Viral genotype |
Ge et al8 | rs12979860 | +3 kbp | C/T | European-American (30%) | NA | Europeans 7.3 (95% CI 5.10 to 10.4)* | 1 |
Hispanic (40%) | African-Americans 6.1 (95% CI 2.3 to 15.9) | ||||||
African-American (60%) | Hispanics 5.6 (95% CI 1.4 to 22.1) | ||||||
Tanaka et al11 | rs12980275 | +3 kbp | A/G | Japanese (15%) | NA | 18.7 (95% CI 6.7 to 51.9)† | 1 |
Tanaka et al11 | rs8099917 | −8 kbp | T/G | Japanese (12%) | NA | 36.5 (95% CI 11.6 to 114.6)† | 1 |
Rauch et al9 | rs8099917 | −8 kbp | T/G | Swiss (17%) | 2.31 (95% CI 1.74 to 3.06) | 5.19 (95% CI 2.90 to 9.30)‡ | 1, 2, 3, 4 |
Suppiah et al10 | rs8099917 | −8 kbp | T/G | European Australian (27%) | NA | 1.64 (95% CI 1.15 to 2.32)‡ | 1 |
↵* Homozygotes for the protective allele vs those with the risk allele (heterozygotes and homozygotes) in those who have achieved a sustained viral response (SVR).
↵† Null virological response vs SVR in those with the risk allele (heterozygotes and homozygotes). Null virological response defined as <2 log decline in hepatitis C virus RNA from pretreatment in the first 12 weeks of treatment and detectable viraemia 24 weeks after treatment.
↵‡ Non-SVR vs SVR in those with the risk allele (heterozygotes and homozygotes).
NA, not assessed.