Table 1

Comparison of genome-wide association studies (GWAS) identifying single nucleotide polymorphisms (SNPs) linked to interferon λ3 (IFNλ3) associated with treatment response or spontaneous clearance

GWASSNP (linked to IFNλ3)Position in relation to IFNλ3, + (upstream), − (downstream)Wild type/risk allelePopulation studied (frequency risk allele)OR of spontaneous clearanceOR of treatment outcome (95% CI)Viral genotype
Ge et al8rs12979860+3 kbpC/TEuropean-American (30%)NAEuropeans 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 al11rs12980275+3 kbpA/GJapanese (15%)NA18.7 (95% CI 6.7 to 51.9)1
Tanaka et al11rs8099917−8 kbpT/GJapanese (12%)NA36.5 (95% CI 11.6 to 114.6)1
Rauch et al9rs8099917−8 kbpT/GSwiss (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 al10rs8099917−8 kbpT/GEuropean Australian (27%)NA1.64 (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.