Panel A shows a line graph of AAN IFN 2 positivity rates by age and sex in the interferon alpha treatment positive group. The x axis represents age in years, and the y axis represents positivity percentage. Panel B shows a similar line graph for the interferon alpha treatment negative group. Panel C depicts a line graph of AAN IFN 2 positivity rates by age and sex in healthy controls. Panel D shows a line graph of AAN IFN 2 positivity rates by duration of hepatitis C infection, with separate lines for the interferon alpha treatment positive and interferon alpha treatment negative groups. Panels E, F, G, and H are dot plots showing AAN IFN 2 positivity rates by response to interferon alpha treatment, single nucleotide polymorphism rs8099917 genotype in hepatitis C patients, single nucleotide polymorphism genotype in the interferon alpha treatment positive group, and single nucleotide polymorphism genotype in the interferon alpha treatment negative group, respectively. Each plot has the x axis representing different categories and the y axis representing positivity percentage. The graphs illustrate trends and differences in AAN IFN 2 positivity rates across various demographics and conditions.
AAN-I-IFN detection and clinical characteristics of the patients. (A) AAN-IFN-α2 (100 pg/ml) positivity rates, by age and sex, in the IFN-α treatment (+) group. In men, autoantibodies were detected in 1.7% of individuals aged under 49 years, 3.8% aged in their 50s, 5.0% aged in their 60s, 4.6% aged in their 70s, and 12.9% aged 80 years or older. In women, the corresponding rates were 1.6%, 2.2%, 3.6%, 3.5%, and 0.0%, respectively. (B) AAN-IFN-α2 (100 pg/ml) positivity rates, by age and sex, in the IFN-α treatment (−) group. In men, autoantibodies were detected in 1.8% of individuals under 49 years, 0.9% aged in their 50s, 0.5% aged in their 60s, 4.1% aged in their 70s, and 4.8% aged 80 years or older. In women, the corresponding rates were 1.0%, 0.0%, 0.0%, 1.6%, and 3.0%, respectively. (C) AAN-IFN-α2 (100 pg/ml) positivity rates, by age and sex, in the healthy controls. In men, autoantibodies were detected in 0.0% of individuals aged under 49 years, 2.1% aged in their 50s, 1.2% aged in their 60s, 0.6% aged in their 70s, and 2.4% aged 80 years or older. In women, the corresponding rates were 0.0%, 0.0%, 0.0%, 0.0%, and 2.5%, respectively. (D) AAN-IFN-α2 (100 pg/ml) positivity rates by duration of hepatitis C infection. In the IFN-α treatment (+) group, the rates were 7.1% (duration <1 year), 1.4% (1–5 years), 8.1% (6–10 years), 0.0% (11–15 years), 5.2% (16–20 years), and 5.3% (>21 years). In the IFN-α treatment (−) group, the rates were 0.0%, 3.2%, 0.0%, 0.9%, and 1.9%, respectively. (E) AAN-IFN-α2 positivity rates by response to IFN-α treatment in hepatitis C patients. The rates were 2.7% (21/771) in SVR, 7.1% (16/224) in non-SVR, and 4.8% in patients in whom treatment was discontinued. The positivity rate was significantly higher in the non-SVR group than in the SVR group (P = 0.0041). (F) AAN-IFN-α2 positivity rates by SNP (rs8099917) genotype in hepatitis C patients were 3.0% (51/1709) for TT, 2.5% (12/482) for TG, and 0% (0/29) for GG (P = 0.677). (G) AAN-IFN-α2 positivity rates, by SNP (rs8099917) genotype, in the IFN-α treatment (+) group were 4.2% for TT, 3.0% for TG, and 0% for GG (P = 0.759). (H) AAN-IFN-α2 positivity rates, by SNP (rs8099917) genotype, in the IFN-α treatment (−) group were 1.9% for TT, 2.0% for TG, and 0% for GG (P = 1.000).