BACKGROUND/AIMS: Hepatitis C virus (HCV) RNA is detectable in a proportion of patients with autoimmune hepatitis type 2, which is characterized by liver-kidney microsomal antibodies (LKM). Therefore, the genotype and sequence of HCV were studied in these patients. METHODS: Sera from 43 LKM-positive and anti-HCV-positive patients (15 from Germany and 28 from Italy) and 82 LKM-negative and anti-HCV-positive patients (57 from Germany and 25 from Italy) were examined. RESULTS: Genotyping revealed that the rate of genotype III HCV according to Okamoto's classification in patients with LKM antibody-positive autoimmune hepatitis type 2 was higher than in LKM-negative patients (22.0% vs. 2.4%; P < 0.05). This was because of an increase of genotype III in our patients from Italy. No HCV mutations were found that show a closer sequence homology to cytochrome P450IID6, the major LKM-1 antigen. Deletions in the envelope and nonstructural region 5 were found. CONCLUSIONS: Because a specific HCV sequence is not associated with the induction of LKM-1 autoantibodies, future research must focus on host factors and possibly additional environmental factors.
Analysis of hepatitis C virus genome in patients with autoimmune hepatitis type 2.
DURAZZO, Marilena;
1994-01-01
Abstract
BACKGROUND/AIMS: Hepatitis C virus (HCV) RNA is detectable in a proportion of patients with autoimmune hepatitis type 2, which is characterized by liver-kidney microsomal antibodies (LKM). Therefore, the genotype and sequence of HCV were studied in these patients. METHODS: Sera from 43 LKM-positive and anti-HCV-positive patients (15 from Germany and 28 from Italy) and 82 LKM-negative and anti-HCV-positive patients (57 from Germany and 25 from Italy) were examined. RESULTS: Genotyping revealed that the rate of genotype III HCV according to Okamoto's classification in patients with LKM antibody-positive autoimmune hepatitis type 2 was higher than in LKM-negative patients (22.0% vs. 2.4%; P < 0.05). This was because of an increase of genotype III in our patients from Italy. No HCV mutations were found that show a closer sequence homology to cytochrome P450IID6, the major LKM-1 antigen. Deletions in the envelope and nonstructural region 5 were found. CONCLUSIONS: Because a specific HCV sequence is not associated with the induction of LKM-1 autoantibodies, future research must focus on host factors and possibly additional environmental factors.
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