BACKGROUND & AIMS: The host's immune response may influence the course of hepatitis C virus (HCV) infection. The aim of this study was to investigate the distribution of HLA class II alleles in white subjects who spontaneously recovered from HCV infection compared with that in patients with persistent infection. METHODS: HLA-DRB1 and -DQB1 typing were performed in 103 consecutive patients with persistent HCV infection (HCV antibody positive, HCV RNA positive) and in 25 subjects with transient HCV infection (HCV antibody positive, persistently negative HCV RNA). RESULTS: No significant differences between subjects with transient or persistent infection were observed for age, sex, source of infection, or HCV serotype. The frequency of DQB1*0301 and DRB1*1101 alleles was higher in patients with transient infection than in those with persistent infection (84% vs. 30.8%, 40% vs. 9.8%; P < 0.01 and P < 0.02, respectively [Bonferroni correction]). DRB1 and DQB1 alleles did not influence viral load as an independent factor. Mean Knodell's scores were lower in patients with DQB1*0301 allele (6.12 +/- 0.4) than in those negative for DQB1*0301 (7.37 +/- 0.3; P < 0.05). CONCLUSIONS: Our results suggest that host- rather than virus-related factors are probably involved in the spontaneous clearance of HCV.
BACKGROUND & AIMS: The host's immune response may influence the course of hepatitis C virus (HCV) infection. The aim of this study was to investigate the distribution of HLA class II alleles in white subjects who spontaneously recovered from HCV infection compared with that in patients with persistent infection. METHODS:HLA-DRB1 and -DQB1 typing were performed in 103 consecutive patients with persistent HCV infection (HCV antibody positive, HCV RNA positive) and in 25 subjects with transient HCV infection (HCV antibody positive, persistently negative HCV RNA). RESULTS: No significant differences between subjects with transient or persistent infection were observed for age, sex, source of infection, or HCV serotype. The frequency of DQB1*0301 and DRB1*1101 alleles was higher in patients with transient infection than in those with persistent infection (84% vs. 30.8%, 40% vs. 9.8%; P < 0.01 and P < 0.02, respectively [Bonferroni correction]). DRB1 and DQB1 alleles did not influence viral load as an independent factor. Mean Knodell's scores were lower in patients with DQB1*0301 allele (6.12 +/- 0.4) than in those negative for DQB1*0301 (7.37 +/- 0.3; P < 0.05). CONCLUSIONS: Our results suggest that host- rather than virus-related factors are probably involved in the spontaneous clearance of HCV.
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