| Conclusion | Our study confirms that patients with HuLDi00025 and normal ALT levels have less severe liver disease than those with elevated ALT levels. This particular biochemical outcome may be explained, at least in part, by host immunogenetic factors such as the presence of HLA-DRB1*11.;This suggests a role for a complex host-immunogenetics interplay in the response to IFN-alpha, in patients with chronic HCV infection.;Our results define an association between the slope of change of viral load and HLA class II haplotype in patients infected with genotype 1b of HCV. This suggests a role for host immunogenetic factors in HCV infection in this homogeneous group.;Our findings establish that certain HLA class II alleles strongly influence disease progression following HCV infection.;These results support the hypothesis that specific HLA class II alleles might influence the susceptibility or resistance to persistent HCV infection.;The development of autoimmune disease in patients with HuLDi00025 depends on the interaction of multiple factors.;the immunogenetic basis for HCV clearance differs between ethnic groups and that the association between HLA class II and HCV clearance is not directly explained by antiviral CD4 T cell response.;Our data suggest that among the western Indian population, certain HLA alleles or associated haplotype influence HCV infection as a host genetic factor.Conclusion1 |
