IFN treatment for CH usually results in a high incidence of side effects; therefore, it is important to adjust IFN treatment accurately using a prediction method. Viral factors, host factors, and treatment factors has been utilized in prior research to predict the outcome of combination therapy. Hepatic SR-58611A microRNA expression pattern before anti-viral treatment has also been utilized as a prediction biomarker of drug response in CH, while other studies have shown that there is a RA-9 possible association between two SNPs near the gene interleukin 28B on chromosome 19 and lack of response to combination therapy. In this study, we evaluated the IFN related gene expression profiles in CH patients before administering CH combination treatment. After the anti-viral therapy, patients were classified according to their clinical outcome: sustained viral response, relapse, and non responder. It was observed that in the NR group, the expression level of some IFN related genes was significantly higher than that in normal liver groups, and that the expression level of the other IFN related genes was significantly lower than in NL. Moreover, the significantly high expression of IFN related genes was associated with low response to combination therapy. This suggests that dysregulation of the IFN system can be related to cases of CH combination therapy failure. Our comprehensive analysis identified 66 genes with expression levels that consistently differed depending on the drug response of 87 CH patients and 5 normal liver specimens. Comparing the gene expression pattern in NR and NL showed the expression levels of 31 genes were significantly different. In addition, most genes with expression levels in NR that were higher or lower than in NL, also differed between NR and SVR. Therefore, it is possible that innate immunity in the early period of HCV infection strongly influences IFN reaction. HCV infection induces the impairment of cell subset number and the function of plasmacytoid dendritic cells and natural killer cells. The amount of PDC, which are the most potent producers of antiviral Type-I and III IFN, decreased in patients�� peripheral blood, however, PDC was trapped in the HCV infected liver tissue. Therapeutic non-responders had increased PDC migration to inflammatory chemokines before therapy, compared with therapeutic responders.