Therefore, in patients with the rs12979860 CC and rs8099917 TT genotype, IL28B production, which induces expression of interferon-stimulated genes, including some inflammatory cytokines, was thought to be increased. This may be the underlying cause of the higher inflammation activity and progressed fibrosis in patients with the IFN responsive allele. In analysis with the studies involving only patients without a history of IFN-based treatment, rs12979860 CC and rs8099917 TT genotypes were associated with higher possibility of having severe inflammation activity; however, the differences did not reach to the significant level. Only three studies according to rs12979860 polymorphism and two studies according to rs8099917 polymorphism were included when restricted to studies with only treatment-naı¨ve patients, and may be underpowered to detect the MDV3100 msds effects of IL28B polymorphisms on inflammation activity. The further analyses with larger sample are needed to confirm this association. Additionally, meta-regression analysis showed that the effect of the rs12979860 polymorphism was influenced by viral genotype distribution. This result may imply a different influence of rs12979860 polymorphism on immune response according to viral genotype in treatment-naı¨ve patients. IL28B polymorphisms were also shown to be associated with lipid metabolism. In the present study, the rs8099917 TT genotype was significantly associated with a lower possibility of severe steatosis. This association still remained statistically significant after we restricted to studies in which only treatmentnaı¨ve patients were included. The lower hepatic steatosis in patients with the IFN responsive allele could be explained by a more efficient export of lipids from hepatocytes. Higher interferon expression was shown to lead to suppression of lipoprotein lipase, which would result in decreased conversion of VLDL to LDL and subsequent higher steatosis. The difference in IL28B expression might cause an aberration of lipid metabolism in patients with CHC. We found no significant association of rs12979860 with steatosis. And when we restricted to treatmentnaı¨ve patients, rs12979860 CC genotype was significantly associated with a higher possibility of severe steatosis. Previous studies have shown that racial differences or viral genotypes make a difference in the effects of rs12979860 and rs8099917 polymorphisms. This may explain the discrepancy between the effect of rs12979860 and rs8099917 on hepatic steatosis. However, only four studies were included in the analysis of rs12979860; or when it comes to the studies with only treatment-naı¨ve patients, only two studies were extracted. Thus, we should not make any definite conclusion on this matter right now. Further studies with larger sample sizes are needed to identify their exact correlation. According to the meta-regression analysis, the effect of rs8099917 polymorphisms on steatosis became smaller with the increase in the male proportion.