Several host metabolic pathways tightly control cellular lipid synthesis. Targeted disruption of these pathways [19] [20] [21] by HCVencoded proteins has been linked with liver steatosis [22, 23] in HCV-infected individuals. Importantly, there is a correlation between the degree of steatosis and both the severity of chronic HCV infection [13, 24] and the response to treatment with pegylated-interferon-a and ribavirin [25, 26] .