The hepatitis C virus (HCV) is a major cause of chronic liver disease worldwide. Its spectrum of severity, however, varies widely, as does its rate of progression towards cirrhosis. This depends on several host-related cofactors, such as age, gender, alcohol consumption, over weight and co-infections. The objective of this review is to discuss two of these cofactors: steatosis and insulin resistance. Although both may occur independently of HCV, a direct role of HCV infection in their pathogenesis has been reported. Whereas the virus-induced steatosis does not seem to have major clinical consequences, the so-called 'metabolic' steatosis and underlying insulin resistance may not only modify the clinical and histological course of chronic hepatitis C, but may also influence the response to interferon alpha-based therapy.