Hepatic steatosis is commonly seen in patients with chronic hepatitis C infection, and the two together have a greater association than by chance alone. Hepatitis C virus is closely associated with lipid metabolism throughout its lifecycle. Hepatic steatosis is more common in genotype 3 infection, due to direct viral effects including through microsomal triglyceride transfer protein, peroxisome proliferator activating receptor, and sterol regulatory element binding protein. In non-genotype 3 infection, hepatic steatosis is considered largely to be due to alterations in host metabolism, particularly through insulin resistance. The clinical relevance of this association has yet to be fully explored. Hepatic steatosis is associated with increased hepatic fibrosis and a reduced level of sustained virological response to pegylated interferon and ribavirin. Small studies trialing adjuvant anti-diabetic therapies or HMG-CoA reductase inhibitors with pegylated-interferon and ribavirin have shown an improved sustained virological response and reduced viral titer. Furthermore, simple lifestyle alterations showed positive effects on parameters of disease activity. These insights raise the possibility of novel treatment options.