A large volume of evidence suggests that lipids and lipid receptors are important in hepatitis C infection.

Hepatic steatosis is common, with at least 65% of liver biopsy specimens demonstrating steatosis. In genotype 3 infection, a specific mechanism of steatosis induction exists, via core antigen expression. The incidence of diabetes is higher in hepatitis C virus (HCV) infection and increases with increasing severity of liver disease. The mechanism of this is via insulin resistance, but it is uncertain whether hepatic steatosis is a result of the insulin resistance or plays a pivotal role in its induction.

HCV is associated with lipid in the serum and almost certainly uses lipid receptors to enter hepatocytes. The low-density fractions of serum contain HCV RNA particles and lipoviral particles (LVP) associated with triglyceride (TG)-rich lipoproteins. Such particles rich in TG have been shown to contain viral capsid and RNA.¹ TG is contained within chylomicrons or within very low-density lipoprotein (VLDL). Chylomicrons are synthesised in the intestine and transported via lymph into the circulation where they are broken down by the action of lipoprotein lipase in many cell types. The chylomicron remnant is then taken up by the liver via the low-density lipoprotein (LDL) receptor (LDLr) or the LDL receptor-related protein. Chylomicrons contain apolipoprotein B48 at …