Abstract
The hepatitis C virus (HCV) requires elements of host lipid metabolism for every step
in the viral life cycle. Clinically, it has long been observed that patients with
chronic hepatitis C have lower nonhigh-density lipoprotein cholesterol, and these
levels rise after successful treatment. The HCV itself circulates as a highly lipidated
lipoviral particle, which closely resembles very low-density lipoprotein (VLDL). Several
required coentry factors for the virus to gain access to the hepatocytes have been
described, and several, including SRB1, LDL-R, and the NPC1L1 receptors, are important
receptors for lipoprotein and cholesterol uptake. Inside the cell, the virus induces
lipogenesis, and specifically induces the master regulator sterol response element
binding protein. Viral replication then requires the concerted efforts of viral proteins
combined with several host factors involved in cholesterol synthesis. The virus is
then packaged alongside the cellular machinery for VLDL production. The complex interplay
highlights pathways of hepatic steatosis and unveils drug targets for the treatment
of HCV.
Keywords
hepatitis C - lipid metabolism - host factors - hypocholesterolemia - lipoviral particle
