Published online Jul 21, 2015. doi: 10.3748/wjg.v21.i27.8293
Peer-review started: February 13, 2015
First decision: March 26, 2015
Revised: April 17, 2015
Accepted: June 10, 2015
Article in press: June 10, 2015
Published online: July 21, 2015
Processing time: 159 Days and 0.6 Hours
The hepatitis C virus (HCV) is one of the most common causes of chronic liver disease and the leading indication for liver transplantation worldwide. Every aspect of the HCV life cycle is closely tied to human lipid metabolism. The virus circulates as a lipid-rich particle, utilizing lipoprotein cell receptors to gain entry into the hepatocyte. It has also been shown to upregulate lipid biosynthesis and impair lipid degradation, resulting in significant intracellular lipid accumulation and circulating hypocholesterolemia. Patients with chronic hepatitis C (CHC) are at increased risk of hepatic steatosis, fibrosis, and cardiovascular disease including accelerated atherosclerosis. HMG CoA Reductase inhibitors, or statins, have been shown to play an important role in the modulation of hepatic steatosis and fibrosis, and recent attention has focused upon their potential therapeutic role in CHC. This article reviews the hepatitis C viral life cycle as it impacts host lipoproteins and lipid metabolism. It then describes the pathogenesis of HCV-related hepatic steatosis, hypocholesterolemia and atherosclerosis, and finally describes the promising anti-viral and anti-fibrotic effects of statins, for the treatment of CHC.
Core tip: This article reviews the complex relationship between hepatitis C virus (HCV) infection and human lipid metabolism. It discusses the aspects of the hepatitis C viral life cycle that are entwined with cholesterol homeostasis, as well as the clinical implications of HCV-mediated changes in human lipid profiles. Finally, it describes the current state of knowledge regarding the impact of statin medications on histological, virological and clinical outcomes, among patients with chronic hepatitis C.