Abstract

Hepatitis C virus (HCV) is a human pathogen responsible for acute and chronic liver disease, infecting an estimated 130–170 million persons worldwide. An intriguing feature of HCV infection is its peculiar relationship with lipids: (1) HCV virions circulate in serum bound to lipoproteins; (2) lipids have been shown to modulate (and, indeed, are essential to) the HCV life cycle; and (3) an occasionally severe accumulation of triglycerides is found in a distinct subgroup of patients in the form of hepatic steatosis. As a result, lipid metabolism is overall altered, conferring an idiosyncratic profile to HCV infection. The scope of this review is to discuss these aspects, focusing on both their molecular mechanisms and their clinical consequences.