Steatosis and hepatitis C

Abstract

Hepatitis C virus (HCV) infection is a common liver disease worldwide with a high rate of chronicity (75-80%) in infected individuals. The chronic form of HCV leads to steatosis, cirrhosis and hepatocellualr carcinoma. Steatosis is prevalent in HCV patients (55%) due to a combination of viral factors (effect of viral proteins on some of the intracellular pathways) and host factors (overweight, insulin resistance, diabetes mellitus, and alcohol consumption). The response rates to treatment of chronic HCV with pegylated interferon (PEG-IFN) and (in the case of genotype-1 HCV, the most common infecting genotype in the USA) ribavirin (RBV) is low, with a sustained viral response rate ≤ 40%. Adding direct-acting antiviral agents-recently approved by the FDA-to the standard protocol has increased the response rate; however HCV-related end-stage liver disease is still the primary indication for liver transplantation in the USA. The focus of this article is on the interrelation between HCV, steatosis and metabolic syndrome.

Figure 1.

Natural history of hepatitis C viral infection.

Figure 2.

HCV-induced steatosis.IRS-1 = insulin receptor substrate-1; MTP = microsomal triglyceride transfer protein; PPAR-α = peroxisome proliferator-activated receptor alpha-α; SOCs = suppressor of cytokine signaling; TG = triglyceride; TNF α = tumor necrosis factor α.

Figure 3.

Hyperinsulinemia and liver fibrosis