Genotype 3 Infection: The Last Stand of Hepatitis C Virus

Drugs. 2017 Feb;77(2):131-144. doi: 10.1007/s40265-016-0685-x.

Abstract

Hepatitis C virus (HCV) represents a significant global disease burden, with an estimated 130-150 million people worldwide living with chronic HCV infection. Within the six major clinical HCV genotypes, genotype 3 represents 22-30% of all infection and is described as a unique entity with higher rates of steatosis, faster progression to cirrhosis, and higher rates of hepatocellular carcinoma. Hepatic steatosis in the setting of hepatitis C genotype 3 (HCV-3) is driven by viral influence on three major pathways: microsomal triglyceride transfer protein, sterol regulatory element-binding protein-1c, and peroxisome proliferator-associated receptor-α. Historically with direct-acting antivirals, the rates of cure for HCV-3 therapies lagged behind the other genotypes. As current therapies for HCV-3 continue to close this gap, it is important to be cognizant of common drug interactions such as acid-suppressing medication and amiodarone. In this review, we discuss the rates of steatosis in HCV-3, the mechanisms behind HCV-3-specific steatosis, and current and future therapies.

Publication types

  • Review

MeSH terms

  • Antiviral Agents / pharmacology
  • Antiviral Agents / therapeutic use*
  • Fatty Liver / etiology
  • Fatty Liver / virology
  • Genotype
  • Hepacivirus / classification
  • Hepacivirus / drug effects
  • Hepacivirus / genetics*
  • Hepacivirus / pathogenicity*
  • Hepatitis C / complications
  • Hepatitis C / drug therapy*
  • Hepatitis C / pathology
  • Hepatitis C / virology*
  • Humans

Substances

  • Antiviral Agents