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

Genotype 3 Infection: The Last Stand of Hepatitis C Virus.

Author information

1
Division of Infectious Diseases, Department of Medicine, Duke University School of Medicine, Durham, NC, USA.
2
Infectious Diseases Research, Duke Clinical Research Institute, Durham, NC, USA.
3
Toronto Center for Liver Disease, University of Toronto, Toronto, ON, Canada.
4
Division of Infectious Diseases, Department of Medicine, Duke University School of Medicine, Durham, NC, USA. susanna.naggie@dm.duke.edu.
5
Infectious Diseases Research, Duke Clinical Research Institute, Durham, NC, USA. susanna.naggie@dm.duke.edu.

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.

PMID:
28074358
PMCID:
PMC5726887
DOI:
10.1007/s40265-016-0685-x
[Indexed for MEDLINE]
Free PMC Article

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