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Genotype 3 Infection: The Last Stand of Hepatitis C Virus

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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.

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Correspondence to Susanna Naggie.

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No funding was received for the preparation of this review.

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Keyur Patel has received consulting fees from Gilead Sciences, and Susanna Naggie has received grants from Abbvie, BMS, Gilead Sciences, Janssen Pharmaceuticals, Merck and Tacere, as well as consulting fees from the IDSA and Merck. Austin Wei-Hong Chan has no conflicts of interest to declare.

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Chan, A., Patel, K. & Naggie, S. Genotype 3 Infection: The Last Stand of Hepatitis C Virus. Drugs 77, 131–144 (2017). https://doi.org/10.1007/s40265-016-0685-x

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