Editorial
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 21, 2017; 23(31): 5645-5649
Published online Aug 21, 2017. doi: 10.3748/wjg.v23.i31.5645
Direct-acting antiviral agents against hepatitis C virus and lipid metabolism
Tatsuo Kanda, Mitsuhiko Moriyama
Tatsuo Kanda, Mitsuhiko Moriyama, Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan
Author contributions: Kanda T and Moriyama M contributed to all aspects of this paper.
Conflict-of-interest statement: Kanda T and Moriyama M declare no conflict of interest related to this publication.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Tatsuo Kanda, MD, PhD, Associate Professor, Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-Kamicho, Itabashi-ku, Tokyo 173-8610, Japan. kandat-cib@umin.ac.jp
Telephone: +81-3-39728111 Fax: +81-3-39568496
Received: May 26, 2017
Peer-review started: May 28, 2017
First decision: June 23, 2017
Revised: July 4, 2017
Accepted: July 22, 2017
Article in press: July 24, 2017
Published online: August 21, 2017
Processing time: 85 Days and 8.5 Hours
Abstract

Hepatitis C virus (HCV) infection induces steatosis and is accompanied by multiple metabolic alterations including hyperuricemia, reversible hypocholesterolemia and insulin resistance. Total cholesterol, low-density lipoprotein-cholesterol and triglyceride levels are increased by peginterferon and ribavirin combination therapy when a sustained virologic response (SVR) is achieved in patients with HCV. Steatosis is significantly more common in patients with HCV genotype 3 but interferon-free regimens are not always effective for treating HCV genotype 3 infections. HCV infection increases fatty acid synthase levels, resulting in the accumulation of fatty acids in hepatocytes. Of note, low-density lipoprotein receptor, scavenger receptor class B type I and Niemann-Pick C1-like 1 proteins are candidate receptors that may be involved in HCV. They are also required for the uptake of cholesterol from the external environment of hepatocytes. Among HCV-infected patients with or without human immunodeficiency virus infection, changes in serum lipid profiles are observed during interferon-free treatment and after the achievement of an SVR. It is evident that HCV affects cholesterol metabolism during interferon-free regimens. Although higher SVR rates were achieved with interferon-free treatment of HCV, special attention must also be paid to unexpected adverse events based on host metabolic changes including hyperlipidemia.

Keywords: Cholesterol; Hepatitis C virus; Interferon-free; Lipid metabolism

Core tip: Eradication of hepatitis C virus (HCV) decreases the rate of complications, including liver-related and liver-unrelated death, and improves patient quality of life. Individuals infected with HCV have an increased risk of cardiovascular diseases and intracerebral hemorrhage, which are both associated with lipid metabolism. HCV infection causes abnormal host lipid metabolism. Treatment with interferon-based and interferon-free regimens has an impact on the eradication of HCV, as well as lipid abnormalities, during treatment and after treatment. Further observations are needed to determine the long-term effects on lipid metabolism caused by HCV and by eradication of the virus.