©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 14, 2018; 24(38): 4304-4310
Published online Oct 14, 2018. doi: 10.3748/wjg.v24.i38.4304
Published online Oct 14, 2018. doi: 10.3748/wjg.v24.i38.4304
Challenge to overcome: Nonstructural protein 5A-P32 deletion in direct-acting antiviral-based therapy for hepatitis C virus
Ken Sato, Toshio Uraoka, Department of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi, Gunma 371-8511, Japan
Author contributions: Sato K reviewed the literature and wrote the first draft of the paper; Uraoka T approved the final version of the article.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Correspondence to: Ken Sato, MD, PhD, Associate Professor, Doctor, Department of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan. satoken@gunma-u.ac.jp
Telephone: +81-272-208127 Fax: +81-272-208127
Received: July 17, 2018
Peer-review started: July 17, 2018
First decision: July 25, 2018
Revised: August 2, 2018
Accepted: August 24, 2018
Article in press: August 24, 2018
Published online: October 14, 2018
Processing time: 86 Days and 23.1 Hours
Peer-review started: July 17, 2018
First decision: July 25, 2018
Revised: August 2, 2018
Accepted: August 24, 2018
Article in press: August 24, 2018
Published online: October 14, 2018
Processing time: 86 Days and 23.1 Hours
Core Tip
Core tip: P32 deletion, as a nonstructural protein 5A resistance-associated substitution (RAS), has been gradually noticed in patients who experience treatment failure associated with daclatasvir and asunaprevir as an antiviral therapy for chronic hepatitis C. Information regarding P32 deletion is very limited at the present. Although the prevalence of this RAS is assumed to be low, it was found to be a new threat to current direct-acting antiviral-based combination therapy. There is an urgent need for further basic and clinical studies on this RAS. Exploring and overcoming this RAS is essential for antiviral therapy for chronic hepatitis C.