Kim H, Lee SA, Do SY, Kim BJ. Precore/core region mutations of hepatitis B virus related to clinical severity. World J Gastroenterol 2016; 22(17): 4287-4296 [PMID: 27158197 DOI: 10.3748/wjg.v22.i17.4287]
Corresponding Author of This Article
Bum-Joon Kim, PhD, Department of Biomedical Sciences, Microbiology and Immunology, Liver Research Institute and Cancer Research Institute, College of Medicine, Seoul National University, 28 Yongon-dong, Chongno-gu, Seoul 110-799, South Korea. kbumjoon@snu.ac.kr
Research Domain of This Article
Virology
Article-Type of This Article
Topic Highlight
Open-Access Policy of This Article
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/
World J Gastroenterol. May 7, 2016; 22(17): 4287-4296 Published online May 7, 2016. doi: 10.3748/wjg.v22.i17.4287
Precore/core region mutations of hepatitis B virus related to clinical severity
Hong Kim, Seoung-Ae Lee, Seung Yeon Do, Bum-Joon Kim
Hong Kim, Seoung-Ae Lee, Seung Yeon Do, Bum-Joon Kim, Department of Biomedical Sciences, Microbiology and Immunology, Liver Research Institute and Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110-799, South Korea
Author contributions: Kim H, Do SY and Kim BJ conceived this research and participated in its design and coordination; Kim H, Lee SA and Do SY analyzed and interpreted the data; Kim BJ wrote this manuscript; Kim H and Lee SA reviewed the manuscript; all authors approved the final manuscript.
Supported by A National Research Foundation grant of Ministry of Science, ICT and Future Planning, South Korea, No. NRF-2015R1C1A1A02037267; and a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, the Ministry of Health and Welfare, South Korea, No. HI14C0955.
Conflict-of-interest statement: No conflict of interest.
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: Bum-Joon Kim, PhD, Department of Biomedical Sciences, Microbiology and Immunology, Liver Research Institute and Cancer Research Institute, College of Medicine, Seoul National University, 28 Yongon-dong, Chongno-gu, Seoul 110-799, South Korea. kbumjoon@snu.ac.kr
Telephone: +82-2-7408316 Fax: +82-2-7430881
Received: February 15, 2016 Peer-review started: February 17, 2016 First decision: March 7, 2016 Revised: March 10, 2016 Accepted: April 7, 2016 Article in press: April 7, 2016 Published online: May 7, 2016 Processing time: 74 Days and 4.8 Hours
Core Tip
Core tip: The presence of several distinct types of mutations in HBV infections has been shown to contribute to the progression of liver disease in chronically infected patients. Although the relationships between single mutation types in the preC/C region and clinical severity have rarely been studied to date, it was recently reported that some preC/C mutations, particularly in the MHC class II restricted region, are significantly correlated with hepatocellular carcinoma. Several preC/C mutations, including preC G1896A, are also related to HBeAg sero-negative status, which can affect the disease progression of chronic patients. Mutations such as I97F/L or P135Q, which inhibit core nucleocapsid formation, also contribute to disease progression by evading host innate immunity. In addition, the P5H/L/T mutation may lead to hepatocarcinogenesis by inducing the ER stress-ROS axis. In this review, we mainly focus on the clinical implications of the reported preC/C mutations.
