Review
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 21, 2018; 24(31): 3488-3499
Published online Aug 21, 2018. doi: 10.3748/wjg.v24.i31.3488
Hepatitis B virus infection: Defective surface antigen expression and pathogenesis
Chun-Chen Wu, Ying-Shan Chen, Liang Cao, Xin-Wen Chen, Meng-Ji Lu
Chun-Chen Wu, Ying-Shan Chen, Liang Cao, Xin-Wen Chen, State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, Hubei Province, China
Liang Cao, Department of Microbiology and Immunology, Feinberg School of Medicine Northwestern University, Chicago, IL 60611, United States
Meng-Ji Lu, Institute of Virology, University Hospital of Essen, Essen 45122, Germany
Author contributions: Wu CC contributed to analysis and interpretation of the data and drafting the article; Chen YS and Cao L contributed to revising the article for important intellectual content; Chen XW and Lu MJ contributed to conception and design, analysis and interpretation of data, and drafting and revising the article for important intellectual content.
Supported by the National Nature Science Foundation of China, No. 31770180; and the Youth Innovation Promotion Association CAS, No. 2016303.
Conflict-of-interest statement: The authors have declared that no potential conflict of interest exists.
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: Meng-Ji Lu, PhD, Professor, Institute of Virology, University Hospital Essen, Hufelandstrasse 55, Essen 45122, Germany. mengji.lu@uni-due.de
Telephone: +49-201-7233530 Fax: +49-201-7235929
Received: April 27, 2018
Peer-review started: May 4, 2018
First decision: May 23, 2018
Revised: June 1, 2018
Accepted: June 25, 2018
Article in press: June 25, 2018
Published online: August 21, 2018
Processing time: 106 Days and 4.5 Hours
Abstract

Hepatitis B virus (HBV) infection is a global public health concern. HBV causes chronic infection in patients and can lead to liver cirrhosis, hepatocellular carcinoma, and other severe liver diseases. Thus, understanding HBV-related pathogenesis is of particular importance for prevention and clinical intervention. HBV surface antigens are indispensable for HBV virion formation and are useful viral markers for diagnosis and clinical assessment. During chronic HBV infection, HBV genomes may acquire and accumulate mutations and deletions, leading to the expression of defective HBV surface antigens. These defective HBV surface antigens have been found to play important roles in the progression of HBV-associated liver diseases. In this review, we focus our discussion on the nature of defective HBV surface antigen mutations and their contribution to the pathogenesis of fulminant hepatitis B. The relationship between defective surface antigens and occult HBV infection are also discussed.

Keywords: Hepatitis B surface protein; Defective surface antigen mutants; Endoplasmic reticulum stress; Fulminant hepatitis B; Occult hepatitis B virus infection; Pathogenesis

Core tip: Defective surface antigen mutation is a type of mutation with great clinical relevance. Many previous publications have explored the association of defective surface antigen mutation with the development of hepatitis B virus (HBV)-associated hepatocellular carcinoma. However, there are no reviews available that elaborate on the relationship between defective surface antigen mutation and HBV-associated fulminant hepatitis (FH), as well as occult hepatitis B virus infection (OBI). This review will focus on these two aspects to discuss the nature of defective HBV surface antigen mutations and their contribution to the pathogenesis of FH. The relationship between defective surface antigens and OBI are also discussed.