Published online Aug 21, 2018. doi: 10.3748/wjg.v24.i31.3488
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
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.
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.