Lee IK, Lee SA, Kim H, Won YS, Kim BJ. Induction of endoplasmic reticulum-derived oxidative stress by an occult infection related S surface antigen variant. World J Gastroenterol 2015; 21(22): 6872-6883 [PMID: 26078563 DOI: 10.3748/wjg.v21.i22.6872]
Corresponding Author of This Article
Bum-Joon Kim, Professor, Department of Microbiology and Immunology, Liver Research Institute, Cancer Research Institute and SNUMRC, College of Medicine, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 110-799, South Korea. kbumjoon@snu.ac.kr
Research Domain of This Article
Infectious Diseases
Article-Type of This Article
Basic Study
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. Jun 14, 2015; 21(22): 6872-6883 Published online Jun 14, 2015. doi: 10.3748/wjg.v21.i22.6872
Induction of endoplasmic reticulum-derived oxidative stress by an occult infection related S surface antigen variant
In-Kyung Lee, Seoung-Ae Lee, Hong Kim, You-Sub Won, Bum-Joon Kim
In-Kyung Lee, Seoung-Ae Lee, Hong Kim, You-Sub Won, Bum-Joon Kim, Department of Microbiology and Immunology, Liver Research Institute, Cancer Research Institute and SNUMRC, College of Medicine, Seoul National University, Seoul 110-799, South Korea
Author contributions: Kim BJ conceived this research and participated in its design and coordination; Lee IK and Lee SA performed the experiments; Kim H, Lee SA, and Won YS analyzed and interpreted the data; Lee SA, Kim H, and Won YS contributed the reagents, materials, and analysis tools; Lee IK, Lee SA and Kim BJ wrote and reviewed the manuscript; Lee IK and Lee SA equally contributed to this research; all authors approved the final manuscript.
Supported by National Research Foundation of Korea grant funded by the Korea government (MEST), No. 2013-005810.
Conflict-of-interest: No conflict-of-interest.
Data sharing: No additional data are available.
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, Professor, Department of Microbiology and Immunology, Liver Research Institute, Cancer Research Institute and SNUMRC, College of Medicine, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 110-799, South Korea. kbumjoon@snu.ac.kr
Telephone: +82-2-7408316 Fax: +82-2-7430881
Received: December 19, 2014 Peer-review started: December 21, 2014 First decision: January 8, 2015 Revised: January 28, 2015 Accepted: February 12, 2015 Article in press: February 13, 2015 Published online: June 14, 2015 Processing time: 181 Days and 3.6 Hours
Core Tip
Core tip: The molecular mechanisms underlying the relationships between occult hepatitis B virus infection and liver disease progression remain a mystery. The present study demonstrated that the HBsAg variant KD, which exhibits a secretion defective phenotype, universally induced endoplasmic reticulum (ER) stress pathways in hepatocytes. This induction of ER stress may evoke ER stress-mediated biological actions that induce liver damaging processes, including ROS production, nitric oxide production, and apoptosis induction. In conclusion, occult infection related to hepatitis B virus S surface antigen variants may play a very pivotal role in the progression of liver diseases primarily via ER-derived oxidative stress and apoptosis in hepatocytes.
