Chen C, Zhang SY, Chen L. Review of clinical characteristics, immune responses and regulatory mechanisms of hepatitis E-associated liver failure. World J Clin Cases 2022; 10(19): 6341-6348 [PMID: 35979284 DOI: 10.12998/wjcc.v10.i19.6341]
Corresponding Author of This Article
Liang Chen, MD, Chief Physician, Department of Hepatology, Shanghai Public Health Clinical Center, No. 2901 Caolang Road, Jin-Shan District, Shanghai 201508, China. chenliang@shphc.org.cn
Research Domain of This Article
Infectious Diseases
Article-Type of This Article
Minireviews
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 Clin Cases. Jul 6, 2022; 10(19): 6341-6348 Published online Jul 6, 2022. doi: 10.12998/wjcc.v10.i19.6341
Review of clinical characteristics, immune responses and regulatory mechanisms of hepatitis E-associated liver failure
Chong Chen, Shu-Ye Zhang, Liang Chen
Chong Chen, Department of Infectious Disease, Shanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China
Shu-Ye Zhang, Liang Chen, Department of Hepatology, Shanghai Public Health Clinical Center, Shanghai 201508, China
Author contributions: Chen C, Zhang SY and Chen L contributed equally to all aspects of the work.
Supported byShanghai Shenkang Hospital Development Center, No. SHDC12020109; Shanghai Association for Science and Technology, No. 21S11905600; and Plan of the Research Project Funded by Shanghai Public Health Clinical Centre, No. KY-GW-2022-22.
Conflict-of-interest statement: All the authors declare no conflict of interest related to the manuscript.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Liang Chen, MD, Chief Physician, Department of Hepatology, Shanghai Public Health Clinical Center, No. 2901 Caolang Road, Jin-Shan District, Shanghai 201508, China. chenliang@shphc.org.cn
Received: January 8, 2022 Peer-review started: January 8, 2022 First decision: March 9, 2022 Revised: March 17, 2022 Accepted: May 5, 2022 Article in press: May 5, 2022 Published online: July 6, 2022
Abstract
Hepatitis E virus (HEV) is the most common cause of acute liver failure (LF) and one of the most common factors causing acute injury in acute-on-chronic LF (ACLF). When HEV-related LF occurs, a series of changes take place in both the intrahepatic environment and extrahepatic microenvironment. The changed types and distribution of immune cells (infiltrating macrophages and increased lymphocytes) in liver tissue, as well the increased proinflammatory cytokines and chemokines in the blood, indicate that the occurrence and progression of HEV-related LF are closely related to immune imbalance. The clinical features and immune reaction in the body during HEV-related acute LF (ALF) and ACLF are complicated. This review highlights recent progress in elucidating the clinical manifestations of HEV-associated ALF and ACLF and discusses the corresponding systemic immune changes and possible regulatory mechanisms.
Core Tip: Hepatitis E virus (HEV) is the most common cause of acute liver failure (LF) and a common factor causing acute injury in acute-on-chronic LF (ACLF). The whole immune environment in the body during HEV-related LF is complicated. This review highlights recent progress in elucidating the clinical manifestations of HEV-associated acute LF and ACLF and discusses the corresponding systemic immune changes and possible regulatory mechanisms.
