Review
Copyright ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 7, 2020; 26(9): 883-903
Published online Mar 7, 2020. doi: 10.3748/wjg.v26.i9.883
Role of alcohol in pathogenesis of hepatitis B virus infection
Murali Ganesan, Allison Eikenberry, Larisa Y Poluektova, Kusum K Kharbanda, Natalia A Osna
Murali Ganesan, Allison Eikenberry, Kusum K Kharbanda, Natalia A Osna, Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, United States
Murali Ganesan, Allison Eikenberry, Kusum K Kharbanda, Natalia A Osna, Department of Internal Medicine, Division of Gastroenterology and Hepatology, University of Nebraska Medical Center, Omaha, NE 68105, United States
Larisa Y Poluektova, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, United States
Author contributions: All authors contributed to this review with conception and design, literature review, drafting and critical revision, editing, and approval of the final version.
Supported by National Institutes of Health, No. NIAAA- K01AA026864.
Conflict-of-interest statement: No potential conflicts of interest.
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: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Murali Ganesan, PhD, Assistant Professor, Department of Internal Medicine, Division of Gastroenterology and Hepatology, University of Nebraska Medical Center, Omaha, NE 68198, United States. murali.ganesan@unmc.edu
Received: December 5, 2019
Peer-review started: December 5, 2019
First decision: December 30, 2019
Revised: February 9, 2020
Accepted: February 15, 2020
Article in press: February 15, 2020
Published online: March 7, 2020
Processing time: 91 Days and 11.2 Hours
Abstract

Hepatitis B virus (HBV) and alcohol abuse often contribute to the development of end-stage liver disease. Alcohol abuse not only causes rapid progression of liver disease in HBV infected patients but also allows HBV to persist chronically. Importantly, the mechanism by which alcohol promotes the progression of HBV-associated liver disease are not completely understood. Potential mechanisms include a suppressed immune response, oxidative stress, endoplasmic reticulum and Golgi apparatus stresses, and increased HBV replication. Certainly, more research is necessary to gain a better understanding of these mechanisms such that treatment(s) to prevent rapid liver disease progression in alcohol-abusing HBV patients could be developed. In this review, we discuss the aforementioned factors for the higher risk of liver diseases in alcohol-induced HBV pathogenies and suggest the areas for future studies in this field.

Keywords: Hepatitis B virus; Alcohol; Immunity; Oxidative stress; Liver disease

Core tip: In this review, we discussed the literature and some of our recent findings on the combined effects of alcohol and hepatitis B virus (HBV)-infection in the progression of liver diseases, such as steatosis, fibrosis, cirrhosis and hepatocellular carcinoma. Worldwide, 1.5 billion people had chronic liver disease in 2017, most commonly resulting from HBV (29%) and alcoholic liver disease (2%). Clinical evidence supports the synergistic effect of alcohol and HBV- infection on progression of end-stage liver diseases. The possible mechanisms for the chronic liver diseases induced by the combination of alcohol and HBV-infection are increased HBV replication, oxidative stress, cell organelles stress [such as endoplasmic reticulum and Golgi stress] and importantly, weakened immune responses. Better understanding of these mechanisms will improve the treatment options for the HBV-alcoholic patients.