Copyright ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 28, 2019; 25(4): 398-410
Published online Jan 28, 2019. doi: 10.3748/wjg.v25.i4.398
Human immunodeficiency virus and hepatotropic viruses co-morbidities as the inducers of liver injury progression
Murali Ganesan, Larisa Y Poluektova, Kusum K Kharbanda, Natalia A Osna
Murali Ganesan, Kusum K Kharbanda, Natalia A Osna, Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, United States
Murali Ganesan, Kusum K Kharbanda, Natalia A Osna, Department of Internal Medicine, 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 equally 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 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:
Corresponding author: Murali Ganesan, PhD, Instructor, Research Service (151), Veterans Affairs Nebraska-Western Iowa Health Care System, 4101 Woolworth Ave, Omaha, NE 68105, United States.
Telephone: +1-402-9953576 Fax: +1-402-4490604
Received: November 30, 2018
Peer-review started: November 30, 2018
First decision: January 11, 2019
Revised: January 15, 2019
Accepted: January 18, 2019
Article in press: January 18, 2019
Published online: January 28, 2019

Hepatotropic viruses induced hepatitis progresses much faster and causes more liver- related health problems in people co-infected with human immunodeficiency virus (HIV). Although treatment with antiretroviral therapy has extended the life expectancy of people with HIV, liver disease induced by hepatitis B virus (HBV) and hepatitis C virus (HCV) causes significant numbers of non-acquired immune deficiency syndrome (AIDS)-related deaths in co-infected patients. In recent years, new insights into the mechanisms of accelerated fibrosis and liver disease progression in HIV/HCV and HIV/HBV co-infections have been reported. In this paper, we review recent studies examining the natural history and pathogenesis of liver disease in HIV-HCV/HBV co-infection in the era of direct acting antivirals (DAA) and antiretroviral therapy (ART). We also review the novel therapeutics for management of HIV/HCV and HIV/HBV co-infected individuals.

Keywords: Human immunodeficiency virus, Hepatitis C virus, Hepatitis B virus, Fibrosis, Stiffness, Treatment

Core tip: In this review, we summarized the literature and our recent findings on liver damage associated with co-infection with human immunodeficiency virus (HIV) and hepatotropic viruses [hepatitis C virus (HCV), hepatitis B virus (HBV)]. The combination of HIV with HCV or HBV causes progressive liver injury and chronic liver inflammation ultimately leading to end-stage liver disease, such as cirrhosis and hepatocellular carcinoma. These outcomes are related to many events including apoptosis-mediated cross-talk between liver parenchymal and non-parenchymal cells, accumulation of inflammatory cells in the liver, microbial translocation and impaired immune responses. The treatment of these co-infections requires the combination of direct acting antiviral (DAA) and antiretroviral therapy (ART) for HCV + HIV and comparatively high doses of DAA for HBV, which should be controlled for drug-drug interactions to avoid hepatotoxicity.