Ganesan M, Poluektova LY, Kharbanda KK, Osna NA. Human immunodeficiency virus and hepatotropic viruses co-morbidities as the inducers of liver injury progression. World J Gastroenterol 2019; 25(4): 398-410 [PMID: 30700937 DOI: 10.3748/wjg.v25.i4.398]
Corresponding Author of This Article
Murali Ganesan, PhD, Instructor, Research Service (151), Veterans Affairs Nebraska-Western Iowa Health Care System, 4101 Woolworth Ave, Omaha, NE 68105, United States. murali.ganesan@unmc.edu
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
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. 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 byNational 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: http://creativecommons.org/licenses/by-nc/4.0/
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. murali.ganesan@unmc.edu
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 Processing time: 57 Days and 14.7 Hours
Core Tip
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.
