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      Human immunodeficiency virus and hepatotropic viruses co-morbidities as the inducers of liver injury progression

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          Abstract

          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.

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          Hepatocyte death: a clear and present danger.

          Maria Guicciardi, Gregory J. Gores, Harmeet Malhi (2010)
          The hepatocyte is especially vulnerable to injury due to its central role in xenobiotic metabolism including drugs and alcohol, participation in lipid and fatty acid metabolism, its unique role in the enterohepatic circulation of bile acids, the widespread prevalence of hepatotropic viruses, and its existence within a milieu of innate immune responding cells. Apoptosis and necrosis are the most widely recognized forms of hepatocyte cell death. The hepatocyte displays many unique features regarding cell death by apoptosis. It is quite susceptible to death receptor-mediated injury, and its death receptor signaling pathways involve the mitochondrial pathway for efficient cell killing. Also, death receptors can trigger lysosomal disruption in hepatocytes which further promote cell and tissue injury. Interestingly, hepatocytes are protected from cell death by only two anti-apoptotic proteins, Bcl-x(L) and Mcl-1, which have nonredundant functions. Endoplasmic reticulum stress or the unfolded protein response contributes to hepatocyte cell death during alterations of lipid and fatty acid metabolism. Finally, the current information implicating RIP kinases in necrosis provides an approach to more fully address this mode of cell death in hepatocyte injury. All of these processes contributing to hepatocyte injury are discussed in the context of potential therapeutic strategies.
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            The natural history of hepatitis C virus infection: host, viral, and environmental factors.

            T. Nelson, Jordan Vlahov, J Boitnott … (2000)
            Hepatitis C virus (HCV) infection may resolve (viral clearance), persist without complications, or cause end-stage liver disease (ESLD). The frequency and determinants of these outcomes are poorly understood. To assess the incidence and determinants of viral clearance and ESLD among persons who acquired HCV infection from injection drug use. Community-based prospective cohort study with enrollment in 1988-1989 and a median follow-up of 8.8 years. A total of 1667 persons aged 17 years or older with a history of injection drug use and an HCV antibody-positive test result during follow-up. Viral clearance was assessed in a subset of 919 patients and defined as failure to detect HCV RNA in at least 2 consecutive samples collected 5 or more months apart. End-stage liver disease was assessed at semiannual visits and by review of medical records and death certificates and defined by the presence of ascites, esophageal varices, or hepatic encephalopathy, or when ESLD was stated as a cause of death. Viral clearance was observed in 90 persons who were compared with 722 with persistent viremia, while the viremia of 107 was not resolved. Viral clearance occurred more often in nonblacks (adjusted odds ratio [OR], 5.15; 95% confidence interval [CI], 2.60-10.17) and those not infected with human immunodeficiency virus (HIV) (adjusted OR, 2.19; 95% CI, 1.26-3.47). Forty cases of ESLD were observed throughout follow-up (incidence, 3.1 per 1000 person-years). In a multivariate model, risk of ESLD was higher for persons aged 38 years or older at enrollment (adjusted relative incidence, 3.67; 95% CI, 1.96-6.88) and who reported ingestion of more than 260 g of alcohol per week (adjusted relative incidence, 3.60; 95% CI, 1.73-7.52). Of 210 patients without ESLD randomly selected for biopsy, only 2 had cirrhosis. Our results indicate that although HCV infection can be self-limited or associated with ESLD, the majority of adults have persistent viremia without clinically demonstrable liver disease. Further research is needed to explain the less frequent clearance of HCV infection among black persons and to improve utilization of treatment for those infected in the context of injection drug use. JAMA. 2000;284:450-456
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              The natural history of community-acquired hepatitis C in the United States. The Sentinel Counties Chronic non-A, non-B Hepatitis Study Team.

              M J Alter, H Margolis, K Krawczynski … (1992)
              Chronic liver disease develops in more than half of patients with post-transfusion hepatitis C, but little is known about the natural history of community-acquired hepatitis C. In 1985 and 1986 we identified adults with acute non-A, non-B hepatitis in four counties in the United States and followed them prospectively. We used three markers to detect hepatitis C virus (HCV) infection in stored samples of serum: antibody to HCV (anti-HCV) detected by second-generation serologic assays; HCV RNA detected by polymerase-chain-reaction assay; and antibody to HCV antigen (anti-HCVAg) detected by fluorescent-antibody-blocking assay. Of 130 patients with non-A, non-B hepatitis, 106 (82 percent) had HCV infection, 93 were positive for anti-HCV, and 13 were positive only for HCV RNA or anti-HCVAg. Chronic hepatitis developed in 60 (62 percent) of 97 HCV-infected patients followed for 9 to 48 months, with no relation to the risk factors for infection. Ten of the 30 patients who had liver biopsies had chronic active hepatitis. In samples collected 42 to 48 months after the onset of hepatitis, HCV RNA was detected in 12 of 13 tested patients with chronic hepatitis and in all 15 tested patients with hepatitis that had resolved. Anti-HCV persisted in all but two of the initially positive patients, for a rate of antibody loss of 0.6 per 100 person-years. Patients with community-acquired hepatitis C have a high rate of chronic hepatitis. HCV may be a major cause of chronic liver disease in the United States, and in most patients HCV infection seems to persist for at least several years, even in the absence of active liver disease.
              Article 0 comments Cited 119 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Murali Ganesan
                Larisa Y Poluektova
                Kusum K Kharbanda
                Natalia A Osna
                Journal
                Journal ID (nlm-ta): World J Gastroenterol
                Journal ID (iso-abbrev): World J. Gastroenterol
                Journal ID (publisher-id): WJG
                Title: World Journal of Gastroenterology
                Publisher: Baishideng Publishing Group Inc
                ISSN (Print): 1007-9327
                ISSN (Electronic): 2219-2840
                Publication date (Print): 28 January 2019
                Publication date (Electronic): 28 January 2019
                Volume: 25
                Issue: 4
                Pages: 398-410
                Affiliations
                Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, United States
                Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, United States. murali.ganesan@ 123456unmc.edu
                Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, United States
                Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, United States
                Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, United States
                Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, United States
                Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, United States
                Author notes

                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.

                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@ 123456unmc.edu

                Telephone: +1-402-9953576 Fax: +1-402-4490604

                Article
                Other ID: jWJG.v25.i4.pg398
                DOI: 10.3748/wjg.v25.i4.398
                PMC ID: 6350175
                PubMed ID: 30700937
                SO-VID: a7c00737-b667-4e8e-9875-1ed8b6303fb7
                Copyright © ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
                License:

                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.

                History
                Date received : 30 November 2018
                Date revision received : 15 January 2019
                Date accepted : 18 January 2019
                Categories
                Subject: Review

                Keywords: human immunodeficiency virus,hepatitis c virus,hepatitis b virus,fibrosis,stiffness,treatment
                Data availability:
                Keywords: human immunodeficiency virus, hepatitis c virus, hepatitis b virus, fibrosis, stiffness, treatment

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