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      HBV-HCV Coinfection: Viral Interactions, Management, and Viral Reactivation

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          Abstract

          Hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection is a complex clinical entity that has an estimated worldwide prevalence of 1–15%. Most clinical studies have shown that progression of disease is faster in HBV-HCV coinfected patients compared to those with monoinfection. Hepatocellular carcinoma development appears to have higher rate in coinfections. Viral replication in coinfected cells is characterized by a dominance of HCV over HBV replication. There are no established guidelines for treatment of HBV-HCV coinfection. Studies on interferon-based therapies and direct-acting antivirals have shown varying levels of efficacy. Clinical reports have indicated that treatment of HCV without suppression of HBV increases the risk for HBV reactivation. In this review, we appraise studies on both direct-acting antivirals and interferon-based therapies to evaluate the efficacy and rates of reactivation with each regimen. Screening for and prevention of coinfection are important to prevent serious HBV reactivations.

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          Hepatitis B reactivation in hepatitis B and C coinfected patients treated with antiviral agents: A systematic review and meta-analysis.

          Guofeng Chen, Cheng Wang, Jing Chen … (2017)
          There is an increased awareness of hepatitis B (HBV) reactivation in chronic hepatitis C (CHC) patients coinfected with HBV treated with pan-oral direct-acting antiviral agents (DAAs). We performed a systematic review and meta-analysis to compare the rate of HBV reactivation in CHC patients coinfected with overt HBV (hepatitis B surface antigen [HBsAg] positive) and occult HBV (HBsAg negative with positive HBV DNA) infection separately, treated with interferon (IFN)-based therapy to those with pan-oral DAAs. The primary outcome was HBV reactivation, and the secondary outcomes included hepatitis due to HBV reactivation, sustained virologic response (SVR) for CHC, loss of HBV DNA and HBsAg seroclearance. Although the pooled incidence rate of HBV reactivation, among CHC patients with overt HBV (n = 779), was similar among those treated with IFN-based therapy (14.5%, P < 0.001) and DAAs (12.2%, P = 0.03; P = 0.91 for heterogeneity between subgroups), it was reported to occur much earlier in those treated with DAAs (4-12 weeks during treatment) than in those treated with IFN-based therapies (most at the end of treatment and some during follow-up). Also, studies with DAA-based therapies were more likely to report incidence of hepatitis due to HBV reactivation (12.2% in DAAs vs. 0% in IFN; P = 0.009 for heterogeneity between subgroups). HBV reactivation and hepatitis due to HBV reactivation also occurred, though less frequently in CHC patients with occult HBV infection. CHC SVR was not affected by HBV reactivation (P = 0.27).
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            Rate of incidence of hepatocellular carcinoma in patients with compensated viral cirrhosis.

            M Chiaramonte, T Stroffolini, S Lobello … (1999)
            Cirrhosis of viral etiology due to hepatitis B virus (HBV) or hepatitis C virus (HCV) infection is a risk factor for hepatocellular carcinoma (HCC). The current study evaluated the rate of incidence of HCC in patients with compensated cirrhosis of viral etiology. Two hundred fifty-nine cirrhotic patients (66 hepatitis B surface antigen [HBsAg] positive, 166 HCV positive, and 27 HBsAg/HCV positive) were longitudinally examined every 6 months by serum alpha-fetoprotein test and liver ultrasonography. The rates of incidence of HCC were calculated by the person-years method. The Kaplan-Meier method was used to estimate the cumulative probability of HCC development. Differences in survival time were evaluated by a log rank test. Independent predictors of HCC development were estimated by Cox proportional hazard regression analysis. During a mean follow-up of 64.5 months, HCC developed in 51 (19.7%) patients: in 34 of 166 HCV positive subjects (20.5%) (mean follow-up, 66.3 months), in 6 of 66 of those HBsAg positive (9.1%) (mean follow-up, 55.06 months), and in 11 of 27 of those with dual HBsAg/HCV infection (40.7%) (mean follow-up, 76.4 months). The rate of incidence of HCC per 100 person-years of follow-up was 3.7 in HCV positive subjects, 2.0 in those HBsAg positive, and 6.4 in those with dual infection. Cumulative HCC appearance rates in HBsAg positive, HCV positive, and HBsAg/HCV positive subgroups were 10%, 21%, and 23% at 5 years, 16%, 28%, and 45% at 10 years, and 16%, 40%, and 55% at 13 years, respectively. Multivariate analysis indicated that age >50 years (hazard risk [HR], 4.5; 95% confidence interval [CI] = 2.1-9.4), male gender (HR, 2.8; 95% CI = 1.1-5.3), and HBsAg/HCV coinfection (HR, 2.3; 95% CI = 1.1-4.6) were independent predictors of HCC development. These findings confirm that male gender and more advanced age (>50 years) are risk factors for HCC in patients with cirrhosis. Furthermore, the data indicate that subjects with dual HBsAg/HCV infection are at highest risk for HCC. Surveillance programs for early detection of HCC should focus especially on these patients.
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              Peginterferon alfa-2a plus ribavirin for the treatment of dual chronic infection with hepatitis B and C viruses.

              Chun-Jen Liu, Wan-Long Chuang, Chuan-Mo Lee … (2009)
              Dual chronic infection with hepatitis C virus (HCV) and hepatitis B virus (HBV) is common in areas endemic for either virus. Combination therapy with ribavirin and pegylated interferon (peginterferon) is the standard of care for patients with HCV monoinfection. We investigated the effects of combination therapy in patients infected with both HBV and HCV (genotypes 1, 2, or 3). The study included 321 Taiwanese patients with active HCV infection; 161 also tested positive for hepatitis B surface antigen (HBsAg) and 160 were HBsAg-negative (controls). Patients with HCV genotype 1 infection received peginterferon alfa-2a (180 mug) weekly for 48 weeks and ribavirin (1000-1200 mg) daily. Patients with HCV genotypes 2 or 3 received peginterferon alfa-2a weekly for 24 weeks and ribavirin (800 mg) daily. At 24 weeks posttreatment, patient samples were examined for a sustained virologic response (SVR) against HCV (serum HCV levels decreased to <25 IU/mL). In patients with HCV genotype 1 infection, the SVR was 72.2% in dually infected patients vs 77.3% in monoinfected patients after treatment. For patients with HCV genotype 2/3 infections, the SVR values were 82.8% and 84.0%, respectively, after treatment. Serum HBV DNA eventually appeared in 36.3% of 77 dual-infected patients with undetectable pretreatment levels of HBV DNA; this was not accompanied by significant hepatitis. Posttreatment HBsAg clearance was observed in 11.2% of 161 dual-infected patients. Combination therapy with peginterferon alfa-2a and ribavirin is equally effective in patients with HCV monoinfection and in those with dual chronic HCV/HBV infection.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Clin Transl Hepatol
                Journal ID (iso-abbrev): J Clin Transl Hepatol
                Journal ID (publisher-id): JCTH
                Title: Journal of Clinical and Translational Hepatology
                Publisher: XIA & HE Publishing Inc.
                ISSN (Print): 2225-0719
                ISSN (Electronic): 2310-8819
                Publication date (Electronic): 6 July 2018
                Publication date (Print): 28 September 2018
                Volume: 6
                Issue: 3
                Pages: 296-305
                Affiliations
                [1]Department of Medicine, Division of Gastroenterology-Hepatology, University of Connecticut Health Center, Farmington, CT, USA
                Author notes
                * Correspondence to: Marianna G. Mavilia, Department of Medicine, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06032, USA. Tel: +1-860-679-2509, Fax: +1-860-679-6582, E-mail: mmavilia@ 123456uchc.edu

                The authors have no conflict of interests related to this publication.

                Drafting manuscript and development of figures (MGM), proposing concept for review and revising the manuscript with critical revisions (GYW).

                Article
                Publisher ID: JCTH.2018.00016
                DOI: 10.14218/JCTH.2018.00016
                PMC ID: 6160312
                PubMed ID: 30271742
                SO-VID: 7067b905-ec7c-43fb-a07a-482502d91852
                Copyright © © 2018 Authors.
                License:

                This article has been published under the terms of Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0), which permits noncommercial unrestricted use, distribution, and reproduction in any medium, provided that the following statement is provided. “This article has been published in Journal of Clinical and Translational Hepatology at DOI: 10.14218/JCTH.2018.00016 and can also be viewed on the Journal’s website at http://www.jcthnet.com”.

                History
                Date received : 1 March 2018
                Date revision received : 25 April 2018
                Date accepted : 1 May 2018
                Categories
                Subject: Review Article

                Keywords: hepatitis b virus,hepatitis c virus,coinfection,viral reactivation
                Data availability:
                Keywords: hepatitis b virus, hepatitis c virus, coinfection, viral reactivation

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