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      Spontaneous clearance of chronic hepatitis C is rare in HIV-infected patients after effective use of combination antiretroviral therapy

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      Author(s): 1 , 1 , 2 , 2 , 1 , 1 , 2 , 1 , 1 , * , for the Grupo de Estudio de Hepatitis Virales (HEPAVIR) of the Sociedad Andaluza de Enfermedades Infecciosas (SAEI)
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      Publication date (Electronic):
      Journal: PLoS ONE
      Publisher: Public Library of Science

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          Abstract

          Objective

          To evaluate the rate of spontaneous resolution of chronic hepatitis C (CHC) infection in a cohort of HIV-infected patients.

          Methods

          A retrospective analysis of 509 HIV-infected patients with chronic HCV infection was performed at two reference hospitals in Andalusia. The main variable of the study was spontaneous clearance of CHC, defined as a negative HCV RNA result after at least two previous quantitative measurements of HCV RNA separated by a minimum of 12 months.

          Results

          Of 509 patients, 3 (0.59%; 95% CI: 0.15%-1.6%) experienced spontaneous clearance of CHC. After combination antiretroviral therapy (cART) initiation, two of three cases experienced an increased CD4 + count, coinciding with HCV viral clearance. All patients were IL28B CC carriers, 2 were co-infected with HCV genotype 3 (the HCV genotype of the remaining patient was not available).

          Conclusions

          Spontaneous clearance of CHC is a rare event in the context of HIV/HCV co-infected patients and may be associated with the effective use of cART and thus HIV suppression.

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          Most cited references15

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          Innate and Adaptive Immune Regulation During Chronic Viral Infections.

          Elina I. Zuniga, Monica Macal, Gavin Lewis … (2015)
          Chronic viral infections represent a unique challenge to the infected host. Persistently replicating viruses outcompete or subvert the initial antiviral response, allowing the establishment of chronic infections that result in continuous stimulation of both the innate and adaptive immune compartments. This causes a profound reprogramming of the host immune system, including attenuation and persistent low levels of type I interferons, progressive loss (or exhaustion) of CD8(+) T cell functions, and specialization of CD4(+) T cells to produce interleukin-21 and promote antibody-mediated immunity and immune regulation. Epigenetic, transcriptional, posttranscriptional, and metabolic changes underlie this adaptation or recalibration of immune cells to the emerging new environment in order to strike an often imperfect balance between the host and the infectious pathogen. In this review we discuss the common immunological hallmarks observed across a range of different persistently replicating viruses and host species, the underlying molecular mechanisms, and the biological and clinical implications.
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            Activation of natural killer cells during acute infection with hepatitis C virus.

            Angelica M Cazaly, Barbara Amadei, Simona Urbani … (2010)
            Natural killer (NK) cells are essential early after infection, not only for viral containment but also for timely and efficient induction of adaptive responses. An inhibitory effect of hepatitis C virus (HCV)-E2 proteins on NK cells has been reported, but the features of NK cell responses in the acute phase of hepatitis C are still largely undefined. Therefore, the aim of this study was to characterize the function and phenotype of NK cells in the acute phase of infection and compare individuals with chronic and self-limited outcomes. Twenty-two individuals with acute HCV infection, 14 with chronic evolution, and 8 with self-limited infection, were studied using NK phenotypic and functional assays. An increased expression of NKG2D on both CD56(bright) and CD56(dim) NK cells was detected in patients with acute HCV, irrespective of the outcome, as compared with healthy controls. Also, interferon gamma production and cytotoxicity by NK cells were higher in individuals with acute HCV infection than in healthy controls. Subset analysis showed increased interferon gamma production in both NK cell subsets carrying group 1 and group 2 HLA-C-specific killer cell immunoglobulin-like receptors. However, increased CD107a was noted only on NK cells expressing the group 1 HLA-C-specific killer cell immunoglobulin-like receptor and was maximal in self-limited infection. Our data show that in the acute phase of HCV infection, NK cells are activated regardless of outcome, with no evidence of a suppressive effect of HCV on NK cell function. 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
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              HCV and HIV co-infection: mechanisms and management.

              Jennifer Y. Chen, Eoin Feeney, Raymond Chung (2014)
              HCV and HIV co-infection is associated with accelerated hepatic fibrosis progression and higher rates of liver decompensation and death compared to HCV monoinfection, and liver disease is a leading cause of non-AIDS-related mortality among HIV-infected patients. New insights have revealed multiple mechanisms by which HCV and HIV lead to accelerated disease progression, specifically that HIV infection increases HCV replication, augments HCV-induced hepatic inflammation, increases hepatocyte apoptosis, increases microbial translocation from the gut and leads to an impairment of HCV-specific immune responses. Treatment of HIV with antiretroviral therapy and treatment of HCV have independently been shown to delay the progression of fibrosis and reduce complications from end-stage liver disease among co-infected patients. However, rates of sustained virologic response with PEG-IFN and ribavirin have been significantly inferior among co-infected patients compared with HCV-monoinfected patients, and treatment uptake has remained low given the limited efficacy and tolerability of current HCV regimens. With multiple direct-acting antiviral agents in development to treat HCV, a unique opportunity exists to redefine the treatment paradigm for co-infected patients, which incorporates data on fibrosis stage as well as potential drug interactions with antiretroviral therapy.
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                Author and article information

                Contributors
                Wenyu Lin: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 4 May 2017
                Publication date Collection: 2017
                Volume: 12
                Issue: 5
                Electronic Location Identifier: e0177141
                Affiliations
                [1 ]Infectious Diseases Unit, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofía de Córdoba, Córdoba, Spain
                [2 ]Infectious Diseases and Microbiology Unit, Hospital La Línea, AGS Campo de Gibraltar, Cádiz, Spain
                Harvard Medical School, UNITED STATES
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                • Conceptualization: ARJ FT AR.

                • Data curation: MF MPP AC IM SLM PLL AR.

                • Formal analysis: MF ARJ FT MPP IM SLM PLL AR.

                • Funding acquisition: AC AR.

                • Investigation: MF ARJ FT MPP AC SLM AR.

                • Methodology: MF ARJ FT AC IM AR.

                • Project administration: ARJ AR.

                • Software: MF ARJ.

                • Supervision: ARJ FT AR.

                • Validation: ARJ FT AR.

                • Writing – original draft: MF ARJ AR.

                • Writing – review & editing: MF ARJ AR FT MPP AC IM SLM PLL AR.

                ¶ Membership of the Grupo de Estudio de Hepatitis Virales (HEPAVIR) of the Sociedad Andaluza de Enfermedades Infecciosas (SAEI) is provided in the Acknowledgments.

                Author information
                http://orcid.org/0000-0001-5005-8268
                Article
                Publisher ID: PONE-D-17-06896
                DOI: 10.1371/journal.pone.0177141
                PMC ID: 5417670
                PubMed ID: 28472191
                SO-VID: f4b86429-631f-4d86-a370-8ef224047701
                Copyright © © 2017 Frias et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 20 February 2017
                Date accepted : 21 April 2017
                Page count
                Figures: 1, Tables: 1, Pages: 8
                Funding
                Funded by: Spanish AIDS Research Network (RIS)
                Award ID: RD16/0025/0034
                Award Recipient :
                ORCID: http://orcid.org/0000-0001-5005-8268
                Funded by: Fundación Progreso y Salud de la Junta de Andalucía
                Award ID: PI0187/2013
                Award Recipient :
                Funded by: Fundación para la Investigación en Salud del Instituto de Salud Carlos III
                Award ID: PI15/01017
                Award Recipient :
                ORCID: http://orcid.org/0000-0001-5005-8268
                Funded by: Consejería de Salud de la Junta de Andalucía
                Award ID: A-0025-2016
                Award Recipient :
                ORCID: http://orcid.org/0000-0001-5005-8268
                This work was supported by the SPANISH AIDS Research Network (RIS) RD16/0025/0034-ISCIII-FEDER, Fundación Progreso y Salud de la Junta de Andalucía (0187/2013), and Fundación para la Investigación en Salud del Instituto de Salud Carlos III (PI15/01017). A.R is the recipient of a Research Support grant from the Consejería de Salud de la Junta de Andalucía (A-0025-2016). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology and life sciences
                Subject: Organisms
                Subject: Viruses
                Subject: RNA viruses
                Subject: Flaviviruses
                Subject: Hepacivirus
                Subject: Hepatitis C virus
                Subject: Biology and life sciences
                Subject: Microbiology
                Subject: Medical microbiology
                Subject: Microbial pathogens
                Subject: Viral pathogens
                Subject: Flaviviruses
                Subject: Hepacivirus
                Subject: Hepatitis C virus
                Subject: Medicine and health sciences
                Subject: Pathology and laboratory medicine
                Subject: Pathogens
                Subject: Microbial pathogens
                Subject: Viral pathogens
                Subject: Flaviviruses
                Subject: Hepacivirus
                Subject: Hepatitis C virus
                Subject: Biology and life sciences
                Subject: Organisms
                Subject: Viruses
                Subject: Viral pathogens
                Subject: Flaviviruses
                Subject: Hepacivirus
                Subject: Hepatitis C virus
                Subject: Biology and life sciences
                Subject: Microbiology
                Subject: Medical microbiology
                Subject: Microbial pathogens
                Subject: Viral pathogens
                Subject: Hepatitis viruses
                Subject: Hepatitis C virus
                Subject: Medicine and health sciences
                Subject: Pathology and laboratory medicine
                Subject: Pathogens
                Subject: Microbial pathogens
                Subject: Viral pathogens
                Subject: Hepatitis viruses
                Subject: Hepatitis C virus
                Subject: Biology and life sciences
                Subject: Organisms
                Subject: Viruses
                Subject: Viral pathogens
                Subject: Hepatitis viruses
                Subject: Hepatitis C virus
                Subject: Biology and Life Sciences
                Subject: Microbiology
                Subject: Virology
                Subject: Viral Transmission and Infection
                Subject: Viral Load
                Subject: Biology and Life Sciences
                Subject: Microbiology
                Subject: Medical Microbiology
                Subject: Microbial Pathogens
                Subject: Viral Pathogens
                Subject: Immunodeficiency Viruses
                Subject: HIV
                Subject: Medicine and Health Sciences
                Subject: Pathology and Laboratory Medicine
                Subject: Pathogens
                Subject: Microbial Pathogens
                Subject: Viral Pathogens
                Subject: Immunodeficiency Viruses
                Subject: HIV
                Subject: Biology and Life Sciences
                Subject: Organisms
                Subject: Viruses
                Subject: Viral Pathogens
                Subject: Immunodeficiency Viruses
                Subject: HIV
                Subject: Biology and Life Sciences
                Subject: Organisms
                Subject: Viruses
                Subject: Immunodeficiency Viruses
                Subject: HIV
                Subject: Biology and life sciences
                Subject: Organisms
                Subject: Viruses
                Subject: RNA viruses
                Subject: Retroviruses
                Subject: Lentivirus
                Subject: HIV
                Subject: Biology and Life Sciences
                Subject: Microbiology
                Subject: Medical Microbiology
                Subject: Microbial Pathogens
                Subject: Viral Pathogens
                Subject: Retroviruses
                Subject: Lentivirus
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                Subject: Medicine and Health Sciences
                Subject: Pathology and Laboratory Medicine
                Subject: Pathogens
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                Subject: Retroviruses
                Subject: Lentivirus
                Subject: HIV
                Subject: Biology and Life Sciences
                Subject: Organisms
                Subject: Viruses
                Subject: Viral Pathogens
                Subject: Retroviruses
                Subject: Lentivirus
                Subject: HIV
                Subject: Medicine and health sciences
                Subject: Diagnostic medicine
                Subject: HIV diagnosis and management
                Subject: Medicine and Health Sciences
                Subject: Gastroenterology and Hepatology
                Subject: Liver Diseases
                Subject: Chronic Liver Disease
                Subject: Chronic Hepatitis
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Vaccination and Immunization
                Subject: Antiviral Therapy
                Subject: Antiretroviral Therapy
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Vaccination and Immunization
                Subject: Antiviral Therapy
                Subject: Antiretroviral Therapy
                Subject: Medicine and Health Sciences
                Subject: Public and Occupational Health
                Subject: Preventive Medicine
                Subject: Vaccination and Immunization
                Subject: Antiviral Therapy
                Subject: Antiretroviral Therapy
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Biology and Life Sciences
                Subject: Microbiology
                Subject: Virology
                Subject: Viral Transmission and Infection
                Subject: Viral Clearance
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