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Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 28, 2016; 22(4): 1433-1448
Published online Jan 28, 2016. doi: 10.3748/wjg.v22.i4.1433
Gut epithelial barrier dysfunction in human immunodeficiency virus-hepatitis C virus coinfected patients: Influence on innate and acquired immunity
Mercedes Márquez, Clotilde Fernández Gutiérrez del Álamo, José Antonio Girón-González
Mercedes Márquez, Clotilde Fernández Gutiérrez del Álamo, José Antonio Girón-González, Department of Internal Medicine, Infectious Disease Unit, Puerta del Mar University Hospital, University of Cadiz, 11009 Cádiz, Spain
José Antonio Girón-González, Servicio de Medicina Interna, Hospital Universitario Puerta del Mar, 11009 Cádiz, Spain
Author contributions: Márquez M and Fernández Gutiérrez del Álamo C performed the bibliographic research, analyzed data and wrote the paper; Girón-González JA designed research, analyzed data and wrote the paper.
Supported by Instituto de Salud Carlos III, Plan Nacional de I+D+I 2008-2011, No. PI11/00605 and Plan Estatal de I+D+I 2013-2016, No. PI14/01779; Co-financed by FEDER (Fondo Europeo de Desarrollo Regional).
Conflict-of-interest statement: All authors declare no conflict 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/
Correspondence to: José Antonio Girón-González, MD, PhD, Department of Internal Medicine, Infectious Disease Unit, Puerta del Mar University Hospital, University of Cadiz, Avda Ana de Viya 21, 11009 Cádiz, Spain. joseantonio.giron@uca.es
Telephone: +34-95-6002879
Received: May 14, 2015
Peer-review started: May 15, 2015
First decision: August 31, 2015
Revised: October 11, 2015
Accepted: November 13, 2015
Article in press: November 13, 2015
Published online: January 28, 2016
Abstract

Even in cases where viral replication has been controlled by antiretroviral therapy for long periods of time, human immunodeficiency virus (HIV)-infected patients have several non-acquired immunodeficiency syndrome (AIDS) related co-morbidities, including liver disease, cardiovascular disease and neurocognitive decline, which have a clear impact on survival. It has been considered that persistent innate and acquired immune activation contributes to the pathogenesis of these non-AIDS related diseases. Immune activation has been related with several conditions, remarkably with the bacterial translocation related with the intestinal barrier damage by the HIV or by hepatitis C virus (HCV)-related liver cirrhosis. Consequently, increased morbidity and mortality must be expected in HIV-HCV coinfected patients. Disrupted gut barrier lead to an increased passage of microbial products and to an activation of the mucosal immune system and secretion of inflammatory mediators, which in turn might increase barrier dysfunction. In the present review, the intestinal barrier structure, measures of intestinal barrier dysfunction and the modifications of them in HIV monoinfection and in HIV-HCV coinfection will be considered. Both pathogenesis and the consequences for the progression of liver disease secondary to gut microbial fragment leakage and immune activation will be assessed.

Keywords: Human immunodeficiency virus infection, Hepatitis C virus infection, Innate immunity, Acquired immunity, Gut barrier

Core tip: Even in patients with a long-term controlled human immunodeficiency virus (HIV) replication by antiretroviral therapy, HIV-infected patients have several non-acquired immunodeficiency virus (AIDS) related co-morbidities, including liver disease. Persistent innate and acquired immune activation contributes to the pathogenesis of these non-AIDS related diseases. Immune activation has been related with bacterial translocation secondary to gut barrier damage by the HIV or the hepatitis C virus (HCV)-related liver cirrhosis. Modifications in gut barrier structure and function and immune activation in HIV-HCV coinfected patients will be reviewed.