Published online Jan 28, 2016. doi: 10.3748/wjg.v22.i4.1433
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
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.
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.