Systemic in ammation and immune dysregulation: role in the pathogenesis of HIV / HCV coinfection

Abstract

The immune dysfunction associated with Human Immunodeficiency Virus (HIV) infection is generated by a chronic stimulation of the immune system, because of the inability to eradicate the virus from the host. This immune dysfunction is exacerbated in the context of coinfection with Hepatitis C Virus (HCV). Systemic inflammation caused by coinfection with both viruses generates an increase in morbidity and mortality in affected individuals. There are several soluble mediators of immunological activation, such as IP-10, TNF-α, IL-6, IL-1β (systemic inflammation markers); IL-17 (CD4+ T cells Th17); IL-2, IFN-γ (CD4+ T cells Th1); IL-8 (neutrophilia); CD23s, ICAMs, CD14s, CD163s, lipopolysaccharide (LPS) (monocyte/macrophage activation markers and bacterial translocation); among others. Currently, more studies are needed to define optimal progression biomarkers for the follow-up of HIV/HCV coinfected individuals. In this review, we focus on the immunopathological mechanisms of HIV/HCV infection involved in inflammation, liver damage and its impact on the morbidity and mortality of affected individuals.