Liver fibrosis, microbial translocation and immune activation markers in HIV and HCV infections and in HIV/HCV co-infection

Background: Liver fibrosis is accelerated in patients co-infected with human immunodeficiency virus and hepatitis C viruses. Aims: We investigated the correlation between liver fibrosis, immune activation and microbial translocation. Methods: This cross-sectional study included patients with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) mono-infections, HIV/HCV co-infection, and healthy controls (20 subjects/group). Peripheral blood was analysed to determine the levels of Forkhead box 3 (Foxp3) T cells, TGF-β1, CD14 (soluble and surface isoforms), IL-17 and bacterial translocation products. These measurements were correlated to the severity of liver fibrosis, measured with the FIB-4 score and transient elastography. Results: Foxp3T cell levels were significantly elevated in HIV mono-infected and co-infected groups (p<. 0.0005). FIB-4 and liver stiffness values inversely correlated with TGF-β1 (p= 0.0155 and p= 0.0498). Bacterial DNA differed significantly in the HIV-positive compared to the other groups: HIV/HCV co-infected subjects had significantly higher serum levels of bacterial translocation products, CD14, and IL-17 levels (p<. 0.001). Conclusions: Fibrosis stage in HIV/HCV co-infection may be influenced by immune activation due either by viral infections or to bacterial translocation.