Exploration of the interaction of immune factors in HIV/HCV infection and its impact on the course of disease

Abstract

The aim of this study was to explore the interaction of immune factors in acquired immune deficiency syndrome (AIDS) patients with hepatitis C infection and its effects on immune and liver function. Fasting venous blood was taken from hepatitis C virus (HCV) patients (HCV group), human immunodeficiency virus (HIV)-treated AIDS patients (HIV group), HIV-infected HCV patients (HIV/HCV group), and healthy controls (control group). Enzyme linked immunosorbent assay (ELISA) was used to detect immune factors (IL-10, IL-6, TNF-α) closely related to disease and intestinal microbial translocation products [Lipopolysaccharide (LPS), bacterial lipopolysaccharide binding protein LPS-binding) Protein (LBP), soluble CD14 molecule (soluble CD14, sCD14), intestinal fatty acid binding protein (IFABP), and anti-endotoxin core antibody (EndoCAb)]. Flow cytometry was used to detect the number of peripheral blood CD4+ T cells. The immune factors closely related to the disease after HIV and HCV infection change in microbial translocation products, and correlations between peripheral blood CD4+ T cell counts and immunization, microbial translocation are compared. The results show that the concentrations of immune factors and intestinal microbial translocation products in the peripheral blood of the HIV/HCV group were higher than those in the HIV and HCV groups. HIV and HCV interact with the intestinal microbial translocation products LPS, LBP, sCD14, and IFABP. There were no significant correlations between immune factor and microbial translocation products in the HIV/HCV group and the number of CD4+ T cells in peripheral blood. In conclusion, after HIV is co-infected with HCV, the systemic immune system is activated, releasing a large number of immunostimulatory factors, further damaging the body. Due to the combined effect of HIV and HCV virus, the liver is further damaged, and the degree of damage mainly depends on the degree of HCV infection and microbial displacement.