Human immunodeficiency virus (HIV) and hepatitis C virus (HCV) are independently and additively associated with higher sCD14, suggesting that microbial translocation contributes to sCD14 elevations in HIV infection, whereas liver fibrosis plays a role in HCV monoinfection. This according to a study that examined the independently contribution of liver fibrosis and microbial translocation to immune activation in HIV and HCV. Multivariable linear regression was used to evaluate whether intestinal fatty acid binding protein (I-FABP) and transient elastography-measured liver fibrosis might mediate the association of HIV and HCV with sCD14 in 120 HIV+/HCV+, 262 HIV+/HCV-, 72 HIV/HCV+, and 170 HIV-/HCV-. Researchers found:
- HIV+/HCV+, HIV+/HCV-, and HIV-/HCV+ had 37%, 21%, and 12% higher sCD14 levels than HIV-/HCV- after multivariable adjustment.
- Additional adjustment for I-FABP modestly attenuated the association of HIV infection, but to a lesser extent in HIV-/HCV+.
- Adjustment for liver fibrosis substantially attenuated the association of HCV infection, but to a lesser extent in HIV+/HCV-.
Reid M, Ma Y, Scherzer R, et al. Contribution of liver fibrosis and microbial translocation to immune activation in HIV and HCV. [Published online ahead of print January 3, 2018]. J Infect Dis. doi:10.1093/infdis/jix688.