Baseline levels of soluble CD14 and CD16⁺56^- natural killer cells are negatively associated with response to interferon/ribavirin therapy during HCV-HIV-1 coinfection

Disease progression of human immunodeficiency virus type 1 (HIV-1) is associated with immune activation. Activation indices are higher during coinfection of hepatitis C virus (HCV) and HIV. The effect of immune activation on interferon (IFN-) therapy response is unknown. We evaluated soluble CD14 (sCD14) and natural killer (NK)-cell subsets at baseline, and during pegIFN-2a/ribavirin therapy in HCV-HIV coinfection. The sCD14 level increased during therapy. Baseline sCD14 positively correlated with baseline HCV level and CD16⁺56^- NK-cell frequency, and both sCD14 and CD16 ⁺56^- NK cells correlated negatively with magnitude of HCV decline. IL28B genotype was associated with therapy response but not sCD14 or CD16⁺56^- NK frequency. Markers of innate immune activation predict poor host response to IFN-based HCV therapy during HCV-HIV coinfection.