Liver Fibrosis Linked to HCV Progression in HIV-Coinfected Patients
Microbial translocation and liver fibrosis are primary mediators of immune activation in patients with human immunodeficiency virus (HIV) monoinfection and hepatitis C virus (HCV) monoinfection, respectively, according to a recent study.
These findings could especially have implications among individuals with HIV/HCV coinfection who, as a result, may have the highest risk of progression, the authors of the study said.
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For their study, the researchers evaluated 120 patients with HIV/HCV coinfection, 262 with HIV monoinfection, 72 with HCV monoinfection, and 170 without infection.
Using multivariable linear regression, the researchers investigated whether intestinal fatty acid binding protein (I-FABP)—a marker of gut epithelial integrity—and transient elastography-measured liver fibrosis affects the association of HIV and HCV with elevated soluble CD14 (sCD14) levels.
Adjusted findings revealed independent associations of HIV and HCV with an elevated sCD14 level. Specifically, it was found that “microbial translocation contributes to an increased sCD14 level during HIV infection, whereas liver fibrosis plays a stronger role during HCV monoinfection,” the researchers wrote.
HIV/HCV coinfection, HIV monoinfection, and HCV monoinfection were found to be associated with 37%, 21%, and 12% higher sCD14 levels, respectively, compared with individuals without infection.
“Coinfected persons may be at greatest risk for progression, because of the independent effects of microbial translocation and liver fibrosis on immune activation,” the researchers concluded.
“Because immune activation has been associated with HIV and HCV disease progression, our findings highlight the importance of treating both HIV and HCV infection to curb immune activation and its clinical sequelae in patients with either or both infections.”
—Christina Vogt
Reference:
Reid M, Ma Y, Scherzer R, et al. Contribution of liver fibrosis and microbial translocation to immune activation in persons infected with HIV and/or hepatitis C virus. J Infect Dis. 2018;217(8):1289-1297. https://doi.org/10.1093/infdis/jix688
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