HLA-B18 as a risk factor of short-term progression to severe liver fibrosis in HIV/HCV co-infected patients with absent or minimal fibrosis: implications for timing of therapy

Abstract

Our aim was to analyze the influence of HLA-B haplotypes on liver fibrosis progression in HIV/hepatitis C virus (HCV) co-infected patients. Retrospective longitudinal study including HIV/HCV, non-cirrhotic and HCV treatment-naïve patients. The main outcome variable was liver fibrosis progression of at least one stage. One hundred and four patients constituted the study population (F0–F1: 62 (59.6%); F2: 22 (21.2%); F3: 20 (19.2%)). During a median follow-up of 54.5 months (IQR: 26.2–77), 45 patients (43.3%) showed an increase in the stage of liver fibrosis (time to event: 29 (IQR: 14–49.5) months). HLA-B18pos patients more frequently had a higher and faster fibrosis progression rate (73.3%; 24 (IQR: 8–29) months) than HLA-B18neg patients (38.2%; 34.5 (IQR: 14.7–51.2) months). This association was also observed in the development of F3–F4 fibrosis among F0–F2 patients (HLA-B18pos: 69.2%; 18 (6.5–37) months vs HLA-B18neg: 28.2%; 37 (IQR: 19–52) months). These results could impact the timing of HCV therapy in F0–F2 patients.