Influence of HLA-B18 on liver fibrosis progression in a cohort of HIV/HCV co-infected individuals.

Liver fibrosis is accelerated in HIV/HCV co-infected compared with HCV mono-infected patients, due to multiple cofactors. Recently, HLA-B18 haplotype has been associated with short-term liver disease progression in this population. Our aim was to assess the influence of HLA-B18 on the fibrosis process in HIV/HCV co-infected individuals, untreated for HCV, during a long-term follow-up. All consecutive HIV/HCV co-infected patients followed in our Centre, with positive HCV-RNA and available HLA haplotypes (determined by SSO-PCR and SSR-PCR using Luminex Technology) were included. Liver fibrosis progression was assessed by means of Fibrosis-4 Index for Liver Fibrosis (FIB-4) and AST to Platelet Ratio Index (APRI). The association between FIB-4 score over time and laboratory and clinical parameters, including HLA, was evaluated by univariate and multivariate multilevel generalized linear models. A total of 29/148 screened patients were excluded because of spontaneous HCV clearance (27% were HLA-B18+). Among the remaining 119 individuals [82% males; median age at first visit=30 years (IQR 26-35); median follow-up=21.5 years (IQR 15-25)], 26% were HLA B18+. No baseline differences were evidenced between HLA B18+ and B18- patients. Fibrosis progression was significantly faster in HLA B18+ than in HLA B18- patients (p<0.001) (Figure 1). At univariate analysis, age (p<0.001), HLA-B18 haplotype (p=0.02) and HIV-RNA viral load over-time (p<0.001) were associated with liver disease progression. At multivariate analysis, only age (p<0.001) remained independently associated with liver fibrosis progression. Our data suggest a possible association between HLA-B18 and an accelerated liver fibrosis in HIV/HCV co-infected with a long-term follow-up. This article is protected by copyright. All rights reserved.