Impact of HIV co-infection on liver fibrosis regression after HCV treatment

Resumen

Chronic hepatitis C virus (HCV) infection is a major cause of liver cirrhosis and hepatocellular carcinoma, which may lead to liver transplantation. Co-infection with HIV may accelerate liver disease and impact treatment response. Monitoring liver fibrosis involves non-invasive methods such as transient hepatic elastography (THE), AST to Platelet Ratio Index (APRI), and Fibrosis-4 (FIB-4). This study compared changes in THE, APRI, and FIB-4 among patients with HCV alone and those with HIV-HCV co-infection before and after direct-acting antiviral (DAA) therapy. We conducted a retrospective cohort study using medical records from patients treated at a reference clinic in Sao Paulo, Brazil, between January 2015 and February 2019. Fibrosis assessments (THE, APRI, FIB-4) were performed pre-treatment and six months post-treatment. APRI and FIB-4 were also evaluated at 12 months. Among 148 participants, 105 (70%) had HCV mono-infection and 43 (30%) had HIV-HCV co-infection. Genotype 1 was most prevalent (86%). At six months post-treatment, greater reductions in THE, APRI, and FIB-4 were observed in the HCV mono-infection group. Pre-treatment THE values positively correlated with subsequent reductions. However, multivariable analysis showed no significant differences between groups in THE reductions, and no significant group differences in APRI or FIB-4 at six and 12 months. DAA treatment led to fibrosis regression in most participants. HIV co-infection did not significantly alter fibrosis outcomes following successful HCV treatment.