부산대학교 도서관

OBJECTIVES:: The absence of direct clinical symptoms clearly associated to HTLV-2 infection may partially explain an underestimate of the real HTLV-2 prevalence rate and its effects in patients concurrently infected with HIV-1 and hepatitis C virus (HCV). Hence, to date, the influence of HTLV-2 on hepatic fibrosis has been poorly studied. DESIGN:: Retrospective study to clarify the influence of HTLV-2 infection in HCV infection and hepatic fibrosis among patients co-infected with HIV-1. METHODS:: This is a comparative cohort study including 39 HTLV-2–HIV-1–HCV co-infected patients and 42 HIV-1–HCV co-infected patients conducted in a tertiary care hospital. They were evaluated for transaminase levels, hepatic fibrosis stage, interleukin (IL)-28B genotype, Th1/Th2/Th17 cytokine levels, immune activation, inflammation, and microbial translocation. RESULTS:: HTLV-2–HIV-1–HCV co-infected patients had lower alanine aminotransferase levels (P = 0.023) and hepatic fibrosis (P = 0.012), compared to HIV-1–HCV co-infected patients. Moreover, Kaplan–Meier survival analysis showed a delay in hepatic fibrosis development for up to 5 years (P = 0.032). HTLV-2–HIV-1–HCV co-infected patients also had higher Th1/Th2 ratio (interferon γ/IL-4 ratio, P = 0.043; tumor necrosis factor α/IL-4 ratio, P = 0.010) and Th17 response (P = 0.015), whereas lower CD8 T-cell activation (P = 0.017) and lipopolysaccharide level (P = 0.001). CONCLUSION:: Findings strongly support that HTLV-2 co-infection might delay fibrosis development in HCV–HIV-1 co-infected patients.