Delayed liver fibrosis in HTLV-2-infected patients co-infected with HIV-1 and hepatitis C virus with suppressive antiretroviral therapy.

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.