Delayed liver fibrosis in HTLV-2-infected patients co-infected with HIV-1 and hepatitis C virus with suppressive antiretroviral therapy. (20th February 2015)

• Record Type: Journal Article
• Authors: Abad-Fernández, María; Moreno, Ana; Dronda, Fernando; del Campo, Santos; Quereda, Carmen; Casado, José Luis; Pérez-Elías, María-Jesús; Moreno, Santiago; Vallejo, Alejandro
• Is Part Of: AIDS. Volume 29:Number 4(2015)
• Publication Date: 2015-02-20
• Subjects: IL-6 level -- immune activation -- microbial translocation -- Th1/Th2 ratio -- Th17 response; AIDS (Disease) -- Periodicals; Acquired Immunodeficiency Syndrome; AIDS (Disease); Periodicals; Periodicals; 616.9792005
• DOI: 10.1097/QAD.0000000000000555
• Languages: English
• ISSNs: 0269-9370

Abstract

Abstract : 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. Abstract : Supplemental Digital Content is available in the text