Infection by HTLV-1 Is Associated With High Levels of Proinflammatory Cytokines in HIV-HCV–Coinfected Patients

Abstract

HIV, hepatitis C virus (HCV), and human T-cell lymphotropic virus type 1 (HTLV-1) share the same routes of infection, making coinfection by these viruses a frequent finding in endemic areas. However, there is scarce information on the clinical/immunological consequences of triple infection. Coinfection by HTLV-1 is able to modulate cytokine's production in patients with HIV, but there are no data on the immune response of HIV-HCV-HTLV-1-infected patients. We compared the plasma levels of 25 different cytokines in patients with HIV-HCV, according to their serostatus to HTLV-1 infection. Eligible patients should be on stable highly active antiretroviral therapy and have undetectable HIV-1 plasma viral load for, at least, 12 months. Cytokines levels were also evaluated by CD4 cells count, rates of sustained virological response (SVR) to previous HCV treatment, frequency of spontaneous HCV clearance, and HCV/IFN-λ3 genotypes. Twenty-five patients (15 coinfected by HIV and HCV, 10 coinfected by HIV, HCV, and HTLV-1) were evaluated. Among the triply infected group, 3 had undetectable HCV viremia (spontaneous clearance). All but one remaining patients were previously treated for HCV, with similar SVR rates (∼29%). Cytokines levels did not differ per HCV/IFN-λ3 genotypes, mean CD4 cells count, age, sex, or SVR. However, patients coinfected by HTLV-1 showed significantly higher levels of IL-1b, IL-2, TNF-α, IFN-γ, MIP-1α, RANTES, and interferon-induced protein 10 (IP-10) than HIV-HCV-coinfected ones. Patients presenting HCV spontaneous clearance had the highest levels of cytokines. Coinfection by HTLV-1 increases the plasma levels of proinflammatory cytokines of patients with HIV-HCV and can influence the outcomes of coinfected patients.