Pathogenesis: Co-Infection and Other Viruses
Thursday, 1:30 - 3:30 pm
Background: Human T-cell lymphotropic virus (HTLV)-2 is prevalent among HIV-infected intravenous drug users. It has been suggested that HTLV-2 could play a protective role in HIV disease progression. The aim of this study was to analyzed immunological and virological parameters in a group of HIV+/HTLV-2+ patients.
Methods: Thirty HIV-mono-infected patients and 25 HIV+ subjects co-infected with HTLV-2 were examined. All patients were naïve for antiretroviral therapy. HIV-specific CD8+ cytoxic T lymphocyte (CTL) cells were measured using an interferon-γ (INF-γ) assay in response to 125 optimally defined peptides divided into 5 pools according to the protein of origin. Immune activation was evaluated by measuring levels of CD38 expression on different CD4+ and CD8+ T-cell subsets. In a subgroup of patients, the production of MIP-1b was also examined in parallel with INF-γ in response to Gag peptides.
Results: The mean CD4 count was similar in both groups of patients. However, a significantly lower HIV load was found in HIV+/HTLV-2+ patients. CD38 expression on total CD8+ T cells and in the naïve subset was significantly lower in co-infected patients. CTL levels against each pool of peptides and total CTL responses were similar in both groups, as was the contribution of each pool to the total CTL response. When analyzing in parallel the production of INF-γ and MIP-1b, we found that MIP-1b(+)/INF-g(-) were the cells that most contributed to the HIV-Gag specific CTL response in HIV/HTLV-2 co-infected patients, while in HIV-mono-infected patients the response was largely dominated by MIP-1b(+)/INF-g(+) cells.
Conclusions: HTLV-2 co-infection may exert a protective role on HIV disease progression by lowering HIV replication and immune activation. A predominance of MIP-1b-producing HIV-specific cells in co-infected patients could contribute to reduced HIV replication.
Keywords: HIV/HTLV-2 coinfection; CTL response; MIP-1beta