“
“Retroviral co-infections with human immunodeficiency virus type-1 (HIV-1) and human T cell leukaemia Poziotinib mouse virus type 1 (HTLV-1) or type 2 (HTLV-2) are prevalent in many areas worldwide. It has been observed that HIV-1/HTLV-2 co-infections are associated with slower rates of CD4+ T cell decline and delayed progression to AIDS. This immunological benefit has been linked to the ability of Tax2, the transcriptional activating protein of HTLV-2, to induce the expression of macrophage inflammatory protein (MIP)-1α/CCL3, MIP-1β/CCL4 and regulated upon activation normal T cell expressed and secreted (RANTES)/CCL5 and to down-regulate the expression of the CCR5 co-receptor

in peripheral blood mononuclear cells (PBMCs). This study aimed to assess the role of Tax2-mediated activation of the nuclear factor kappa B (NF-κB) signalling pathway on the production of the anti-viral CC-chemokines MIP-1α, MIP-1β and RANTES. Recombinant Tax1 and Tax2 proteins, or proteins expressed www.selleckchem.com/products/azd3965.html via adenoviral vectors used to infect cells, were tested for their ability to activate the NF-κB pathway in cultured PBMCs in the presence or absence of NF-κB pathway inhibitors. Results showed a significant release of MIP-1α, MIP-1β and RANTES by PBMCs after the activation of p65/RelA

and p50. The secretion of these CC-chemokines was significantly reduced (P < 0·05) by canonical NF-κB signalling inhibitors. In conclusion, Tax2 protein may promote Florfenicol innate anti-viral immune responses through the activation of the canonical NF-κB pathway. The human T cell leukaemia viruses types 1 and 2 (HTLV-1, HTLV-2) infect approximately 15–25 million individuals worldwide [1]. Both viruses have similar biological properties,

genomic structures and tropism for immune cells, and they establish lifelong infection in their hosts with rare expression of clinical disease [2]. The neurological disorder HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) [3, 4], adult T cell leukaemia (ATL) [5, 6] and inflammatory diseases [7-9] have been reported in 3–5% of individuals infected with HTLV-1. In contrast, HTLV-2 has not been linked clearly to any disease, although long-term carriers of HTLV-2 have subtle alterations in their immunological phenotypes [10]. Due to common modes of retroviral transmission [11], co-infections with human immunodeficiency virus type 1 (HIV-1) and HTLV-1 or HIV-1 and HTLV-2 are prevalent in many metropolitan areas in the United States and worldwide (reviewed recently in [12]). In the absence of therapy, HIV-1 results in massive depletion of CD4+ T cells, with development of severe immunodeficiency and death from opportunistic infections.