The infected DCs can rapidly transfer HTLV-1 to autologous primary CD4+ T-cells, resulting in a chronic productive infection of CD4+ T cells ex vivo. The DC-T cell transmission of HTLV-1 is reduced by blocking Neuropilin-1 (NP-1) and heparin sulfate proteoglycans (HSPGs) [78], two molecules involved in the initial interaction of HTLV-1 with CD4+ T-cells [82–85] and in the DC-T cell interaction [86,87]. The gene discussed is CD4; the disease is infection.