Figure 2

Natural course of HTLV-I infection to onset of ATL. HTLV-I is transmitted via three routes, and infected cells are necessary in all three. After infection, HTLV-I promotes clonal proliferation of infected cells by pleiotropic actions of Tax. Tax expression is suppressed by viral accessory gene products, such as Rex, p30 and HBZ proteins. Proliferation of HTLV-I infected cells is controlled by cytotoxic T-cells in vivo. After a long latent period, ATL develops in about 5% of asymptomatic carriers. The expression of Tax is inactivated by several mechanisms, suggesting that Tax is not necessary in this stage. Alternatively, alternations in the host genome accumulate during the latent period, finally leading to onset of ATL.