Genetic control and dynamics of the cellular immune response to the human T–cell leukaemia virus, HTLV–I

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Abstract
About 1% of people infected with the human T–cell leukaemia virus, type 1 (HTLV–I) develop a disabling chronic inflammatory disease of the central nervous system known as HTLV–I–associated myelopathy/tropical spastic paraparesis (HAM/TSP). Patients with HAM/TSP have a vigorous immune response to HTLV–I, and it has been widely suggested that this immune response, particularly the HTLV–I–specific cytotoxic T–lymphocyte (CTL) response, causes the tissue damage that is seen in HAM/TSP. In this paper we summarize recent evidence that a strong CTL response to HTLV–I does in fact protect against HAM/TSP by reducing the proviral load of HTLV–I. We conclude that HTLV–I is persistently replicating at a high level, despite the relative constancy of its genome sequence. These results imply that antiretroviral drugs could reduce the risk of HAM/TSP by reducing the viral load, and that an effective anti–HTLV–I vaccine should elicit a strong CTL response to the virus. The dynamic nature of the infection also has implications for the epidemiology and the evolution of HTLV–I.