The etiology of HAM/TSP is poorly understood, however it is associated with higher HTLV-1 proviral loads, a higher frequency of HTLV-1-specific CD8+ T-cells and greater production of IFN-γ and TNF-α than that observed in asymptomatic HTLV-1-infected subjects, suggesting the involvement of cellular immune responses in the pathogenesis[5-8]. This evidence concerns the gene CD8A and tropical spastic paraparesis.