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Neurologic diseases associated with human T-cell lymphotropic virus type I (HTLV-I) infection have a clinical spectrum that includes myelopathy (HTLV-I-associated myelopathy/tropical spastic paraparesis, HAM/TSP) as the central manifestation. Many clinical signs of involvement outside the central nervous system (CNS) have been described in some patients with HAM/TSP and have triggered and advanced the discovery of some HTLV-I-associated concepts in HTLV-I-infected individuals without signs of CNS involvement. Most of these HTLV-I-associated diseases exhibit common viroimmunologic characteristics that include a distributional bias of HTLV-I activation between the blood flow and the affected lesions and accumulated cellular immune responses in the lesions. These facts suggest that the vulnerable tissue(s) in some HTLV-I-infected individuals may not be defined by an exclusive tissue specificity, but that common steps of HTLV-I-versus-host interactions may have an important role in the pathologic process(es) in these diseases. This review summarizes the recent perspectives of the clinical spectrum and the pathogenesis of HAM/TSP in Japan. Furthermore, the feasible pathogenic involvement of cellular interactions between infected cells and responding immunocompetent cells in the affected tissues is emphasized.