Human T lymphotropic virus type I(HTLV-I) is associated with the nonfatal neurologic disease, HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Many clinical signs of involvement outside the central nervous system (CNS) have been described in some patients with HAM/TSP and have triggered the discovery of some HTLV-I-associated concepts in the infected individuals without signs of CNS involvement. Most of these HTLV-I-associated diseases exhibit common possible 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. This review summarizes the recent perspectives of the molecular pathogenesis of HAM/TSP and other HTLV-I-associated diseases. Furthermore, the feasible pathogenic involvement of cellular interactions between infected cells and responding immunocompetent cells in the affected tissues is emphasized (bystander auto-aggressiveness).