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Figure 1: Hypothesis for the pathogenesis of Human T-cell leukemia virus type 1- (HTLV-1-)associated myelopathy/tropical spastic paraparesis (HAM/TSP). In patients with HAM/TSP, genetically determined less efficient CTL response against HTLV-1 may cause higher proviral load and antigen expression, leading in turn to activation and expansion of antigen-specific T cell responses, subsequent induction of large amounts of proinflammatory cytokines and chemokines, and progression of HAM/TSP development. It is also possible that the immunoglobulin G specific to HTLV-1-Tax, which cross-reacts with heterogeneous nuclear ribonuclear protein-A1 (hnRNP-A1), is associated with subsequent inflammation following initial tissue damage.