Immunopathogenesis of Human T-Cell Leukemia Virus Type-1-Associated Myelopathy/Tropical Spastic Paraparesis: Recent Perspectives

Figure 1

Hypothesis for the pathogenesis of human T-cell leukemia virus type-1 (HTLV-1) -associated myelopathy/tropical spastic paraparesis (HAM/TSP). Accumulating evidence suggests that the virus-host immunologic interactions play a pivotal role in HAM/TSP pathogenesis. Genetically determined less efficient CTL response against HTLV-1 may cause higher proviral load and antigen expression in infected individuals, which lead 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-react with heterogeneous nuclear ribonuclear protein-A1 (hnRNP-A1), is associated with subsequent inflammation following initial tissue damage.