Fig. 1.

Proposed model of the immunopathology in human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis: bystander neural damage. HTLV-1-infected CD4⁺ T cells proliferate in the periphery and circulate in HTLV-1-infected individuals. The infected cells invade the central nervous system across the blood-brain barrier and express viral antigens. HTLV-1-specific cytotoxic T lymphocytes (CTL) are activated and expanded on stimulation by the HTLV-1 antigens and accumulate in the spinal cord. The CTL recognize viral antigens presented by human leukocyte antigen class I molecules on the infiltrating HTLV-1-infected CD4⁺ T cells, leading to the secretion of proinflammatory cytokines, such as interferon-γ and tumor necrosis factor-α. HTLV-1-specific inflammation mediated by the interaction of HTLV-1-infected CD4⁺ T cells with HTLV-1-specific CTL causes apoptosis in adjacent neural cells (bystander damage) in the CNS, resulting in tissue destruction and degeneration. BBB, blood-brain barrier