p 130: the role of host t- cell lymphocyte in immunopathogenesis of htlv-i-associated myelopathy/tropical spastic paraparesis

human t-cell lymphotropic virus type 1 (htlv-1) is associated with adult t-cell leukemia/lymphoma (atl) and htlv-1-associated myelopathy/tropical spastic paraparesis (ham/tsp). only a limited percentage of infected individuals develop disease in response to the virus while the majority remain asymptomatic and ham/tsp is the most common clinical manifestation of the virus. ham/tsp is an inflammatory disease of the central nervous system (cns). the mechanism by which htlv-1 induces ham/tsp is not clear yet. several factors have been hypothesized to contribute to an htlv-i-infected individual’s progress to ham/tsp. one of the most important factors is the host immune response against htlv-i and t cell lymphocytes plays a key role in the immune response against htlv1 virus. htlv1 attacks different types of cells in the body but cd4(+) t lymphocytes are the main target of htlv-1 that have an important role in the immunological response to this retrovirus. htlv-i-infected cd4+ t lymphocytes migrate to the cns tissues and cd8+ htlv-i specific cytotoxic t lymphocyte (ctl) attack htlv-i-infected lymphocytes. recent data indicate that htlv-i and its expression are localized in infiltrated lymphocytes within the spinal cord lesions of ham/tsp patients rather than in resident central nervous system (cns) parenchymal cells. hyperactive cd8(+) cytotoxic t lymphocytes (ctl) that generate in response to htlv-i-infected lymphocytes likely play a key role in the genesis of pathologic abnormalities associated with ham/tsp and also a high htlv-i proviral load in peripheral blood lymphocytes (pbl) increase this pathological response and cause spinal cord lesions in ham/tsp patients. although the exact mechanism underlying the high htlv-i proviral load in pbl in ham/tsp patients is still unknown, we must consider therapeutic approaches in ham/tsp that eliminate htlv-i-infected cd4+ t lymphocytes and also the regulation of efficiency and activity of hyperactive cd8 (+) cytotoxic t lymphocyte (ctl).