Human T lymphotropic virus type 1 (HTLV-1)
Shila Azodi, Steven Jacobson
Abstract
Shila Azodi, Steven Jacobson
Abstract
Human T cell lymphotropic virus type I (HTLV-I) is the etiologic agent in a progressive neurological disease termed HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HAM/TSP is a chronic inflammatory disease of the central nervous system (CNS) characterized by unremitting myelopathic symptoms such as spastic paraparesis, bowel/bladder dysfunction, and lower limb sensory changes. Similar to other infectious and inflammatory diseases, interplay between host genes and antigen-specific immune responses have been suggested to be involved in the pathogenesis of HTLV-I associated disorders. This review will examine clinical, pathological, and immunological events in HAM/TSP with a particular emphasis on the role of cellular immune responses to HTLV-I in patients with HAM/TSP. This large body of information on HTLV-I pathology, disease association, and cellular immune reactivity has set the framework for our understanding of HAM/TSP pathogenesis. Importantly, these observations give a rationale for immunotherapeutic strategies in attempts to clinically intervene in this disease. Moreover, mechanisms defined from these HAM/TSP studies may be applied to other neurologic disorders in which antigen-specific host immune responses may also be immunopathogenic such as neuro-AIDS or multiple sclerosis.
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Human T cell lymphotropic virus type I (HTLV-I) is the etiologic agent in a progressive neurological disease termed HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HAM/TSP is a chronic inflammatory disease of the central nervous system (CNS) characterized by unremitting myelopathic symptoms such as spastic paraparesis, bowel/bladder dysfunction, and lower limb sensory changes. Similar to other infectious and inflammatory diseases, interplay between host genes and antigen-specific immune responses have been suggested to be involved in the pathogenesis of HTLV-I associated disorders. This review will examine clinical, pathological, and immunological events in HAM/TSP with a particular emphasis on the role of cellular immune responses to HTLV-I in patients with HAM/TSP. This large body of information on HTLV-I pathology, disease association, and cellular immune reactivity has set the framework for our understanding of HAM/TSP pathogenesis. Importantly, these observations give a rationale for immunotherapeutic strategies in attempts to clinically intervene in this disease. Moreover, mechanisms defined from these HAM/TSP studies may be applied to other neurologic disorders in which antigen-specific host immune responses may also be immunopathogenic such as neuro-AIDS or multiple sclerosis.
Key concepts: Human T-lymphotropic virus, Virology, Virus, Biology, Neuroscience, Myelopathy, Spinal cord