A new hypothesis for the pathogenesis of Human T-lymphotropic virus type 1 associated myelopathy/tropical spastic paraparesis |
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Authors: | Angelina J Mosley |
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Institution: | a Department of Neuroinflammation, UCL Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK b Department of Immunology, Wright-Fleming Institute, Imperial College London, Norfolk Place, London W2 1PG, UK |
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Abstract: | The exogenous, human retrovirus Human T-lymphotropic virus type 1 (HTLV-1) results in a highly dynamic persistent infection. HTLV-1 usually causes an asymptomatic infection but a small proportion of individuals may develop HTLV-1 associated myelopathy/ tropical spastic paraparesis (HAM/TSP). HAM/TSP is a chronic inflammatory disease of the central nervous system (CNS) that is rarely fatal, but can be severely debilitating. HTLV-1 is found in the CNS primarily within infiltrating, infected CD4+ T lymphocytes. CD4+ T-cell infiltration into the CNS is currently believed to be the pivotal event for the pathogenesis of HAM/TSP but the exact mechanisms by which these T cells result in neurological damage are unknown. Here we explore a current hypothesis of HAM/TSP pathogenesis and suggest a new hypothesis focused on why the majority of HTLV-1-infected individuals do not develop neuroinflammatory disease. In this new hypothesis we highlight the two battles for control over HTLV-1 activity that occur in the peripheral blood and the CNS. We also introduce the idea that HAM/TSP is the result of a disturbed damage:healing ratio within the spinal cord that is dependent on the activity of HTLV-1 proteins, glia and infiltrating immune cells. |
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Keywords: | HTLV-1 HAM/TSP Pathogenesis CD8 CD4 Central nervous system |
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