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Role of resident CNS cell populations in HTLV-1-associated neuroinflammatory disease
Journal article   Open access

Role of resident CNS cell populations in HTLV-1-associated neuroinflammatory disease

Veronique Lepoutre, Pooja Jain, Kevin Quann, Brian Wigdahl and Zafar K Khan
Frontiers in bioscience, v 14(3), pp 1152-1168
01 Jan 2009
PMID: 19273122
url
https://doi.org/10.2741/3300View
Published, Version of Record (VoR) Open

Abstract

Central Nervous System - pathology HTLV-I Infections - pathology Muscular Diseases - pathology Human T-lymphotropic virus 1 - isolation & purification Humans Paraparesis, Tropical Spastic - pathology
Human T cell leukemia virus type 1 (HTLV-1), the first human retrovirus discovered, is the etiologic agent for a number of disorders; the two most common pathologies include adult T cell leukemia (ATL) and a progressive demyelinating neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The neurologic dysfunction associated with HAM/TSP is a result of viral intrusion into the central nervous system (CNS) and the generation of a hyperstimulated host response within the peripheral and central nervous system that includes expanded populations of CD4+ and CD8+ T cells and proinflammatory cytokines/chemokines in the cerebrospinal fluid (CSF). This robust, yet detrimental immune response likely contributes to the death of myelin producing oligodendrocytes and degeneration of neuronal axons. The mechanisms of neurological degeneration in HAM/TSP have yet to be fully delineated in vivo and may involve the immunogenic properties of the HTLV-1 transactivator protein Tax. This comprehensive review characterizes the available knowledge to date concerning the effects of HTLV-1 on CNS resident cell populations with emphasis on both viral and host factors contributing to the genesis of HAM/TSP.

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Web of Science research areas
Biochemistry & Molecular Biology
Cell Biology
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