Open Access
Article
Role of resident CNS cell populations in HTLV-1-associated neuroinflammatory disease
Veronique Lepoutre1,Pooja Jain1,Kevin Quann1,Brian Wigdahl1,Zafar K Khan1
1
Department of Microbiology and Immunology, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Philadelphia, Pennsylvania 19102, USA
DOI: 10.2741/3300 Volume 14 Issue 3, pp.1152-1168
Published: 01 January 2009
(This article belongs to the Special Issue Molecular mechanisms of neurological disorders)
Abstract

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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Veronique Lepoutre, Pooja Jain, Kevin Quann, Brian Wigdahl, Zafar K Khan. Role of resident CNS cell populations in HTLV-1-associated neuroinflammatory disease. Frontiers in Bioscience-Landmark. 2009. 14(3); 1152-1168.