1. HTLV‐1 and Neurological‐Associated Disease
- Author
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Philippe V. Afonso, Antoine Gessain, Olivier Cassar, Epidémiologie et Physiopathologie des Virus Oncogènes / Oncogenic Virus Epidemiology and Pathophysiology (EPVO (UMR_3569 / U-Pasteur_3)), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Fabrice Chretien, Kum Thong Wong, Leroy R. Sharer, Katy Keohane, Francoise Gray, International Society of Neuropathology, and Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)
- Subjects
0303 health sciences ,business.industry ,virus diseases ,Disease ,3. Good health ,03 medical and health sciences ,0302 clinical medicine ,immune system diseases ,[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology ,Immunology ,Medicine ,business ,030217 neurology & neurosurgery ,030304 developmental biology - Abstract
International audience; Human T-cell leukemia/lymphoma virus-1 (HTLV-1), the first human oncoretrovirus, is the etiological agent of a chronic neuromyelopathy named “tropical spastic paraparesis/HTLV-1–associated myelopathy (TSP/HAM). At least 5–10 million individuals are infected worldwide. The areas of highest prevalence are southwestern Japan and parts of the Caribbean, South America, intertropical Africa, and the Middle East. The lifetime risk of developing TSP/HAM in HTLV-1 carriers is estimated at 0.25–4%, depending on the endemic area. The neurological characteristics include spasticity or hyper-reflexia of the lower limbs, urinary bladder disturbances often with lower limb muscle weakness, sensory disturbance, and low back pain. TSP/HAM pathology is characterized by chronic inflammation with perivascular lymphocyte cuffs and mild parenchymal lymphocytic infiltrates, foamy macrophages, astrocyte proliferation, and fibrillary gliosis. Pyramidal tract degenerative lesions with myelin and axonal loss are observed, mainly in the lower thoracic spinal cord; these are linked to inflammatory foci in the CNS. The treatment of TSP/HAM remains largely symptomatic because there is no current disease-modifying therapy with definite long-term clinical benefit.
- Published
- 2020