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Differentiation of HAM/TSP from patients with multiple sclerosis infected with HTLV-I

From the Neurological Service (M.P.-S., C.C.F.V., R.P.-A.), Gaffree Guinle University Hospital, Federal University of Rio de Janeiro State, Neurolife Cerebrospinal Fluid Laboratory (M.P.-S.), Instituto Estadual de Hematologia Arthur de S. Cavalcanti, and Neurological Service (C.C.F.V.), Antonio Pedro Hospital, Fluminense Federal University, Rio de Janeiro, Brazil; and Neuroimmunology Branch (Y.Y., S.J.), National Institutes of Neurological Disorders and Stroke, NIH, and Center for Biological Evaluation and Research (M.R.), US Food and Drug Administration, Bethesda, MD.

Address correspondence and reprint requests to Dr. M. Puccioni-Sohler, Rua Dezenove de Fevereiro 185/705, 22280 030, Rio de Janeiro/RJ, Brazil; e-mail: mpuccioni{at}hucff.ufrj.br

Objective: To better differentiate patients with human T lymphotropic virus type I (HTLV-I)–associated myelopathy/tropical spastic paraparesis (HAM/TSP) from patients with multiple sclerosis (MS) who are HTLV-I seropositive, we compared the HTLV-I antibodies and HTLV-I proviral DNA loads in CSF and peripheral blood mononuclear cells (PBMC).

Methods: Intrathecal synthesis of HTLV-I antibodies and HTLV-I proviral DNA loads in CSF and PBMC were measured and compared in 39 Brazilian patients: 17 HAM/TSP and 22 HTLV-I-seropositive non-HAM/TSP (7 with other neurologic diseases, 11 asymptomatic carriers, and 4 HTLV-I-seropositive patients with an MS-like phenotype). In addition, we followed immunologic and virologic markers in comparison to the clinical course (by Kurtzke Expanded Disability Status Scale) of seven patients (five with HAM/TSP and two with an MS-like phenotype) for a mean period of 16 (SD ± 5) months.

Results: The proviral load in CSF and PBMC was higher in HAM/TSP than in non-HAM/TSP patients, except in the two HTLV-I-seropositive patients with an MS-like phenotype that also fulfilled the criteria for HAM/TSP. Higher HTLV-I proviral DNA load in CSF was associated with the higher proviral DNA load in PBMC and lower intrathecal synthesis of HTLV-I antibodies. These laboratory findings remained stable during follow-up.

Conclusion: The high proviral load in peripheral blood mononuclear cells or in CSF or both may be a good marker of human T lymphotropic virus type I (HTLV-I)–associated myelopathy/tropical spastic paraparesis (HAM/TSP) and can differentiate patients with HAM/TSP from patients with multiple sclerosis infected with HTLV-I.

Performed in part as a collaborative research and development agreement between Biogen and NIH and supported by the FAPERJ (Fundação de Amparo a Pesquisa do Rio de Janeiro) and a fellowship from CAPES (Fundação Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, Brazil) to M.P.-S.

Disclosure: The authors report no conflicts of interest.

Received March 27, 2006. Accepted in final form September 29, 2006.