Por favor, use este identificador para citar o enlazar este ítem: https://repositorio.bahiana.edu.br:8443/jspui/handle/bahiana/2967
Título : Association of Tuberculosis Status with Neurologic Disease and Immune Response in HTLV-1 Infection
Otros títulos : Aids research and human retroviruses
Autor : Arruda, Sérgio Marcos
Souza, Anselmo
Carvalho, Natália
Neves, Yuri
Santos, Silvane Braga
Astos, Maria de Lourdes B
Martins Netto, Eduardo
Glesby, Marshall J.
Carvalho, Edgar
Palabras clave : HTLV-1; Tuberculosis; Immune response
Fecha de publicación : 2017
Resumen : The human T cell lymphotropic virus type 1 (HTLV-1) is the etiologic agent of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 infected individuals have increased susceptibility to Mycobacterium tuberculosis infection but the influence of tuberculosis (TB) on the course of HTLV-1 infection is unknown. The aim of this study was to evaluate the influence of TB on immunological, virologic, and neurologic features of HTLV-1 infection. This is a retrospective analysis of individuals enrolled in a cohort study from an HTLV-1 clinic who were evaluated for past or latent tuberculosis (LTB) and classified clinically as HTLV-1 carriers, probable HAM/TSP and definite AM/TSP. Spontaneous cytokine production (interferongamma [IFN-c], tumor necrosis factor [TNF], and interleukin[IL]-10), serum chemokines (CXCL9 and CXCL10) and HTLV-1 proviral load were evaluated. Of 172 participants, 64 did not have histories of TB (TBgroup), 81 had LTB and 27 had TB in the past (TB+ group). In the TB+ group, there was a higher frequency of HAM/TSP patients (35%) than in HTLV-1 carriers (10%) (OR= 3.8, p = .0001). HAM/TSP patients with histories of TB had higher IFN-c/IL-10 and TNF/IL-10 ratios when compared with HAM/TSP patients without histories of TB. There were no differences in serum chemokine production and proviral load across TB groups stratified on HTLV-1 clinical status. In conclusion, TB may influence the development of HAM/TSP, and patients with these two diseases have an impairment in the modulation of immune response.
URI : http://www7.bahiana.edu.br//jspui/handle/bahiana/2967
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