Volume 11 Supplement 1

16th Interntional Conference on Human Retroviruses: HTLV and Related Viruses

Open Access

Prevalence and influence of tuberculosis in the neurologic manifestations of the Human T cell lymphotropic virus type 1 (HTLV-1)

  • Maria de Lourdes Bastos1, 2, 3,
  • Anselmo Souza1,
  • Natália Carvalho1,
  • Yuri Neves1,
  • Silvane Santos1, 4 and
  • Edgar M Carvalho1, 2, 4
Retrovirology201411(Suppl 1):P6

https://doi.org/10.1186/1742-4690-11-S1-P6

Published: 7 January 2014

HTLV-1 infects mainly T cells, leading to activation and cellular proliferation with exaggerated production of pro-inflammatory cytokines. The majority of HTLV-1 infected patients are considered as HTLV-1 carriers, but 5% will develop HTLV-1 associated myelopathy (HAM) and about 15% overactive bladder, an oligosymptomatic form of HAM. HTLV-1 is associated with increased susceptibility to Mycobacterium tuberculosis infection but up to now it is unknown if HTLV-1 influences the severity of tuberculosis and if tuberculosis may influence the outcome of HTLV-1. The aims of this study were to determine the prevalence and severity of tuberculosis (TB) in HTLV-1 infected patients and analyze whether TB influences the outcome of HTLV-1 infection. This is a cross-sectional study, in which the prevalence of tuberculosis was analyzed in 166 HTLV-1 infected individuals. Cytokine productions were determined by ELISA, the proviral load was evaluated by PCR. Tuberculosis occurred in 33 (22%) of cases and 70 (42%) had a positive tuberculin skin test (TST) (latent tuberculosis). The majority of the cases did not have severe tuberculosis. There was no difference in the proviral load, but there was a higher frequency of HAM/TSP in the group with tuberculosis than in HTLV-1 infected subjects without TB (P<0.05). This study shows that the prevalence of M.tuberculosis infection is 6 fold higher in HTLV-1 infected individuals than that described in the Brazilian population the majority of co-infected had latent tuberculosis and HTLV-1 may influence progression from infection to HAM/TSP.

Funded by

National Institute of Health (NIH AI 079238) and CNPq.

Authors’ Affiliations

(1)
Serviço de Imunologia, Complexo Hospitalar Universitário Professor Edgard Santos, Universidade Federal da Bahia
(2)
Escola Bahiana de Medicina e Saúde Pública
(3)
Hospital Especializado Octávio Mangabeira
(4)
Instituto Nacional de Ciência e Tecnologia de Doenças Tropicais (INCT-DT)

Copyright

© de Lourdes Bastos et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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