RT Journal Article
SR Electronic
T1 Clinic and immunologic features of the co-infection tuberculosis and HTLV-1
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P2634
VO 44
IS Suppl 58
A1 Maria de Lourdes Bastos
A1 Yuri Neves
A1 Natália Carvalho
A1 Nathália Lisboa
A1 Anselmo Souza
A1 Silvane Santos
A1 Eduardo Netto
A1 Edgar M. Carvalho
YR 2014
UL http://erj.ersjournals.com/content/44/Suppl_58/P2634.abstract
AB Introduction: The human T cell lymphotropic virus type 1 (HTLV-1) infection increases up to 4 fold the susceptibility for tuberculosis (TB) but very little is known about the pathogenesis and clinical consequences of this co-infection. Objectives: The aims of this study were to determine the prevalence of TB in a cohort of HTLV-1, to evaluate the immunologic response that may explain the clinical consequences of this co-infection. Methods: A total of 190 HTLV-1 infected subjects followed at the HTLV-1 clinic in the Federal University of Bahia, were enrolled in the study. The diagnosis of HTLV-1 was performed by an ELISA serological test and confirmed by Western blot. They answer a questionnaire, had a complete physical and neurological examinations, chest X ray and a tuberculin skin test (TST). HTLV-1 infected subjects were classified as asymptomatic, neurogenic bladder and HTLV-1 associated myelopathy (HAM). Cytokines were measured by ELISA in supernatants of lymphocyte cultures and the pro-viral load by PCR. Results: There were 39 (20,5%) cases of TB and 76 (46%) of latent TB (P<0.05). Patients with TB and HTLV-1 had a lower production of TNF-α and higher ratio of IFN : IL-10 (P<0.05) than HTLV-1 + LTB or HTLV-1 without TB. Moreover the frequency of HAM was higher (P< 0.001) in the TB group compared to LTB and without TB. Conclusion: Our data did not support that HTLV-1 make M.tuberculosis infection more severe. While the increased susceptibility for TB in HTLV-1 may be due to a decreasing in TNF-α production, TB by inducing a more exaggerated inflammatory response in HTLV-1 influences the clinical outcome of the viral infection, contributing for the development of HAM.