Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/28270
Title: HIV-1 infection and HIV-1 Tat protein permit the survival and replication of a non-pathogenic trypanosomatid in macrophages through TGF-beta1 production
Authors: Souza, Victor Barreto de
Medeiros, Thalyta Xavier
Motta, Maria Cristina Machado
Bou-Habib, Dumith Chequer
Saraiva, Elvira M.
Affilliation: Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunologia Clínica. Rio de Janeiro, RJ. Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunologia Clínica. Rio de Janeiro, RJ. Brasil.
Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biofísica Carlos Chagas Filho. Laboratório de Ultraestrutura Celular Herta Meyer. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunologia Clínica. Rio de Janeiro, RJ. Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Microbiologia Professor Paulo de Góes. Departamento de Imunologia. Laboratório de Imunobiologia das Leishmanioses. Rio de Janeiro, RJ, Brasil.
Abstract: Monoxenic trypanosomatids, which usually are non-pathogenic in humans, have been detected in AIDS patients, but the mechanisms underlying the establishment of these protozoa in HIV-1-infected individuals are poorly understood. Here we addressed the role of HIV-1 and the HIV-1 Tat protein in the replication of the monoxenic trypanosomatid Blastocrithidia culicis in HIV-1-infected primary human macrophages. We found that HIV-1 and B. culicis replication augmented almost three times in co-infected macrophages, and that Tat antiserum significantly reduced the exacerbated protozoan growth. Exposure of B. culicis only infected macrophages to Tat protein also resulted in enhanced protozoan proliferation, reaching a twofold increase at 100 ng/mL. Electron microscopy analysis revealed that B. culicis and HIV-1 co-habit the same cells, and showed protozoan dividing forms inside macrophages. Protozoan replication diminished when B. culicis only infected macrophages were treated with Tat protein in the presence of anti-TGF-beta1 antibodies, suggesting a participation of this cytokine in the augmentation of protozoan multiplication. In fact, exogenous TGF-beta1 promoted the trypanosomatid replication in macrophages. Overall, our results suggest that HIV-1 infection deactivates the macrophage microbicidal activity, permitting the survival and multiplication of an otherwise non-pathogenic protozoan in these cells, a process partially mediated by Tat protein, via TGF-beta1 secretion.
Keywords: Monoxenic trypanosomatid
HIV-1
HIV-1 Tat protein
Blastocrithidia culicis
HIV-1/non-pathogenic trypanosomatid co-infection
TGF-b1
keywords: HIV-1
coinfecção por tripanossomatídeos não patogênicos
Blastocrithidia culicis
Tripanossomatídeo monoxênico
DeCS: Produtos do Gene tat
Issue Date: 2008
Publisher: Elsevier
Citation: SOUZA, Victor Barreto de; et al. HIV-1 infection and HIV-1 Tat protein permit the survival and replication of a non-pathogenic trypanosomatid in macrophages through TGF-b1 production. Microbes and Infection, v.10, n.6, p.642-649, 2008.
DOI: 10.1016/j.micinf.2008.02.014
ISSN: 1286-4579
Copyright: restricted access
Appears in Collections:IOC - Artigos de Periódicos

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