| Author | Souza, Victor Barreto de | |
| Author | Medeiros, Thalyta Xavier | |
| Author | Motta, Maria Cristina Machado | |
| Author | Bou-Habib, Dumith Chequer | |
| Author | Saraiva, Elvira M. | |
| Access date | 2018-08-21T14:09:39Z | |
| Available date | 2018-08-21T14:09:39Z | |
| Document date | 2008 | |
| 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. | pt_BR |
| ISSN | 1286-4579 | pt_BR |
| URI | https://www.arca.fiocruz.br/handle/icict/28270 | |
| Language | eng | pt_BR |
| Publisher | Elsevier | pt_BR |
| Rights | restricted access | |
| Subject in Portuguese | HIV-1 | pt_BR |
| Subject in Portuguese | coinfecção por tripanossomatídeos não patogênicos | pt_BR |
| Subject in Portuguese | Blastocrithidia culicis | pt_BR |
| Subject in Portuguese | Tripanossomatídeo monoxênico | pt_BR |
| 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 | pt_BR |
| Type | Article | |
| DOI | 10.1016/j.micinf.2008.02.014 | |
| 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. | pt_BR |
| Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunologia Clínica. Rio de Janeiro, RJ. Brasil. | pt_BR |
| Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunologia Clínica. Rio de Janeiro, RJ. Brasil. | pt_BR |
| Affilliation | 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. | pt_BR |
| Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunologia Clínica. Rio de Janeiro, RJ. Brasil. | pt_BR |
| Affilliation | 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. | pt_BR |
| Subject | Monoxenic trypanosomatid | pt_BR |
| Subject | HIV-1 | pt_BR |
| Subject | HIV-1 Tat protein | pt_BR |
| Subject | Blastocrithidia culicis | pt_BR |
| Subject | HIV-1/non-pathogenic trypanosomatid co-infection | pt_BR |
| Subject | TGF-b1 | pt_BR |
| DeCS | Produtos do Gene tat | pt_BR |
| e-ISSN | 1769-714X | |
| Embargo date | 2030-01-01 | |
