Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/10683
Title: HIV-1 and Its gp120 Inhibits the Influenza A(H1N1)pdm09 Life Cycle in an IFITM3-Dependent Fashion
Authors: Mesquita, Milene
Rodrigues, Natalia Fintelman
Sacramento, Carolina Q.
Abrantes, Juliana L.
Costa, Eduardo
Temerozo, Jairo R.
Siqueira, Marilda M.
Bou-Habib, Dumith Chequer
Souza, Thiago Moreno L.
Affilliation: Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virus Respiratório e do Sarampo. WHO/NIC. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virus Respiratório e do Sarampo. WHO/NIC. Rio de Janeiro, RJ, Brasi
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virus Respiratório e do Sarampo. WHO/NIC. Rio de Janeiro, RJ, Brasi
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virus Respiratório e do Sarampo. WHO/NIC. Rio de Janeiro, RJ, Brasi
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virus Respiratório e do Sarampo. WHO/NIC. Rio de Janeiro, RJ, Brasi
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virus Respiratório e do Sarampo. WHO/NIC. Rio de Janeiro, RJ, Brasi
undação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virus Respiratório e do Sarampo. WHO/NIC. Rio de Janeiro, RJ, Brasil.
Abstract: HIV-1-infected patients co-infected with A(H1N1)pdm09 surprisingly presented benign clinical outcome. The knowledge that HIV-1 changes the host homeostatic equilibrium, which may favor the patient resistance to some co-pathogens, prompted us to investigate whether HIV-1 infection could influence A(H1N1)pdm09 life cycle in vitro. We show here that exposure of A(H1N1)pdm09-infected epithelial cells to HIV-1 viral particles or its gp120 enhanced by 25% the IFITM3 content, resulting in a decrease in influenza replication. This event was dependent on toll-like receptor 2 and 4. Moreover, knockdown of IFITM3 prevented HIV-1 ability to inhibit A(H1N1)pdm09 replication. HIV-1 infection also increased IFITM3 levels in human primary macrophages by almost 100%. Consequently, the arrival of influenza ribonucleoproteins (RNPs) to nucleus of macrophages was inhibited, as evaluated by different approaches. Reduction of influenza RNPs entry into the nucleus tolled A(H1N1)pdm09 life cycle in macrophages earlier than usual, limiting influenza’s ability to induce TNF-a. As judged by analysis of the influenza hemagglutin (HA) gene from in vitro experiments and from samples of HIV-1/ A(H1N1)pdm09 co-infected individuals, the HIV-1-induced reduction of influenza replication resulted in delayed viral evolution. Our results may provide insights on the mechanisms that may have attenuated the clinical course of Influenza in HIV-1/A(H1N1)pdm09 co-infected patients during the recent influenza form 2009/2010.
Keywords: HIV-1
Influenza A(H1N1)pdm09
DeCS: HIV-1
Issue Date: 2014
Publisher: Plos One
Citation: MESQUITA, Milene et al. HIV-1 and Its gp120 Inhibits the Influenza A(H1N1)pdm09 Life Cycle in an IFITM3-Dependent Fashion. Plos One, v.9, n.6, 14p, jun. 2014.
DOI: 10.1371/journal.pone.0101056
Copyright: open access
Appears in Collections:IOC - Artigos de Periódicos

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