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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/56489
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dc.creatorAndres Mojoli Le Quesnept_BR
dc.creatorDumith Chequer Bou Habibpt_BR
dc.creatorBarbara Simonson Gonçalvespt_BR
dc.creatorJairo Temerozopt_BR
dc.creatorBruno Cister Alvespt_BR
dc.creatorVictor Geddespt_BR
dc.creatorAlice Herlingerpt_BR
dc.creatorRenato Santana de Aguiarpt_BR
dc.creatorJosé Henrique Pilottopt_BR
dc.creatorElvira Saraivapt_BR
dc.date.accessioned2023-07-17T20:10:07Z-
dc.date.available2023-07-17T20:10:07Z-
dc.date.issued2020-
dc.citation.volume10pt_BR
dc.citation.issue19603pt_BR
dc.identifier.issn2045-2322pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/56489-
dc.description.resumoNeutrophils release extracellular traps (NETs) after interaction with microorganisms and physiological or synthetic products. NETs consist of decondensed chromatin complexed with proteins, some of them with microbicidal properties. Because NETs can modulate the functioning of HIV-1 target cells, we aimed to verify whether they modify HIV-1 replication in macrophages. We found that exposure of HIV-1-infected macrophages to NETs resulted in significant inhibition of viral replication. The NET anti-HIV-1 action was independent of other soluble factors released by the activated neutrophils, but otherwise dependent on the molecular integrity of NETs, since NET-treatment with protease or DNase abolished this effect. NETs induced macrophage production of the anti-HIV-1 β-chemokines Rantes and MIP-1β, and reduced the levels of integrated HIV-1 DNA in the macrophage genome, which may explain the decreased virus production by infected macrophages. Moreover, the residual virions released by NET-treated HIV-1-infected macrophages lost infectivity. In addition, elevated levels of DNA-elastase complexes were detected in the plasma from HIV-1-infected individuals, and neutrophils from these patients released NETs, which also inhibited HIV-1 replication in in vitro infected macrophages. Our results reveal that NETs may function as an innate immunity mechanism able to restrain HIV-1 production in macrophages.pt_BR
dc.languageporpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - INSTITUTO DE CIÊNCIAS BIOLOGICASpt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofScientific Reportspt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectNeutrophilspt_BR
dc.subjectHIV-1pt_BR
dc.subjectProduction in macrophagespt_BR
dc.subject.otherNeutrofilospt_BR
dc.subject.otherHIV (Virus)pt_BR
dc.subject.otherMacrofagospt_BR
dc.titleNeutrophil extracellular traps from healthy donors and HIV-1-infected individuals restrict HIV-1 production in macrophagespt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.nature.com/articles/s41598-020-75357-2pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4654-2257pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0552-9045pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9378-0418pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-8092-2149pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0723-3873pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7660-7058pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-5180-3717pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0521-8597pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6388-5286pt_BR
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