Neutrophil extracellular traps from healthy donors and HIV-1-infected individuals restrict HIV-1 production in macrophages

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dc.creatorAndres Mojoli Le Quesne
dc.creatorDumith Chequer Bou Habib
dc.creatorBarbara Simonson Gonçalves
dc.creatorJairo Temerozo
dc.creatorBruno Cister Alves
dc.creatorVictor Geddes
dc.creatorAlice Herlinger
dc.creatorRenato Santana de Aguiar
dc.creatorJosé Henrique Pilotto
dc.creatorElvira Saraiva
dc.date.accessioned2023-07-17T20:10:07Z
dc.date.accessioned2025-09-09T01:25:22Z
dc.date.available2023-07-17T20:10:07Z
dc.date.issued2020
dc.identifier.issn2045-2322
dc.identifier.urihttps://hdl.handle.net/1843/56489
dc.languagepor
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofScientific Reports
dc.rightsAcesso Aberto
dc.subjectNeutrofilos
dc.subjectHIV (Virus)
dc.subjectMacrofagos
dc.subject.otherNeutrophils
dc.subject.otherHIV-1
dc.subject.otherProduction in macrophages
dc.titleNeutrophil extracellular traps from healthy donors and HIV-1-infected individuals restrict HIV-1 production in macrophages
dc.typeArtigo de periódico
local.citation.issue19603
local.citation.volume10
local.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.
local.identifier.orcidhttps://orcid.org/0000-0002-4654-2257
local.identifier.orcidhttps://orcid.org/0000-0003-0552-9045
local.identifier.orcidhttps://orcid.org/0000-0002-9378-0418
local.identifier.orcidhttps://orcid.org/0000-0002-8092-2149
local.identifier.orcidhttps://orcid.org/0000-0002-0723-3873
local.identifier.orcidhttps://orcid.org/0000-0002-7660-7058
local.identifier.orcidhttps://orcid.org/0000-0001-5180-3717
local.identifier.orcidhttps://orcid.org/0000-0003-0521-8597
local.identifier.orcidhttps://orcid.org/0000-0002-6388-5286
local.publisher.countryBrasil
local.publisher.departmentICB - INSTITUTO DE CIÊNCIAS BIOLOGICAS
local.publisher.initialsUFMG
local.url.externahttps://www.nature.com/articles/s41598-020-75357-2

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