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HIV controllers have low inflammation associated with a strong HIV-specific immune response in blood

dc.rights.licenseopenen_US
dc.contributor.authorHOCINI, H.
hal.structure.identifierStatistics In System biology and Translational Medicine [SISTM]
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorBONNABAU, Henri
dc.contributor.authorLACABARATZ, C.
dc.contributor.authorLEFEBVRE, C.
dc.contributor.authorTISSERAND, P.
dc.contributor.authorFOUCAT, E.
dc.contributor.authorLELIEVRE, J. D.
dc.contributor.authorLAMBOTTE, O.
dc.contributor.authorSAEZ-CIRION, A.
dc.contributor.authorVERSMISSE, P.
hal.structure.identifierStatistics In System biology and Translational Medicine [SISTM]
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorTHIEBAUT, Rodolphe
dc.contributor.authorLEVY, Y.
dc.date.accessioned2020-06-23T08:19:35Z
dc.date.available2020-06-23T08:19:35Z
dc.date.issued2019-05-15
dc.identifier.issn1098-5514 (Electronic) 0022-538X (Linking)en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/8092
dc.description.abstractEnHIV-Controllers (HIC) maintain control of HIV replication without combined antiretroviral treatment (cART). The mechanisms leading to virus control are not fully known. We used gene expression and cellular analyses to compare HIC and HIV-1 infected individuals under cART. In the blood, HIC are characterized by a low inflammation, a down modulation of NK inhibitory cell signaling and an up regulation of T-cell activation gene expression. This balance that persists following stimulation of cells with HIV antigens, was consistent with functional analyses showing a bias towards a Th1 and cytotoxic T cell response and a lower production of inflammatory cytokines. Taking advantage of the characterization of HIC based upon their CD8+ T lymphocyte capacity to suppress HIV-infection, we show that unsupervised analysis of differentially expressed genes fits clearly with this cytotoxic activity allowing the characterization of a specific signature of HIC. These results reveal significant features of HIC making the bridge between cellular function, gene signatures and the regulation of inflammation and killing capacity of HIV-specific CD8+T cells. Moreover, these genetic profiles are consistent through analyses performed from blood to PBMC and T-cells. HIV controllers maintain strong HIV-specific immune responses with low levels of inflammation. Our findings may pave the way for new immunotherapeutic approaches leading to strong HIV-1-specific immune responses while minimizing inflammation.IMPORTANCE A small minority of HIV infected patients, called "HIV Controllers" (HIC) maintains spontaneous control of HIV replication. It is therefore important to identify mechanisms that contribute to the control of HIV replication that may have implications for vaccine design. We observed a low inflammation, a down modulation of natural killer inhibitory cell signaling and an up regulation of T-cell activation gene expression in blood of HIC compared to patients under combined antiretroviral treatment. This profile persists following in vitro stimulation of peripheral blood mononuclear cells with HIV antigens, and was consistent with functional analyses showing a Th1 and cytotoxic T cell response and a lower production of inflammatory cytokines. These results reveal significant features of HIV controllers that maintain strong HIV-specific immune responses with low levels of inflammation. These findings define the immune status of HIC that is probably associated with the control of viral load.
dc.language.isoENen_US
dc.subject.enSISTM
dc.title.enHIV controllers have low inflammation associated with a strong HIV-specific immune response in blood
dc.title.alternativeJ Virolen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1128/jvi.01690-18en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed30814287en_US
bordeaux.journalJournal of Virologyen_US
bordeaux.page14en_US
bordeaux.volume93en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - U1219en_US
bordeaux.issue10en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.teamSISTM_BPH
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03160730
hal.version2
hal.date.transferred2021-03-06T02:39:31Z
hal.exporttrue
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