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HIV-2 infection is associated with preserved GALT homeostasis and epithelial integrity despite ongoing mucosal viral replication

2017Journal article Restricted access
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dc.contributor.authorFernandes, S. M.
dc.contributor.authorPires, A. R.
dc.contributor.authorMatoso, P.
dc.contributor.authorFerreira, C.
dc.contributor.authorNunes-Cabaço, Helena
dc.contributor.authorCorreia, L.
dc.contributor.authorValadas, Emília
dc.contributor.authorPoças, J.
dc.contributor.authorPacheco, P.
dc.contributor.authorVeiga-Fernandes, Henrique
dc.contributor.authorFoxall, Russell
dc.contributor.authorSousa, Ana E.
dc.date.accessioned2022-02-28T16:32:42Z
dc.date.available2022-02-28T16:32:42Z
dc.date.issued2017
dc.description© 2018 Society for Mucosal Immunologypt_PT
dc.description.abstractThe mechanisms that enable preservation of gut mucosal integrity during persistent viral replication and inherent inflammation remain unclear. Here, we investigated, for the first time, gut homeostasis in HIV-2 infection, a naturally occurring form of attenuated HIV disease. We found viral replication in both sigmoid and ileum of asymptomatic HIV-2+ patients (range: 240-851 circulating CD4+T-cells per μl) despite their undetectable viremia, accompanied by interferon-γ-producing CD8 T-cell expansion, irrespective of antiretroviral treatment. Nevertheless, there was no CD4 T-cell depletion, and Foxp3+ and IL-17- or IL-22-producing CD4 T-cell numbers were unaffected. Moreover, IL-22-producing innate lymphoid cells and IL-22-induced antimicrobial peptides and mucins were maintained. In agreement, the epithelium histology was preserved, including tight junction protein zonula occludens (ZO-1) levels. Furthermore, in vitro infection of colon epithelia with primary isolates revealed no HIV-2 impact on ZO-1 expression. Notably, sigmoid transcriptional levels of CCL20 and CCL28 were significantly increased, in direct correlation with GM-CSF, indicating a local response able to enhance CD4 T-cell recruitment. In conclusion, maintenance of mucosal integrity in HIV-2 infection was associated with T-cell recruitment responses, potentially counteracting CD4 T-cell depletion due to HIV-2 replication. These data have unique implications for the design of therapies targeting gut homeostasis in HIV-1 infection and other chronic inflammatory settings.pt_PT
dc.description.sponsorshipThis work was supported by the Fundação para a Ciência e Tecnologia (FCT), and the Programa Operacional Ciência e Inovação 2010 (EXPL/DTP-PIC/0854/2013 to RBF, and PIC/IC/82712/2007 to AES), as well a Fundação Calouste Gulbenkian (P132532/2013 to AES). SMF, ARP, HNC, and RBF received FCT scholarships.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMucosal Immunol. 2018 Jan;11(1):236-248pt_PT
dc.identifier.doi10.1038/mi.2017.44pt_PT
dc.identifier.eissn1935-3456
dc.identifier.issn1933-0219
dc.identifier.urihttp://hdl.handle.net/10451/51555
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherSpringer Naturept_PT
dc.relationAchieving gut integrity in HIV/AIDS through IL-22
dc.relation.publisherversionhttps://www.nature.com/mi/pt_PT
dc.titleHIV-2 infection is associated with preserved GALT homeostasis and epithelial integrity despite ongoing mucosal viral replicationpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleAchieving gut integrity in HIV/AIDS through IL-22
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/EXPL%2FDTP-PIC%2F0854%2F2013/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5646-ICCMS/PIC%2FIC%2F82712%2F2007/PT
oaire.citation.endPage248pt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage236pt_PT
oaire.citation.titleMucosal Immunologypt_PT
oaire.citation.volume11pt_PT
oaire.fundingStream3599-PPCDT
oaire.fundingStream5646-ICCMS
person.familyNameNunes Cabaço
person.familyNameValadas
person.familyNameVeiga-Fernandes
person.familyNameFoxall
person.familyNameSousa
person.givenNameHelena Isabel Marques
person.givenNameEmília
person.givenNameHenrique
person.givenNameRussell
person.givenNameAna E.
person.identifier61187
person.identifier.ciencia-idD01D-34B6-6C79
person.identifier.ciencia-idC919-1B92-794F
person.identifier.ciencia-idD015-D3A2-992D
person.identifier.orcid0000-0001-7213-2879
person.identifier.orcid0000-0001-5213-1473
person.identifier.orcid0000-0001-6216-1836
person.identifier.orcid0000-0001-9821-0708
person.identifier.orcid0000-0002-4618-9799
person.identifier.ridL-2642-2014
person.identifier.scopus-author-id6603593138
person.identifier.scopus-author-id6508113770
person.identifier.scopus-author-id6701559470
person.identifier.scopus-author-id7202484563
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsrestrictedAccesspt_PT
rcaap.typearticlept_PT
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