Publication
HIV-2 infection is associated with preserved GALT homeostasis and epithelial integrity despite ongoing mucosal viral replication.
| dc.contributor.author | Fernandes, S | |
| dc.contributor.author | Pires, A | |
| dc.contributor.author | Matoso, P | |
| dc.contributor.author | Ferreira, C | |
| dc.contributor.author | Nunes-Cabaço, H | |
| dc.contributor.author | Correia, L | |
| dc.contributor.author | Valadas, E | |
| dc.contributor.author | Poças, J | |
| dc.contributor.author | Pacheco, P, et al. | |
| dc.date.accessioned | 2019-02-22T15:43:26Z | |
| dc.date.available | 2019-02-22T15:43:26Z | |
| dc.date.issued | 2018 | |
| dc.description.abstract | The 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.version | info:eu-repo/semantics/publishedVersion | pt_PT |
| dc.identifier.citation | Mucosal Immunol. 2018 Jan;11(1):236-248 | pt_PT |
| dc.identifier.doi | 10.1038/mi.2017.44 | pt_PT |
| dc.identifier.issn | 1935-3456 | |
| dc.identifier.uri | http://hdl.handle.net/10400.10/2138 | |
| dc.language.iso | eng | pt_PT |
| dc.peerreviewed | yes | pt_PT |
| dc.publisher | Nature Pub. Group, | pt_PT |
| dc.subject | HIV infections | pt_PT |
| dc.subject | Asymptomatic diseases | pt_PT |
| dc.title | HIV-2 infection is associated with preserved GALT homeostasis and epithelial integrity despite ongoing mucosal viral replication. | pt_PT |
| dc.type | journal article | |
| dspace.entity.type | Publication | |
| oaire.citation.conferencePlace | New York | pt_PT |
| oaire.citation.endPage | 248 | pt_PT |
| oaire.citation.startPage | 236 | pt_PT |
| oaire.citation.title | Mucosal Immunology | pt_PT |
| oaire.citation.volume | 11 | pt_PT |
| rcaap.rights | closedAccess | pt_PT |
| rcaap.type | article | pt_PT |