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HIV-2 integrase polymorphisms and longitudinal genotypic analysis of HIV-2 infected patients failing a raltegravir-containing regimen

2014Journal article Open access
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dc.contributor.authorCavaco-Silva, J.
dc.contributor.authorAbecasis, A.
dc.contributor.authorMiranda, A.
dc.contributor.authorPoças, J.
dc.contributor.authorNarciso, J.
dc.contributor.authorÁguas, M.
dc.contributor.authorMaltez, F.
dc.contributor.authorAlmeida, I.
dc.contributor.authorGermano, I.
dc.contributor.authorDiniz, A.
dc.contributor.authorGonçalves, M.
dc.contributor.authorGomes, P.
dc.contributor.authorCunha, C.
dc.contributor.authorCamacho, R.
dc.date.accessioned2015-10-27T11:43:07Z
dc.date.available2015-10-27T11:43:07Z
dc.date.issued2014
dc.description.abstractTo characterize the HIV-2 integrase gene polymorphisms and the pathways to resistance of HIV-2 patients failing a raltegravir-containing regimen, we studied 63 integrase strand transfer inhibitors (INSTI)-naïve patients, and 10 heavily pretreated patients exhibiting virological failure while receiving a salvage raltegravir-containing regimen. All patients were infected by HIV-2 group A. 61.4% of the integrase residues were conserved, including the catalytic motif residues. No INSTI-major resistance mutations were detected in the virus population from naïve patients, but two amino acids that are secondary resistance mutations to INSTIs in HIV-1 were observed. The 10 raltegravir-experienced patients exhibited resistance mutations via three main genetic pathways: N155H, Q148R, and eventually E92Q - T97A. The 155 pathway was preferentially used (7/10 patients). Other mutations associated to raltegravir resistance in HIV-1 were also observed in our HIV-2 population (V151I and D232N), along with several novel mutations previously unreported. Data retrieved from this study should help build a more robust HIV-2-specific algorithm for the genotypic interpretation of raltegravir resistance, and contribute to improve the clinical monitoring of HIV-2-infected patients.pt_PT
dc.description.sponsorshipThis work was funded by a research grant from Merck & Co., Inc., Whitehouse Station, N.J., USA, and by the European Commission's Seventh Framework Programme (FP7/2007–2013) under the project “Collaborative HIV and Anti-HIV Drug Resistance Network” (CHAIN, grant 223131). J.C.-S. was supported by Fundação para a Ciência e Tecnologia (FCT) with a PhD grant no. SFRH/BD/61141/2009. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.pt_PT
dc.identifier10.1371/journal.pone.0092747
dc.identifier.citationPLoS One. 2014;9(3):e92747pt_PT
dc.identifier.doi10.1371/journal.pone.0092747
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/10400.16/1872
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherPublic Library of Sciencept_PT
dc.relation.publisherversionhttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0092747pt_PT
dc.titleHIV-2 integrase polymorphisms and longitudinal genotypic analysis of HIV-2 infected patients failing a raltegravir-containing regimenpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.conferencePlaceUnited States of Americapt_PT
oaire.citation.titlePloS onept_PT
oaire.citation.volume9(3)pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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