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dc.contributor.authorWang, Feng-Xiang
dc.contributor.authorXu, Yan
dc.contributor.authorSullivan, Julie
dc.contributor.authorSouder, Emily
dc.contributor.authorArgyris, Elias G
dc.contributor.authorAcheampong, Edward A
dc.contributor.authorFisher, Jaime
dc.contributor.authorSierra, Maria Angeles 
dc.contributor.authorThomson, Michael M 
dc.contributor.authorNajera-Morrondo, Rafael 
dc.contributor.authorFrank, Ian
dc.contributor.authorKulkosky, Joseph
dc.contributor.authorPomerantz, Roger J
dc.contributor.authorNunnari, Giuseppe
dc.date.accessioned2019-01-11T12:41:51Z
dc.date.available2019-01-11T12:41:51Z
dc.date.issued2005-01
dc.identifier.citationJ Clin Invest. 2005;115(1):128-37.es_ES
dc.identifier.issn0021-9738es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/6997
dc.description.abstractThe persistence of HIV-1 in virally suppressed infected individuals on highly active antiretroviral therapy (HAART) remains a major therapeutic problem. The use of cytokines has been envisioned as an additional therapeutic strategy to stimulate latent proviruses in these individuals. Immune activation therapy using IL-2 has shown some promise. In the present study, we found that IL-7 was significantly more effective at enhancing HIV-1 proviral reactivation than either IL-2 alone or IL-2 combined with phytohemagglutinin (PHA) in CD8-depleted PBMCs. IL-7 also showed a positive trend for inducing proviral reactivation from resting CD4(+) T lymphocytes from HIV-1-infected patients on suppressive HAART. Moreover, the phylogenetic analyses of viral envelope gp120 genes from induced viruses indicated that distinct proviral quasispecies had been activated by IL-7, as compared with those activated by the PHA/IL-2 treatment. These studies thus demonstrate that different activators of proviral latency may perturb and potentially deplete only selected, specific portions of the proviral archive in virally suppressed individuals. The known immunomodulatory effects of IL-7 could be combined with its ability to stimulate HIV-1 replication from resting CD4(+) T lymphocytes, in addition to other moieties, to potentially deplete HIV-1 reservoirs and lead to the rational design of immune-antiretroviral approaches.es_ES
dc.description.sponsorshipThis work was supported in part by US Public Health Services grants AI43289 and NS41864 (to R.J.Pomerantz), and the Center for AIDS research (CFAR) AI45008 at the University of Pennsylvania.es_ES
dc.language.isoenges_ES
dc.publisherAmerican Society for Clinical Investigation (ASCI) es_ES
dc.type.hasVersionVoRes_ES
dc.subject.meshAnti-HIV Agents es_ES
dc.subject.meshAntiretroviral Therapy, Highly Activees_ES
dc.subject.meshCD4-Positive T-Lymphocytes es_ES
dc.subject.meshCells, Cultured es_ES
dc.subject.meshGene Expression Regulation, Viral es_ES
dc.subject.meshHIV Envelope Protein gp120 es_ES
dc.subject.meshHIV Infections es_ES
dc.subject.meshHIV Long Terminal Repeat es_ES
dc.subject.meshHIV-1 es_ES
dc.subject.meshHumans es_ES
dc.subject.meshInterleukin-2 es_ES
dc.subject.meshLymphocyte Activation es_ES
dc.subject.meshPhylogeny es_ES
dc.subject.meshPhytohemagglutinins es_ES
dc.subject.meshProviruses es_ES
dc.subject.meshRNA, Viral es_ES
dc.subject.meshSpecies Specificity es_ES
dc.subject.meshVirus Activation es_ES
dc.subject.meshVirus Replication es_ES
dc.titleIL-7 is a potent and proviral strain-specific inducer of latent HIV-1 cellular reservoirs of infected individuals on virally suppressive HAARTes_ES
dc.typejournal articlees_ES
dc.identifier.pubmedID15630452es_ES
dc.format.volume115es_ES
dc.format.number1es_ES
dc.format.page128-37es_ES
dc.identifier.doi10.1172/JCI22574es_ES
dc.contributor.funderUnited States Public Health Services
dc.contributor.funderUniversity of Pennsylvania (Estados Unidos)
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1172/JCI22574es_ES
dc.identifier.journalThe Journal of Clinical Investigationes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES


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