Publication:
Molecular mechanisms involved in HIV latency and implications for HIV treatment and eradication

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dc.contributor.authorAlcamí, José
dc.contributor.authorCoiras, Mayte
dc.contributor.authorLopez-Huertas, Maria Rosa
dc.contributor.authorPerez-Olmeda, Mayte
dc.date.accessioned2019-04-02T09:36:51Z
dc.date.available2019-04-02T09:36:51Z
dc.date.issued2010-05-11
dc.description.abstractAim: The aim of this presentation is to review the molecular mechanisms necessary for the establishment of HIV-1 latency, their relationship with different cellular and anatomic reservoirs, as well as the current treatment strategies targeting viral persistence in latent reservoirs, their main limitations and future perspectives. Methods: For years, the molecular mechanisms leading to HIV-1 reactivation have been characterised in detail but the study of latency has remained elusive due to the technical limitations that arise when a negative phenomenon, like the absence of replication, is studied. Development of new techniques for studying HIV-1 latency, the identification of factors that restrict retroviral infections, the characterisation of chromatin structure in the setting of viral integration, and the discovery of new systems regulating gene expression. Results: Resting lymphocytes represent an extremely restrictive environment for HIV-1 replication. In contrast, immune activation of CD4+ T lymphocytes provides an optimal context for robust HIV-1 replication. Most mechanisms to maintain HIV-1 latency operate at transcriptional level such as the chromosome environment at the site of integration or the availability of viral and host transcription factors. In addition, HIV-1 integration and expression can be restrained or enhanced by different host cell factors such as IkBa, COMMD1, APOBEC3G, LEDGF and Emerin. Finally, both cellular and viral miRNAs could be involved in maintaining HIV-1 latency or in controlling low-ongoing viral replication. Identification of new cellular elements restricting the viral cycle provides a new paradigm on HIV-1 latency. Discussion: As a lentivirus, HIV-1 is able to infect resting, non-dividing cells where the viral genome can be permanently integrated into the host cell chromosomes. Latent HIV-1 reservoirs are established early during primary infection in lymphocytes and macrophages and constitute a major barrier to eradication even in the presence of highly active antiretroviral therapy (HAART). HIV-1 latency should no longer be considered a merely passive event due to the lack of positive factors but as an active process that is maintained by cellular elements that regulate the gene expression program in the infected cell.es_ES
dc.description.peerreviewedSíes_ES
dc.format.numberS1es_ES
dc.format.page15es_ES
dc.format.volume7es_ES
dc.identifier.citationRetrovirology 2010 7(Suppl 1):I15.es_ES
dc.identifier.doi10.1186/1742-4690-7-S1-I15es_ES
dc.identifier.issn1742-4690es_ES
dc.identifier.journalRetrovirologyes_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7421
dc.language.isoenges_ES
dc.publisherBioMed Central (BMC)es_ES
dc.relation.publisherversionhttps://doi.org/10.1186/1742-4690-7-S1-I15es_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectGene Expression Programes_ES
dc.subjectCellular Elementes_ES
dc.subjectCurrent Treatment Strategyes_ES
dc.subjectLatent Reservoires_ES
dc.subjectViral miRNAses_ES
dc.titleMolecular mechanisms involved in HIV latency and implications for HIV treatment and eradicationes_ES
dc.typeconference presentationes_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
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relation.isAuthorOfPublicationf729e106-ee5d-450a-b046-63b14e24c1a3
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relation.isAuthorOfPublicationd01866d4-34ba-4cd6-b995-3c4199bf0c59
relation.isAuthorOfPublication.latestForDiscovery2fc55aca-54b0-411c-b170-c2149068a902
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