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dc.contributor.author
Mohammadi, Pejman
dc.contributor.author
di Iulio, Julia
dc.contributor.author
Muñoz, Miguel
dc.contributor.author
Martinez, Raquel
dc.contributor.author
Bartha, István
dc.contributor.author
Cavassini, Matthias
dc.contributor.author
Thorball, Christian
dc.contributor.author
Fellay, Jacques
dc.contributor.author
Beerenwinkel, Niko
dc.contributor.author
Ciuffi, Angela
dc.contributor.author
Telenti, Amalio
dc.date.accessioned
2019-08-16T10:13:50Z
dc.date.available
2017-06-11T10:57:18Z
dc.date.available
2019-08-16T10:13:50Z
dc.date.issued
2014-05-29
dc.identifier.issn
1553-7366
dc.identifier.issn
1553-7374
dc.identifier.other
10.1371/journal.ppat.1004156
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/86708
dc.identifier.doi
10.3929/ethz-b-000086708
dc.description.abstract
HIV latency is a major obstacle to curing infection. Current strategies to eradicate HIV aim at increasing transcription of the latent provirus. In the present study we observed that latently infected CD4+ T cells from HIV-infected individuals failed to produce viral particles upon ex vivo exposure to SAHA (vorinostat), despite effective inhibition of histone deacetylases. To identify steps that were not susceptible to the action of SAHA or other latency reverting agents, we used a primary CD4+ T cell model, joint host and viral RNA sequencing, and a viral-encoded reporter. This model served to investigate the characteristics of latently infected cells, the dynamics of HIV latency, and the process of reactivation induced by various stimuli. During latency, we observed persistence of viral transcripts but only limited viral translation. Similarly, the reactivating agents SAHA and disulfiram successfully increased viral transcription, but failed to effectively enhance viral translation, mirroring the ex vivo data. This study highlights the importance of post-transcriptional blocks as one mechanism leading to HIV latency that needs to be relieved in order to purge the viral reservoir.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Public Library of Science
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.title
Dynamics of HIV Latency and Reactivation in a Primary CD4+T Cell Model
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
ethz.journal.title
PLoS Pathogens
ethz.journal.volume
10
en_US
ethz.journal.issue
5
en_US
ethz.journal.abbreviated
PLoS Pathog
ethz.pages.start
e1004156
en_US
ethz.size
14 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.grant
Dynamics of HIV latency and reactivation at population and single-cell level
en_US
ethz.identifier.wos
ethz.identifier.nebis
005409548
ethz.publication.place
Lawrence, KS
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02060 - Dep. Biosysteme / Dep. of Biosystems Science and Eng.::03790 - Beerenwinkel, Niko / Beerenwinkel, Niko
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02060 - Dep. Biosysteme / Dep. of Biosystems Science and Eng.::03790 - Beerenwinkel, Niko / Beerenwinkel, Niko
ethz.grant.agreementno
146579
ethz.grant.fundername
SNF
ethz.grant.funderDoi
10.13039/501100001711
ethz.grant.program
Projektförderung in Biologie und Medizin (Abteilung III)
ethz.date.deposited
2017-06-11T10:59:48Z
ethz.source
ECIT
ethz.identifier.importid
imp593652197da9173768
ethz.ecitpid
pub:136489
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-12T20:59:40Z
ethz.rosetta.lastUpdated
2019-08-16T10:14:03Z
ethz.rosetta.versionExported
true
ethz.COinS
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