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The mTOR Complex Controls HIV Latency
In: Cell Host & Microbe, Jg. 20 (2016-12-01), Heft 6
Online
academicJournal
- 785 - 797
A population of CD4 T lymphocytes harboring latent HIV genomes can persist in patients on antiretroviral therapy, posing a barrier to HIV eradication. To examine cellular complexes controlling HIV latency, we conducted a genome-wide screen with a pooled ultracomplex shRNA library and in vitro system modeling HIV latency and identified the mTOR complex as a modulator of HIV latency. Knockdown of mTOR complex subunits or pharmacological inhibition of mTOR activity suppresses reversal of latency in various HIV-1 latency models and HIV-infected patient cells. mTOR inhibitors suppress HIV transcription both through the viral transactivator Tat and via Tat-independent mechanisms. This inhibition occurs at least in part via blocking the phosphorylation of CDK9, a p-TEFb complex member that serves as a cofactor for Tat-mediated transcription. The control of HIV latency by mTOR signaling identifies a pathway that may have significant therapeutic opportunities.
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The mTOR Complex Controls HIV Latency
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Autor/in / Beteiligte Person: | Besnard, Emilie ; Hakre, Shweta ; Kampmann, Martin ; Lim, Hyung W ; Hosmane, Nina N ; Martin, Alyssa ; Bassik, Michael C ; Verschueren, Erik ; Battivelli, Emilie ; Chan, Jonathan ; Svensson, J Peter ; Gramatica, Andrea ; Conrad, Ryan J ; Ott, Melanie ; Greene, Warner C ; Krogan, Nevan J ; Siliciano, Robert F ; Weissman, Jonathan S ; Verdin, Eric |
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Zeitschrift: | Cell Host & Microbe, Jg. 20 (2016-12-01), Heft 6 |
Veröffentlichung: | eScholarship, University of California, 2016 |
Medientyp: | academicJournal |
Umfang: | 785 - 797 |
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