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High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing
Published on: January 22, 2019
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MicroRNA-155 Reinforces HIV Latency
Debbie S Ruelas1, Jonathan K Chan2, Eugene Oh3
1From the Gladstone Institute of Virology and Immunology, San Francisco, California 94158, the Biomedical Sciences Program and.
The Journal of Biological Chemistry
|April 16, 2015
Summary
Researchers identified a cellular circuit involving TRIM32 and miR-155 that impacts HIV latency. Understanding this pathway is key to developing a cure for HIV infection.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- A small population of dormant, infected cells prevents a cure for HIV.
- Reactivation of latent HIV can lead to cell death or a return to latency.
Purpose of the Study:
- To uncover the dynamics of HIV gene expression and silencing in the latent reservoir.
- To identify key molecular players in the reactivation from HIV latency.
Main Methods:
- Characterization of an intracellular circuit involving TRIM32 and miR-155.
- Investigation of TRIM32's role as an HIV activator and its mechanism of action.
Main Results:
- TRIM32, an E3 ubiquitin ligase, activates HIV.
- TRIM32 directly modifies IκBα, inducing a novel NF-κB pathway.
- miR-155 may promote the return to latency in reactivated cells.
Conclusions:
- The identified TRIM32-miR-155 circuit is crucial for understanding HIV latency dynamics.
- Targeting this circuit could offer new strategies for an HIV-1 cure.
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