Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 290, Issue 22, Pages 13736-13748Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M115.641837
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Funding
- Martin Delaney CARE Collaboratory (National Institutes of Health) [NIAID U19 AI096113]
- UCSF Microbial Pathogenesis and Host Defense Program (National Institutes of Health) [NIAID 5 T32 AI60537-9]
- Jane Coffin Childs Postdoctoral Fellowship
- Centers for AIDS Research (CFAR), a National Institutes of Health [P30 AI027763]
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The presence of a small number of infected but transcriptionally dormant cells currently thwarts a cure for the more than 35 million individuals infected with HIV. Reactivation of these latently infected cells may result in three fates: 1) cell death due to a viral cytopathic effect, 2) cell death due to immune clearance, or 3) a retreat into latency. Uncovering the dynamics of HIV gene expression and silencing in the latent reservoir will be crucial for developing an HIV-1 cure. Here we identify and characterize an intracellular circuit involving TRIM32, an HIV activator, and miR-155, a microRNA that may promote a return to latency in these transiently activated reservoir cells. Notably, we demonstrate that TRIM32, an E3 ubiquitin ligase, promotes reactivation from latency by directly modifying I kappa B alpha, leading to a novel mechanism of NF-kappa B induction not involving I kappa B kinase activation.
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