ArticleJournal of virology2012
Kinase control prevents HIV-1 reactivation in spite of high levels of induced NF-κB activity.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Effect of Kinases in Extracellular Vesicles from HIV-1-Infected Cells on Bystander Cells.Cells · 2025Article
- Lentiviral Nef Proteins Differentially Govern the Establishment of Viral Latency.Journal of virology · 2022Article
- Host T Cell Dedifferentiation Effects Drive HIV-1 Latency Stability.Journal of virology · 2022Article
- The Cultured TMethods in molecular biology (Clifton, N.J.) · 2022Article
- Extensive proteomic and transcriptomic changes quench the TCR/CD3 activation signal of latently HIV-1 infected T cells.PLoS pathogens · 2021Article
- Maraviroc Is Associated with Latent HIV-1 Reactivation through NF-κB Activation in Resting CD4Journal of virology · 2018Article
- JNK, p38, ERK, and SGK1 Inhibitors in Cancer.Cancers · 2017Article
- Systems analysis of latent HIV reversal reveals altered stress kinase signaling and increased cell death in infected T cells.Scientific reports · 2017Article
- Deficiency in DNA damage response, a new characteristic of cells infected with latent HIV-1.Cell cycle (Georgetown, Tex.) · 2017Article
- Role of Host Factors on the Regulation of Tat-Mediated HIV-1 Transcription.Current pharmaceutical design · 2017Review
- The host cell side of latent HIV-1 infection.Oncotarget · 2015Article
- Stable Phenotypic Changes of the Host T Cells Are Essential to the Long-Term Stability of Latent HIV-1 Infection.Journal of virology · 2015Article
- Direct non-productive HIV-1 infection in a T-cell line is driven by cellular activation state and NFκB.Retrovirology · 2014Article
- Kinase control of latent HIV-1 infection: PIM-1 kinase as a major contributor to HIV-1 reactivation.Journal of virology · 2014Article
- HIV-1 transcription and latency: an update.Retrovirology · 2013Review
- Barriers to a cure for HIV: new ways to target and eradicate HIV-1 reservoirs.Lancet (London, England) · 2013Review
- A doubly fluorescent HIV-1 reporter shows that the majority of integrated HIV-1 is latent shortly after infection.Journal of virology · 2013Article
- Dendritic cell-induced activation of latent HIV-1 provirus in actively proliferating primary T lymphocytes.PLoS pathogens · 2013Article
- An AP-1 binding site in the enhancer/core element of the HIV-1 promoter controls the ability of HIV-1 to establish latent infection.Journal of virology · 2013Article
- TNF and TNF receptor superfamily members in HIV infection: new cellular targets for therapy?Mediators of inflammation · 2013Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Despite its clinical importance, the molecular biology of HIV-1 latency control is at best partially understood, and the literature remains conflicting. The most recent description that latent HIV-1 is integrated into actively expressed host genes has further confounded the situation. This lack of molecular understanding complicates our efforts to identify therapeutic compounds or strategies that could reactivate latent HIV-1 infection in patients, a prerequisite for the eradication of HIV-1 infection. Currently, many therapeutic development efforts operate under the assumption that a restrictive histone code could govern latent infection and that either dissipation of the histone-based restrictions or NF-κB activation could be sufficient to trigger HIV-1 reactivation. We here present data that suggest an additional, higher level of molecular control. During a high-content drug screening effort, we identified AS601245 as a potent inhibitor of HIV-1 reactivation in latently infected primary T cells and T cell lines. In either system, AS601245 inhibited HIV-1 reactivation despite high levels of induced NF-κB activation. This finding suggests the presence of a gatekeeper kinase activity that controls latent HIV-1 infection even in the presence of high levels of NF-κB activity. Potential therapeutic stimuli that do not target this gatekeeper kinase will likely fail to trigger efficient system-wide HIV-1 reactivation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.