ArticleProceedings of the National Academy of Sciences of the United States of America2003
Identification of T cell-signaling pathways that stimulate latent HIV in primary cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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Who cites it
70 citing papers in PubMed, 106 citations in OpenAlex.
- Heat shock protein 90 is a chaperone regulator of HIV-1 latency.PLoS pathogens · 2025Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- CD4+ T cells with latent HIV-1 have reduced proliferative responses to T cell receptor stimulation.The Journal of experimental medicine · 2024Article
- Article
- The latent reservoir of inducible, infectious HIV-1 does not decrease despite decades of antiretroviral therapy.The Journal of clinical investigation · 2023Article
- Upstream Stimulatory Factors Regulate HIV-1 Latency and Are Required for Robust T Cell Activation.Viruses · 2023Article
- The role of tunneling nanotubes during early stages of HIV infection and reactivation: implications in HIV cure.NeuroImmune pharmacology and therapeutics · 2023Review
- TRIM24 controls induction of latent HIV-1 by stimulating transcriptional elongation.Communications biology · 2023Article
- Genome-wide CRISPR screens identify combinations of candidate latency reversing agents for targeting the latent HIV-1 reservoir.Science translational medicine · 2022Article
- Hydrogen sulfide blocks HIV rebound by maintaining mitochondrial bioenergetics and redox homeostasis.eLife · 2021Article
- AP-1 and NF-κB synergize to transcriptionally activate latent HIV upon T-cell receptor activation.FEBS letters · 2021Article
- HSF1 inhibition attenuates HIV-1 latency reversal mediated by several candidate LRAs In Vitro and Ex Vivo.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- HIV-1 Proviral Transcription and Latency in the New Era.Viruses · 2020Review
- Diversity of small molecule HIV-1 latency reversing agents identified in low- and high-throughput small molecule screens.Medicinal research reviews · 2020Review
- Benefits and limitations of humanized mice in HIV persistence studies.Retrovirology · 2020Review
- Semen Exosomes Promote Transcriptional Silencing of HIV-1 by Disrupting NF-κB/Sp1/Tat Circuitry.Journal of virology · 2018Article
- Myeloid Dendritic Cells Induce HIV Latency in Proliferating CD4Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Humanized Mouse Models for Human Immunodeficiency Virus Infection.Annual review of virology · 2017Review
- Targeting type I interferon-mediated activation restores immune function in chronic HIV infection.The Journal of clinical investigation · 2017Article
- Using animal models to overcome temporal, spatial and combinatorial challenges in HIV persistence research.Journal of translational medicine · 2016Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Eradication of HIV infection depends on the elimination of a small, but stable population of latently infected T cells. After the discontinuation of therapy, activation of latent virus can rekindle infection. To purge this reservoir, it is necessary to define cellular signaling pathways that lead to activation of latent HIV. We used the SCID-hu (Thy/Liv) mouse model of HIV latency to analyze a broad array of T cell-signaling pathways and show in primary, quiescent cells that viral induction depends on the activation of two primary intracellular signaling pathways, protein kinase C or nuclear factor of activated T cells (NF-AT). In contrast, inhibition or activation of other important T cell stimulatory pathways (such as mitogen-activated protein kinase, calcium flux, or histone deacetylation) do not significantly induce virus expression. We found that the activation of NF-kappaB is critical to viral reactivation; however, all pathways that stimulate NF-kappaBdonot reactivate latent virus. Our studies further show that inhibition of NF-kappaB does not prevent activation of HIV by NF-AT, indicating that these pathways can function independently to activate the HIV LTR. Thus, we define several molecular pathways that trigger HIV reactivation from latency and provide evidence that latent HIV infection is maintained by the functional lack of particular transcription factors in quiescent cells.
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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.