ArticleBlood2009
Induction of HIV-1 latency and reactivation in primary memory CD4+ T cells.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 258 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
258 citing papers in PubMed, 345 citations in OpenAlex.
- The Depsipeptide Romidepsin Reverses HIV-1 Latency In Vivo.PLoS pathogens · 2015Trial
- Histone deacetylase inhibitor romidepsin induces HIV expression in CD4 T cells from patients on suppressive antiretroviral therapy at concentrations achieved by clinical dosing.PLoS pathogens · 2014Trial
- Pharmacological METTL3 inhibition attenuates HIV-1 latency reversal in CD4Antimicrobial agents and chemotherapy · 2026Article
- Quantitative limits of host-driven HIV transcription and host gene control by the viral transactivator Tat.Nucleic acids research · 2026Article
- Histone decrotonylation plays a distinct role in HIV latency.Science advances · 2026Article
- Clonal dynamics of HIV-infected and uninfected T cells.EBioMedicine · 2026Article
- HIV-seq reveals gene expression differences between HIV-transcribing cells from viremic and suppressed people with HIV.Nature communications · 2026Article
- HIV-1 Integration Site Determines the Transcriptional Fate and Persistence of Integrated Proviruses.bioRxiv : the preprint server for biology · 2026Article
- HIV Nef amplifies mechanical heterogeneity to promote immune evasion.bioRxiv : the preprint server for biology · 2025Article
- Single cell technologies and the biology of HIV-infected CD4 T-cell reservoirs.Current opinion in HIV and AIDS · 2025Review
- Using single cell technologies to understand HIV latency models.Current opinion in HIV and AIDS · 2025Review
- The p400 complex promotes HIV-1 latency by suppressing viral transcription and altering the host cell state.Nucleic acids research · 2025Article
- Modeling simian immunodeficiency virus (SIV) latency in primary rhesus macaque CD4bioRxiv : the preprint server for biology · 2025Article
- Fragment-Based Immune Cell Engager Antibodies in Treatment of Cancer, Infectious and Autoimmune Diseases: Lessons and Insights from Clinical and Translational Studies.Antibodies (Basel, Switzerland) · 2025Review
- Yoda1, a Piezo1 agonist, induced latent HIV reactivation associated with upregulation of CD3/TCR complex and HLA genes.Research square · 2025Article
- Article
- Heat shock protein 90 is a chaperone regulator of HIV-1 latency.PLoS pathogens · 2025Article
- The Complex Interactions Between HIV-1 and Human Host Cell Genome: From Molecular Mechanisms to Clinical Practice.International journal of molecular sciences · 2025Review
- A First-in-Class Dual Degrader of Bcl-2/Bcl-xL Reverses HIV Latency and Minimizes Ex Vivo Reservoirs from Patients.International journal of molecular sciences · 2025Article
- Tracking HIV persistence across T cell lineages during early ART-treated HIV-1-infection using a reservoir-marking humanized mouse model.Nature communications · 2025Article
198 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The use of antiretroviral therapy in HIV type 1 (HIV-1)-infected patients does not lead to virus eradication. This is due, to a significant degree, to the fact that HIV-1 can establish a highly stable reservoir of latently infected cells. In this work, we describe an ex vivo experimental system that generates high levels of HIV-1 latently infected memory cells using primary CD4+ T cells. Using this model, we were able to dissect the T cell-signaling pathways and to characterize the long terminal repeat (LTR) cis-acting elements involved in reactivation of HIV-1 in memory CD4+ T cells. We conclude that Lck and nuclear factor of activated T cells (NFAT), but not NF-kappaB, are required for optimal latent virus reactivation in memory T cells. We also found that the cis-acting elements which are critical toward HIV-1 reactivation are the Sp1 and kappaB/NFAT transcription factor binding sites.
Indexed as
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What OpenQuestion holds
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.