ArticleJournal of virology2020
A Stronger Transcription Regulatory Circuit of HIV-1C Drives the Rapid Establishment of Latency with Implications for the Direct Involvement of Tat.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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
9 citing papers in PubMed, 12 citations in OpenAlex.
- HIV-1 Tat: Molecular Switch in Viral Persistence and Emerging Technologies for Functional Cure.International journal of molecular sciences · 2025Review
- Development of a latency model for HIV-1 subtype C and the impact of long terminal repeat element genetic variation on latency reversal.Journal of virus eradication · 2024Article
- Proximity Ligation Assay to Detect the Proximity Between Host Proteins and Viral Proteins of HIV-1.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Experimental models for HIV latency and molecular tools for reservoir quantification-an update.Clinical microbiology reviews · 2023Review
- Review
- Enhanced Transcriptional Strength of HIV-1 Subtype C Minimizes Gene Expression Noise and Confers Stability to the Viral Latent State.Journal of virology · 2023Article
- An emerging and variant viral promoter of HIV-1 subtype C exhibits low-level gene expression noise.Retrovirology · 2021Article
- Addressing an HIV cure in LMIC.Retrovirology · 2021Review
- Balance between Retroviral Latency and Transcription: Based on HIV Model.Pathogens (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The magnitude of transcription factor binding site variation emerging in HIV-1 subtype C (HIV-1C), especially the addition of NF-κB motifs by sequence duplication, makes the examination of transcriptional silence challenging. How can HIV-1 establish and maintain latency despite having a strong long terminal repeat (LTR)? We constructed panels of subgenomic reporter viral vectors with varying copy numbers of NF-κB motifs (0 to 4 copies) and examined the profile of latency establishment in Jurkat cells. Surprisingly, we found that the stronger the viral promoter, the faster the latency establishment. Importantly, at the time of commitment to latency and subsequent points, Tat levels in the cell were not limiting. Using highly sensitive strategies, we demonstrate the presence of Tat in the latent cell, recruited to the latent LTR. Our data allude, for the first time, to Tat establishing a negative feedback loop during the late phases of viral infection, leading to the rapid silencing of the viral promoter.
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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.