ReviewThe Journal of clinical investigation2016
Molecular mechanisms of HIV latency.
Review in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
105 citing papers in PubMed, 139 citations in OpenAlex.
- Trial
- Cell heterogeneity contributes to the variable response of HIV-1 to latency-reversing agents.Science advances · 2026Article
- A novel synergistic phycobiliprotein combination against HIV-1 shows potent antiviral activity.AMB Express · 2026Article
- Targeting NF-κB signaling for HIV latency reversal: Mechanisms, challenges, and therapeutic perspectives.Virus research · 2026Review
- Identification of the cellular factor KLF16 as a novel epigenetic repressor of HIV-1 transcription.Research square · 2026Article
- Identification of the cellular transcription factor KLF16 as a novel repressive epigenetic repressor of HIV-1 transcription.bioRxiv : the preprint server for biology · 2026Article
- The HIV reservoir landscape in elite controllers.Current opinion in HIV and AIDS · 2026Review
- Fueling silence: Metabolic control of latent viral infection.PLoS pathogens · 2026Article
- Integrative genomic and immunoinformatic approach for characterizing HIV-1 pol, vpr, and Nef genes and designing a multi-epitope vaccine.Scientific reports · 2025Article
- Novel bioinformatics approaches to design epitope-based vaccine against HIV latency by inquiring CTL epitopes and built-in adjuvants.Scientific reports · 2025Article
- HIV-1 Tat: Molecular Switch in Viral Persistence and Emerging Technologies for Functional Cure.International journal of molecular sciences · 2025Review
- Bird's eye view of natural products for the development of new anti-HIV agents: Understanding from a therapeutic viewpoint.Animal models and experimental medicine · 2025Review
- Magnetoelectric Extracellular Vesicle Latency-Targeting (MELT) Nanotherapeutic for the Block-Lock-and-Kill HIV Eradication Strategy.Biomedicines · 2025Article
- Article
- The role of genetic diversity, epigenetic regulation, and sex-based differences in HIV cure research: a comprehensive review.Epigenetics & chromatin · 2025Review
- The Proviral Reservoirs of Human Immunodeficiency Virus (HIV) Infection.Pathogens (Basel, Switzerland) · 2024Review
- Breaking the Silence: Regulation of HIV Transcription and Latency on the Road to a Cure.Viruses · 2023Review
- Characteristics and mechanisms of latency-reversing agents in the activation of the human immunodeficiency virus 1 reservoir.Archives of virology · 2023Review
- Scopoletin Reactivates Latent HIV-1 by Inducing NF-κB Expression without Global T Cell Activation.International journal of molecular sciences · 2023Article
- Humanized Mice for Studies of HIV-1 Persistence and Elimination.Pathogens (Basel, Switzerland) · 2023Review
45 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
3 authors at 1 institution in 1 country.
Funding
Abstract
HIV seeds reservoirs of latent proviruses in the earliest phases of infection. These reservoirs are found in many sites, including circulating cells, the lymphoid system, the brain, and other tissues. The "shock and kill" strategy, where HIV transcription is reactivated so that antiretroviral therapy and the immune system clear the infection, has been proposed as one approach to curing AIDS. In addition to many defective viruses, resting hematopoietic cells harbor transcriptionally latent HIV. Understanding basic mechanisms of HIV gene expression provides a road map for this strategy, allowing for manipulation of critical cellular and viral transcription factors in such a way as to maximize HIV gene expression while avoiding global T cell activation. These transcription factors include NF-κB and the HIV transactivator of transcription (Tat) as well as the cyclin-dependent kinases CDK13 and CDK11 and positive transcription elongation factor b (P-TEFb). Possible therapies involve agents that activate these proteins or release P-TEFb from the inactive 7SK small nuclear ribonucleoprotein (snRNP). These proposed therapies include PKC and MAPK agonists as well as histone deacetylase inhibitors (HDACis) and bromodomain and extraterminal (BET) bromodomain inhibitors (BETis), which act synergistically to reactivate HIV in latently infected cells.
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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.