ReviewExpert opinion on therapeutic targets2016
Cyclin-dependent kinases as therapeutic targets for HIV-1 infection.
Review in Expert opinion on therapeutic targets, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 24 citations in OpenAlex.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- Decoding cross-talk between Mpox and HIV: insights from transcriptomics and network-based analyses.Virology journal · 2025Article
- FUBP3 enhances HIV-1 transcriptional activity and regulates immune response pathways in T cells.Molecular therapy. Nucleic acids · 2025Article
- Uncovering potential CDK9 inhibitors from natural compound databases through docking-based virtual screening and MD simulations.Journal of molecular modeling · 2024Article
- Controversies in the Design of Strategies for the Cure of HIV Infection.Pathogens (Basel, Switzerland) · 2023Review
- When cyclin-dependent kinases meet viral infections, including SARS-CoV-2.Journal of medical virology · 2022Review
- Insights Into Persistent HIV-1 Infection and Functional Cure: Novel Capabilities and Strategies.Frontiers in microbiology · 2022Review
- Are BET Inhibitors yet Promising Latency-Reversing Agents for HIV-1 Reactivation in AIDS Therapy?Viruses · 2021Review
- CVB3 VP1 interacts with MAT1 to inhibit cell proliferation by interfering with Cdk-activating kinase complex activity in CVB3-induced acute pancreatitis.PLoS pathogens · 2021Article
- Humanized Mice for the Evaluation of Novel HIV-1 Therapies.Frontiers in immunology · 2021Review
- Review
- The Dual-Specificity Kinase DYRK1A Modulates the Levels of Cyclin L2 To Control HIV Replication in Macrophages.Journal of virology · 2020Article
- HIV Transcription Is Independent of Mediator Kinases.AIDS research and human retroviruses · 2019Article
- Inhibitors of Signaling Pathways That Block Reversal of HIV-1 Latency.Antimicrobial agents and chemotherapy · 2019Article
- Microglial Cells: The Main HIV-1 Reservoir in the Brain.Frontiers in cellular and infection microbiology · 2019Review
- HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies.Molecules (Basel, Switzerland) · 2018Review
- Post-translational Modification-Based Regulation of HIV Replication.Frontiers in microbiology · 2018Review
- Reactivation of HIV-1 from Latency by an Ingenol Derivative from Euphorbia Kansui.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
introductionA number of cyclin-dependent kinases (CDKs) mediate key steps in the HIV-1 replication cycle and therefore have potential to serve as therapeutic targets for HIV-1 infection, especially in HIV-1 cure strategies. Current HIV-1 cure strategies involve the development of small molecules that are able to activate HIV-1 from latent infection, thereby allowing the immune system to recognize and clear infected cells. Areas covered: The role of seven CDK family members in the HIV-1 replication cycle is reviewed, with a focus on CDK9, as the mechanism whereby the viral Tat protein utilizes CDK9 to enhance viral replication is known in considerable detail. Expert opinion: Given the essential roles of CDKs in cellular proliferation and gene expression, small molecules that inhibit CDKs are unlikely to be feasible therapeutics for HIV-1 infection. However, small molecules that activate CDK9 and other select CDKs such as CDK11 have potential to reactivate latent HIV-1 and contribute to a functional cure of infection.
Indexed as
Identifiers
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.