ArticlePLoS pathogens2023
A modular CRISPR screen identifies individual and combination pathways contributing to HIV-1 latency.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- BRD proteins in human retroviral infection: emerging evidence from HIV-1 and future perspectives for HTLV-1.Molecular biology reports · 2026Review
- CypA is a molecular barrier to HIV emergence from Eastern chimpanzees.bioRxiv : the preprint server for biology · 2026Article
- The human chromatin remodeling complex p400 restricts HIV-1 transcription in a Tat-dependent manner.Nucleic acids research · 2025Article
- HIV-1 latency reversing agents converge on phosphoregulation of nuclear protein complexes.bioRxiv : the preprint server for biology · 2025Article
- Retinol Binding Protein 4 reactivates latent HIV-1 by triggering canonical NF-κB, JAK/STAT5 and JNK signalling.Signal transduction and targeted therapy · 2025Article
- Using single cell technologies to understand HIV latency models.Current opinion in HIV and AIDS · 2025Review
- BET degraders reveal BRD4 disruption of 7SK and P-TEFb is critical for effective reactivation of latent HIV in CD4+ T-cells.Journal of virology · 2025Article
- Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal.eLife · 2025Article
- A targeted CRISPR screen identifies ETS1 as a regulator of HIV-1 latency.PLoS pathogens · 2025Article
- Synergistic Activity of Second Mitochondrial-Derived Activator of Caspases Mimetic with Toll-like Receptor 8 Agonist Reverses HIV-1-Latency and Enhances Antiviral Immunity.International journal of molecular sciences · 2025Article
- A high-throughput, microplate reader-based method to monitor in vitro HIV latency reversal in the absence of flow cytometry.Virology · 2025Article
- CBP/p300 lysine acetyltransferases inhibit HIV-1 expression in latently infected T cells.iScience · 2024Article
- Replication competent HIV-guided CRISPR screen identifies antiviral factors including targets of the accessory protein Nef.Nature communications · 2024Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- IDR-targeting compounds suppress HPV genome replication via disruption of phospho-BRD4 association with DNA damage response factors.Molecular cell · 2024Article
- A CRISPR Screen of HIV Dependency Factors Reveals ThatViruses · 2023Article
- A CRISPR screen of HIV dependency factors revealsbioRxiv : the preprint server for biology · 2023Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Transcriptional silencing of latent HIV-1 proviruses entails complex and overlapping mechanisms that pose a major barrier to in vivo elimination of HIV-1. We developed a new latency CRISPR screening strategy, called Latency HIV-CRISPR which uses the packaging of guideRNA-encoding lentiviral vector genomes into the supernatant of budding virions as a direct readout of factors involved in the maintenance of HIV-1 latency. We developed a custom guideRNA library targeting epigenetic regulatory genes and paired the screen with and without a latency reversal agent-AZD5582, an activator of the non-canonical NFκB pathway-to examine a combination of mechanisms controlling HIV-1 latency. A component of the Nucleosome Acetyltransferase of H4 histone acetylation (NuA4 HAT) complex, ING3, acts in concert with AZD5582 to activate proviruses in J-Lat cell lines and in a primary CD4+ T cell model of HIV-1 latency. We found that the knockout of ING3 reduces acetylation of the H4 histone tail and BRD4 occupancy on the HIV-1 LTR. However, the combination of ING3 knockout accompanied with the activation of the non-canonical NFκB pathway via AZD5582 resulted in a dramatic increase in initiation and elongation of RNA Polymerase II on the HIV-1 provirus in a manner that is nearly unique among all cellular promoters.
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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.