ArticleThe Journal of clinical investigation2020
Filgotinib suppresses HIV-1-driven gene transcription by inhibiting HIV-1 splicing and T cell activation.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- Clonal dynamics of HIV-infected and uninfected T cells.EBioMedicine · 2026Article
- Filgotinib inhibits METTL3-mediated mNPJ precision oncology · 2026Article
- HIV-1-encoded circular RNA enhances viral transcription through Tat binding.Nature microbiology · 2026Article
- Article
- Modulation of IRF7-driven transcription as a strategy to control HIV-1 latency.Frontiers in immunology · 2026Article
- RNA splicing patterns contribute to burst size variation among HIV-1-infected Jurkat cell clones.Journal of virology · 2025Article
- MrHAMER2: high-accuracy long-read RNA sequencing to decode isoform-specific variation in viral transcripts during latency.bioRxiv : the preprint server for biology · 2025Article
- Article
- Article
- CAR-T Therapy in HIV: Pioneering Advances and Navigating Challenges.Infectious diseases & immunity · 2024Article
- Silencing the transcriptionally active HIV reservoir to improve treatment outcomes.Nature microbiology · 2024Article
- Transcription of HIV-1 at sites of intact latent provirus integration.The Journal of experimental medicine · 2024Article
- Mechanisms and efficacy of small molecule latency-promoting agents to inhibit HIV reactivation ex vivo.JCI insight · 2024Article
- Transcription of HIV-1 at sites of intact latent provirus integration.bioRxiv : the preprint server for biology · 2024Article
- Review
- Targeting Viral Transcription for HIV Cure Strategies.Microorganisms · 2024Review
- Article
- Article
- Integration site-dependent HIV-1 promoter activity shapes host chromatin conformation.Genome research · 2023Article
- Machine Learning Bolsters Evidence That D1, Nef, and Tat Influence HIV Reservoir Dynamics.Pathogens & immunity · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Despite effective antiretroviral therapy, HIV-1-infected cells continue to produce viral antigens and induce chronic immune exhaustion. We propose to identify HIV-1-suppressing agents that can inhibit HIV-1 reactivation and reduce HIV-1-induced immune activation. Using a newly developed dual-reporter system and a high-throughput drug screen, we identified FDA-approved drugs that can suppress HIV-1 reactivation in both cell line models and CD4+ T cells from virally suppressed HIV-1-infected individuals. We identified 11 cellular pathways required for HIV-1 reactivation as druggable targets. Using differential expression analysis, gene set enrichment analysis, and exon-intron landscape analysis, we examined the impact of drug treatment on the cellular environment at a genome-wide level. We identified what we believe to be a new function of a JAK inhibitor, filgotinib, that suppresses HIV-1 splicing. First, filgotinib preferentially suppresses spliced HIV-1 RNA transcription. Second, filgotinib suppresses HIV-1-driven aberrant cancer-related gene expression at the integration site. Third, we found that filgotinib suppresses HIV-1 transcription by inhibiting T cell activation and by modulating RNA splicing. Finally, we found that filgotinib treatment reduces the proliferation of HIV-1-infected cells. Overall, the combination of a drug screen and transcriptome analysis provides systematic understanding of cellular targets required for HIV-1 reactivation and drug candidates that may reduce HIV-1-related immune activation.
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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.