ArticlePloS one2013
DDX5 facilitates HIV-1 replication as a cellular co-factor of Rev.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- Human RPL7 and DDX21 function synergistically with HTLV-1 Gag to overcome genomic RNA structural barriers that block tRNAPro primer annealing.Nucleic acids research · 2026Article
- Article
- Comparative Transcriptomics Analyses Identify DDX43 as a Cellular Regulator Involved in Suppressing HSV-2 Replication.Viruses · 2025Article
- Pathogenic SIV infection is associated with acceleration of epigenetic age in rhesus macaques.The Journal of clinical investigation · 2025Article
- Human microRNA miR-197-3p positively regulates HIV-1 virion infectivity through its target DDX52 by stabilizing Vif protein expression.The Journal of biological chemistry · 2025Article
- DEAD box RNA helicase 5 is a new pro-viral host factor for Sindbis virus infection.Virology journal · 2024Article
- Viral Subversion of the Chromosome Region Maintenance 1 Export Pathway and Its Consequences for the Cell Host.Viruses · 2023Review
- DDX5 inhibits type I IFN production by promoting degradation of TBK1 and disrupting formation of TBK1 - TRAF3 complex.Cellular and molecular life sciences : CMLS · 2023Article
- HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal.The Journal of clinical investigation · 2023Article
- Review
- Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19.International journal of molecular sciences · 2022Review
- DDX5: an expectable treater for viral infection- a literature review.Annals of translational medicine · 2022Review
- DEAD-ly Affairs: The Roles of DEAD-Box Proteins on HIV-1 Viral RNA Metabolism.Frontiers in cell and developmental biology · 2022Review
- HibeRNAtion: HIV-1 RNA Metabolism and Viral Latency.Frontiers in cellular and infection microbiology · 2022Review
- DExD/H-box helicases: multifunctional regulators in antiviral innate immunity.Cellular and molecular life sciences : CMLS · 2021Review
- Article
- Selective regulation in ribosome biogenesis and protein production for efficient viral translation.Archives of microbiology · 2021Review
- DDX5 potentiates HIV-1 transcription as a co-factor of Tat.Retrovirology · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
HIV-1 Rev plays an important role in the late phase of HIV-1 replication, which facilitates export of unspliced viral mRNAs from the nucleus to cytoplasm in infected cells. Recent studies have shown that DDX1 and DDX3 are co-factors of Rev for the export of HIV-1 transcripts. In this report, we have demonstrated that DDX5 (p68), which is a multifunctional DEAD-box RNA helicase, functions as a new cellular co-factor of HIV-1 Rev. We found that DDX5 affects Rev function through the Rev-RRE axis and subsequently enhances HIV-1 replication. Confocal microscopy and co-immunoprecipitation analysis indicated that DDX5 binds to Rev and this interaction is largely dependent on RNA. If the DEAD-box motif of DDX5 is mutated, DDX5 loses almost all of its ability to bind to Rev, indicating that the DEAD-box motif of DDX5 is required for the interaction between DDX5 and Rev. Our data indicate that interference of DDX5-Rev interaction could reduce HIV-1 replication and potentially provide a new molecular target for anti-HIV-1 therapeutics.
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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.