ArticleJournal of virology2021
RNA Helicase DDX17 Inhibits Hepatitis B Virus Replication by Blocking Viral Pregenomic RNA Encapsidation.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
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Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- DDX17 and viral infection.Virulence · 2026Review
- DDX17-mediated raptor-dependent mTORC1 activation links autophagy inhibition and metabolic compensation in HCC development.Cellular & molecular biology letters · 2026Article
- DNA synthesis inside the hepatitis B virus creates a high-energy spool.bioRxiv : the preprint server for biology · 2026Article
- DTMUV upregulates DDX17 expression to facilitate viral replication.Veterinary research · 2025Article
- Interferon alpha-inducible protein 27 (IFI27) inhibits hepatitis B virus (HBV) transcription through downregulating cellular transcription factor C/EBPα.Journal of virology · 2025Article
- Hepatitis B Virus Nucleocapsid Assembly.Journal of molecular biology · 2025Review
- 3A and 2B proteins of SVA play chess game with host restriction factor DDX23 by apoptotic pathway.Journal of virology · 2025Article
- HBV p22-interacting protein C1QBP inhibits viral replication through impeding nucleocapsid formation and nuclear import.PLoS pathogens · 2025Article
- Cell-intrinsic regulation of HBV RNAs by the nonsense-mediated mRNA decay pathway controls viral replication.iScience · 2025Article
- RNA helicases, DDX5 and DDX17, facilitate lytic reactivation of gammaherpesviruses.PLoS pathogens · 2025Article
- Established and Emerging Roles of DEAD/H-Box Helicases in Regulating Infection and Immunity.Immunological reviews · 2025Review
- Regulation of viral replication by host restriction factors.Frontiers in immunology · 2025Review
- Helicase protein DDX11 as a novel antiviral factor promoting RIG-I-MAVS-mediated signaling pathway.mBio · 2024Article
- RNA Helicase DDX5 in Association With IFI16 and the Polycomb Repressive Complex 2 Silences Transcription of the Hepatitis B Virus by Interferon.Journal of medical virology · 2024Article
- C G composition in transposon-derived genes is increased in FXD with perturbed immune system.NAR molecular medicine · 2024Article
- [Post-transcriptional regulation mechanism and antiviral strategy of hepatitis B virus RNA].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024Review
- Review
- Versatility of the Zinc-Finger Antiviral Protein (ZAP) As a Modulator of Viral Infections.International journal of biological sciences · 2024Review
- Transcriptome and proteomic analysis of mpox virus F3L-expressing cells.Frontiers in cellular and infection microbiology · 2024Article
- RNA binding protein TIAR modulates HBV replication by tipping the balance of pgRNA translation.Signal transduction and targeted therapy · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
DDX17 is a member of the DEAD-box helicase family proteins involved in cellular RNA folding, splicing, and translation. It has been reported that DDX17 serves as a cofactor of host zinc finger antiviral protein (ZAP)-mediated retroviral RNA degradation and exerts direct antiviral function against Raft Valley fever virus through binding to specific stem-loop structures of viral RNA. Intriguingly, we have previously shown that ZAP inhibits hepatitis B virus (HBV) replication through promoting viral RNA decay, and the ZAP-responsive element (ZRE) of HBV pregenomic RNA (pgRNA) contains a stem-loop structure, specifically epsilon, which serves as the packaging signal for pgRNA encapsidation. In this study, we demonstrated that the endogenous DDX17 is constitutively expressed in human hepatocyte-derived cells but dispensable for ZAP-mediated HBV RNA degradation. However, DDX17 was found to inhibit HBV replication primarily by reducing the level of cytoplasmic encapsidated pgRNA in a helicase-dependent manner. Immunofluorescence assay revealed that DDX17 could gain access to cytoplasm from nucleus in the presence of HBV RNA. In addition, RNA immunoprecipitation and electrophoretic mobility shift assays demonstrated that the enzymatically active DDX17 competes with HBV polymerase to bind to pgRNA at the 5' epsilon motif. In summary, our study suggests that DDX17 serves as an intrinsic host restriction factor against HBV through interfering with pgRNA encapsidation.
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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.