ArticlePLoS pathogens2010
Hepatitis B virus polymerase blocks pattern recognition receptor signaling via interaction with DDX3: implications for immune evasion.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
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.
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Who cites it
119 citing papers in PubMed, 205 citations in OpenAlex.
- Multiple doses of hepatitis B recombinant vaccine for chronic hepatitis B patients with low surface antigen levels: a pilot study.Hepatology international · 2018Trial
- Viral persistence and immune dysfunction in chronic hepatitis B: Mechanisms of post-treatment antigen asynchrony.iScience · 2026Review
- Review
- Engineering a dual-antigen mRNA vaccine to restore immune control in chronic hepatitis B.Nature communications · 2026Article
- Emerging roles of POLR2L of RNA polymerase II dynamics and disease mechanisms (Review).Molecular medicine reports · 2026Review
- At the crossroads of immunity and hijacking: dual roles of DDX proteins during host-virus interactions.Frontiers in cellular and infection microbiology · 2026Review
- Advancements and expanding applications of CAR-T cell therapy.Frontiers in immunology · 2026Review
- The Intrinsic Innate Immunity of Hepatocytes Suppresses HBV Replication and Is Antagonized by HBx.Viruses · 2025Article
- Innate immune recognition in hepatitis B virus infection.Virulence · 2025Review
- Herpes Simplex 2 Virus Depletes Cells of DEAD-Box Helicase 3 Protein by Packaging It into Virions.Viruses · 2025Article
- Hepatocyte-intrinsic innate immunity in hepatitis B virus infection: A focused review.World journal of hepatology · 2025Review
- DDX3X and virus interactions: functional diversity and antiviral strategies.Frontiers in microbiology · 2025Review
- Mechanisms underlying the compromised clinical efficacy of interferon in clearing HBV.Virology journal · 2024Review
- Article
- PRRSV hijacks DDX3X protein and induces ferroptosis to facilitate viral replication.Veterinary research · 2024Article
- Insights into Immune Exhaustion in Chronic Hepatitis B: A Review of Checkpoint Receptor Expression.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Bovine DDX3X Restrains Bovine SP110c-Mediated Activation of Inflammasome in Macrophages.Animals : an open access journal from MDPI · 2024Article
- Hepatitis B surface antigen expression impairs endoplasmic reticulum stress-related autophagic flux by decreasing LAMP2.JHEP reports : innovation in hepatology · 2024Article
- Conserved Functions ofInternational journal of molecular sciences · 2024Article
- Epigenetic addition of mCell death & disease · 2024Article
59 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral infection leads to induction of pattern-recognition receptor signaling, which leads to interferon regulatory factor (IRF) activation and ultimately interferon (IFN) production. To establish infection, many viruses have strategies to evade the innate immunity. For the hepatitis B virus (HBV), which causes chronic infection in the liver, the evasion strategy remains uncertain. We now show that HBV polymerase (Pol) blocks IRF signaling, indicating that HBV Pol is the viral molecule that effectively counteracts host innate immune response. In particular, HBV Pol inhibits TANK-binding kinase 1 (TBK1)/IkappaB kinase-epsilon (IKKepsilon), the effector kinases of IRF signaling. Intriguingly, HBV Pol inhibits TBK1/IKKepsilon activity by disrupting the interaction between IKKepsilon and DDX3 DEAD box RNA helicase, which was recently shown to augment TBK1/IKKepsilon activity. This unexpected role of HBV Pol may explain how HBV evades innate immune response in the early phase of the infection. A therapeutic implication of this work is that a strategy to interfere with the HBV Pol-DDX3 interaction might lead to the resolution of life-long persistent infection.
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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.