ArticlePLoS pathogens2013
Inhibition of hepatitis B virus replication by the host zinc finger antiviral protein.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 2 of them syntheses that pooled it.
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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
166 citing papers in PubMed, 2 syntheses or guidelines pooled it, 241 citations in OpenAlex.
- The Post-Transcriptional Regulatory Element of Hepatitis B Virus: From Discovery to Therapy.Viruses · 2024Pooled it
- Genetic bases of resistance to the rice hoja blanca disease deciphered by a quantitative trait locus approach.G3 (Bethesda, Md.) · 2023Pooled it
- Quantitative Characterization of the Serum Elemental Signatures in HBV Infection.Biological trace element research · 2026Article
- DNA synthesis inside the hepatitis B virus creates a high-energy spool.bioRxiv : the preprint server for biology · 2026Article
- Altered expression of ADAR1, N4BP1, and PSME1 in PBMCs correlated with therapeutic outcomes in HBeAg-negative chronic hepatitis B patients treated with Peg-IFN-α.Frontiers in cellular and infection microbiology · 2026Observational
- 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
- Non canonical BRCA1 promotes cell survival via modulating PARP13-mediated SEC61G mRNA decay.Oncogenesis · 2025Article
- HIV-2 evades restriction by ZAP through adaptations in the U3 LTR region despite increased CpG levels.Nucleic acids research · 2025Article
- Epigenetic drugs against human DNA viruses and retroviruses.Antiviral research · 2025Review
- Cell-intrinsic regulation of HBV RNAs by the nonsense-mediated mRNA decay pathway controls viral replication.iScience · 2025Article
- Identification and validation of a 9-RBPs-related gene signature associated with prognosis and immune infiltration in bladder cancer based on bioinformatics analysis and machine learning.Translational andrology and urology · 2025Article
- Host ZAP activity correlates with the levels of CpG suppression in primate lentiviruses.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- NEDD4-binding protein 1 suppresses hepatitis B virus replication by regulating viral RNAs.The Journal of general virology · 2025Article
- Infectious Subgenomic Amplicon Strategies for Japanese Encephalitis and West Nile Viruses.Journal of medical virology · 2025Article
- Endogenous ZAP is associated with altered Zika virus infection phenotype.Virology journal · 2024Article
- ZC3HAV1 facilitates STING activation and enhances inflammation.Communications biology · 2024Article
- Dual Roles of Host Zinc Finger Proteins in Viral RNA Regulation: Decay or Stabilization.International journal of molecular sciences · 2024Review
- Liver mechanosignaling as a natural anti-hepatitis B virus mechanism.Nature communications · 2024Article
- Identification of Host Proteins Involved in Hepatitis B Virus Genome Packaging.Journal of proteome research · 2024Article
106 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
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The zinc finger antiviral protein (ZAP) is a mammalian host restriction factor that inhibits the replication of a variety of RNA viruses, including retroviruses, alphaviruses and filoviruses, through interaction with the ZAP-responsive elements (ZRE) in viral RNA, and recruiting the exosome to degrade RNA substrate. Hepatitis B virus (HBV) is a pararetrovirus that replicates its genomic DNA via reverse transcription of a viral pregenomic (pg) RNA precursor. Here, we demonstrate that the two isoforms of human ZAP (hZAP-L and -S) inhibit HBV replication in human hepatocyte-derived cells through posttranscriptional down-regulation of viral pgRNA. Mechanistically, the zinc finger motif-containing N-terminus of hZAP is responsible for the reduction of HBV RNA, and the integrity of the four zinc finger motifs is essential for ZAP to bind to HBV RNA and fulfill its antiviral function. The ZRE sequences conferring the susceptibility of viral RNA to ZAP-mediated RNA decay were mapped to the terminal redundant region (nt 1820-1918) of HBV pgRNA. In agreement with its role as a host restriction factor and as an innate immune mediator for HBV infection, ZAP was upregulated in cultured primary human hepatocytes and hepatocyte-derived cells upon IFN-α treatment or IPS-1 activation, and in the livers of hepatitis B patients during immune active phase. Knock down of ZAP expression increased the level of HBV RNA and partially attenuated the antiviral effect elicited by IPS-1 in cell cultures. In summary, we demonstrated that ZAP is an intrinsic host antiviral factor with activity against HBV through down-regulation of viral RNA, and that ZAP plays a role in the innate control of HBV replication. Our findings thus shed light on virus-host interaction, viral pathogenesis, and antiviral approaches.
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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.