ArticlePLoS pathogens2018
Inhibition of Japanese encephalitis virus infection by the host zinc-finger antiviral protein.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- The Post-Transcriptional Regulatory Element of Hepatitis B Virus: From Discovery to Therapy.Viruses · 2024Pooled it
- Increased or decreased numbers of CpG dinucleotide motifs in the genome of influenza A virus do not affectJournal of virology · 2026Article
- Japanese Encephalitis Virus and Host Innate Immunity: Insights Into TLR Signaling, PRR Crosstalk, and Viral Immune Evasion.Cell biochemistry and function · 2026Review
- Lost in translation: interferon-stimulated genes targeting flavivirus protein synthesis.Journal of virology · 2026Review
- SPRY domains encode ubiquitin ligase specificity for ZAP and RIG-I.PLoS pathogens · 2026Article
- Annexin A2 facilitates Japanese encephalitis virus replication by regulating endocytosis and intracellular transport in PK15 cells.Frontiers in microbiology · 2026Article
- Analysis of the Porcine Reproductive and Respiratory Syndrome Virus Nucleocapsid Interactome.Journal of proteome research · 2025Article
- West Nile virus vaccine candidates attenuated by dinucleotide enrichment are immunogenic and protective against lethal infection.PLoS pathogens · 2025Article
- HIV-2 evades restriction by ZAP through adaptations in the U3 LTR region despite increased CpG levels.Nucleic acids research · 2025Article
- Zika virus impairs non-homologous end joining and exacerbates DNA damage in neural progenitors derived from Huntington's disease iPSCs via mutant huntingtin-elicited Ku70/Ku80 complex disruption.Stem cell research & therapy · 2025Article
- Mono-ADP-ribosylating PARP enzymes in cellular signaling and disease.Journal of cell science · 2025Review
- The zinc finger protein ZFP36L2 inhibits flavivirus infection via the 5'-3' XRN1-mediated RNA decay pathway in the replication complexes.Journal of biomedical science · 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
- Review
- Review
- Endogenous ZAP affects Zika virus RNA interactome.RNA biology · 2024Article
- Versatility of the Zinc-Finger Antiviral Protein (ZAP) As a Modulator of Viral Infections.International journal of biological sciences · 2024Review
- Antiviral Activity of Zinc Finger Antiviral Protein (ZAP) in Different Virus Families.Pathogens (Basel, Switzerland) · 2023Review
- Sensing nucleotide composition in virus RNA.Bioscience reports · 2023Review
13 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
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CCCH-type zinc-finger antiviral protein (ZAP) is a host factor that restricts the infection of many viruses mainly through RNA degradation, translation inhibition and innate immune responses. So far, only one flavivirus, yellow fever virus, has been reported to be ZAP-resistant. Here, we investigated the antiviral potential of human ZAP (isoform ZAP-L and ZAP-S) against three flaviviruses, Japanese encephalitis virus (JEV), dengue virus (DENV) and Zika virus (ZIKV). Infection of JEV but not DENV or ZIKV was blocked by ZAP overexpression, and depletion of endogenous ZAP enhanced JEV replication. ZAP hampered JEV translation and targeted viral RNA for 3'-5' RNA exosome-mediated degradation. The zinc-finger motifs of ZAP were essential for RNA targeting and anti-JEV activity. JEV 3'-UTR, especially in the region with dumbbell structures and high content of CG dinucleotide, was mapped to bind ZAP and confer sensitivity to ZAP. In summary, we identified JEV as the first ZAP-sensitive flavivirus. ZAP may act as an intrinsic antiviral factor through specific RNA binding to fight against JEV 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.