ArticleScientific reports2016
The ORF3 Protein of Genotype 1 Hepatitis E Virus Suppresses TLR3-induced NF-κB Signaling via TRADD and RIP1.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
35 citing papers in PubMed, 57 citations in OpenAlex.
- The hepatitis E virus capsid protein ORF2 counteracts cell-intrinsic antiviral responses to enable persistent replication in cell culture.PLoS pathogens · 2025Article
- Cell line-dependent release of quasi-enveloped hepatitis E virus reveals alternative Golgi-associated egress in the absence of pORF3.Frontiers in cellular and infection microbiology · 2025Article
- Hepatitis E virus: from innate sensing to adaptive immune responses.Nature reviews. Gastroenterology & hepatology · 2024Review
- Multiple Functions of Hepatitis E Virus ORF3.Microorganisms · 2024Review
- Multi-epitope vaccine design for hepatitis E virus based on protein ORF2 and ORF3.Frontiers in microbiology · 2024Article
- Amino acid pattern reveals multi-functionality of ORF3 protein from HEV.Bioinformation · 2024Article
- Virus-Host Protein Interaction Network of the Hepatitis E Virus ORF2-4 by Mammalian Two-Hybrid Assays.Viruses · 2023Article
- Hepatitis E Virus Protease Inhibits the Activity of Eukaryotic Initiation Factor 2-Alpha Kinase 4 and Promotes Virus Survival.Journal of virology · 2023Article
- RIPK1 in the inflammatory response and sepsis: Recent advances, drug discovery and beyond.Frontiers in immunology · 2023Review
- Structural aspects of hepatitis E virus.Archives of virology · 2022Review
- An Arginine-Rich Motif in the ORF2 capsid protein regulates the hepatitis E virus lifecycle and interactions with the host cell.PLoS pathogens · 2022Article
- Analysis of codon usage patterns in open reading frame 4 of hepatitis E viruses.Beni-Suef University journal of basic and applied sciences · 2022Article
- Beyond the Usual Suspects: Hepatitis E Virus and Its Implications in Hepatocellular Carcinoma.Cancers · 2021Review
- Role of "dual-personality" fragments in HEV adaptation-analysis of Y-domain region.Journal, genetic engineering & biotechnology · 2021Article
- Hepatitis E Virus Immunopathogenesis.Pathogens (Basel, Switzerland) · 2021Review
- Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors.International journal of molecular sciences · 2021Review
- Research progress on Toll-like receptor signal transduction and its roles in antimicrobial immune responses.Applied microbiology and biotechnology · 2021Review
- Open reading frame 3 protein of hepatitis E virus: Multi-function protein with endless potential.World journal of gastroenterology · 2021Review
- Review
- Structural and molecular biology of hepatitis E virus.Computational and structural biotechnology journal · 2021Review
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
Hepatitis E virus (HEV) genotype 1 infection is common and can emerge as outbreaks in developing areas, thus posing a threat to public health. However, due to the absence of feasible animal models, the mechanism of HE pathogenesis remains obscure. The HEV pathogenic mechanism has been suggested to be mediated by the immune system and not by direct viral duplication. We firstly discovered that the open reading frame 3 (ORF3) protein of genotype 1 HEV downregulates TLR3-mediated NF-κB signaling in Human A549 Lung Epithelial Cells (A549 cells) which were exposed to different TLR agonists associated with viral nucleic acids. Additionally, we identified the P2 domain of ORF3 as being responsible for this inhibition. Intriguingly, tumor necrosis factor receptor 1-associated death domain protein (TRADD) expression and receptor-interacting protein kinase 1 (RIP1) K63-ubiquitination were reduced in the presence of both ORF3 and Poly(I:C). Furthermore, we found that Lys377 of RIP1 acts as the functional ubiquitination site for ORF3-associated inhibition. Overall, we found that ORF3 protein downregulates TLR3-mediated NF-κB signaling via TRADD and RIP1. Our findings provide a new perspective on the cellular response in HEV infection and expand our understanding of the molecular mechanisms of HEV pathogenesis in innate immunity.
Indexed as
Identifiers
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.