ArticleJournal of virology2018
Potent Inhibition of Hepatitis E Virus Release by a Cyclic Peptide Inhibitor of the Interaction between Viral Open Reading Frame 3 Protein and Host Tumor Susceptibility Gene 101.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Impact of hepatitis E virus host- and virus-derived insertions on the antiviral response in primary human hepatocytes.bioRxiv : the preprint server for biology · 2026Article
- Network controllability analysis reveals the antiviral potential of Etravirine against hepatitis E virus infection.mSystems · 2025Article
- Exosome: an overview on enhanced biogenesis by small molecules.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- A Review: The Antiviral Activity of Cyclic Peptides.International journal of peptide research and therapeutics · 2023Review
- Characterizing (un)binding mechanism of USP7 inhibitors to unravel the cause of enhanced binding potencies at allosteric checkpoint.Protein science : a publication of the Protein Society · 2022Article
- Antimicrobial peptides and their potential application in antiviral coating agents.Colloids and surfaces. B, Biointerfaces · 2022Review
- Prospecting forJournal of biomolecular structure & dynamics · 2022Article
- Antiviral Activity of Zinc Oxide Nanoparticles and Tetrapods Against the Hepatitis E and Hepatitis C Viruses.Frontiers in microbiology · 2022Article
- Identification of potential molecules against COVID-19 main protease through structure-guided virtual screening approach.Journal of biomolecular structure & dynamics · 2021Article
- Screening and Molecular Modeling Evaluation of Food Peptides to Inhibit Key Targets of COVID-19 Virus.Biomolecules · 2021Article
- Molecular Dynamics Simulations Reveal the Interaction Fingerprint of Remdesivir Triphosphate Pivotal in Allosteric Regulation of SARS-CoV-2 RdRp.Frontiers in molecular biosciences · 2021Article
- Conformational Characterization of the Co-Activator Binding Site Revealed the Mechanism to Achieve the Bioactive State of FXR.Frontiers in molecular biosciences · 2021Article
- Hepatitis E Virus Infection: Circulation, Molecular Epidemiology, and Impact on Global Health.Pathogens (Basel, Switzerland) · 2020Review
- Intercellular Transmission of Naked Viruses through Extracellular Vesicles: Focus on Polyomaviruses.Viruses · 2020Review
- BK Polyomavirus Hijacks Extracellular Vesicles forJournal of virology · 2020Article
- Hepatitis E Virus Drug Development.Viruses · 2019Review
- Spicatoside A derived from Liriope platyphylla root ethanol extract inhibits hepatitis E virus genotype 3 replication in vitro.Scientific reports · 2019Article
- Life cycle and morphogenesis of the hepatitis E virus.Emerging microbes & infections · 2018Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis E virus (HEV) generally causes self-limiting acute viral hepatitis in normal individuals. It causes a more severe disease in immunocompromised persons and pregnant women. Due to the lack of an efficient cell culture system or animal model, the life cycle of the virus is understudied, few antiviral targets are known, and very few antiviral candidates against HEV infection have been identified. Inhibition of virus release is one possible antiviral development strategy, which limits the spread of the virus. Previous studies have demonstrated the essential role of the interaction between the PSAP motif of the viral open reading frame 3 protein (ORF3-PSAP) and the UEV domain of the host tumor susceptibility gene 101 (TSG101) protein (UEV-TSG101) in mediating the release of genotype 3 HEV. Cyclic peptide (CP) inhibitors of the interaction between the human immunodeficiency virus (HIV) gag-PTAP motif and UEV-TSG101 are known to block the release of HIV. Using a molecular dynamic simulation, we observed that both gag-PTAP and ORF3-PSAP motifs bind to the same site in UEV-TSG101 by hydrogen bonding. HIV-released inhibitory CPs also displayed binding to the same site in UEV-TSG101, indicating that they may compete with ORF3-PSAP or gag-PTAP for binding to UEV-TSG101. Two independent assays confirmed the ability of a cyclic peptide (CP11) to inhibit the ORF3-TSG101 interaction. CP11 treatment also reduced the release of both genotype 1 and genotype 3 HEV by approximately 90%, with a 50% inhibitory concentration (IC
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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.