ArticleJournal of virology2010
Viral entry inhibitors targeted to the membrane site of action.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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
71 citing papers in PubMed, 95 citations in OpenAlex.
- A first-in-human study of the novel HIV-fusion inhibitor C34-PEGScientific reports · 2017Trial
- A highly potent, stable, and safe dePEGylated lipopeptide against Nipah virus and related henipaviruses.Emerging microbes & infections · 2026Article
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- Enhancing the solubility of SARS-CoV-2 inhibitors to increase future prospects for clinical development.Journal of virology · 2025Article
- Development of nebulized inhalation delivery for fusion-inhibitory lipopeptides to protect non-human primates against Nipah-Bangladesh infection.Antiviral research · 2025Article
- Intranasally administrated fusion-inhibitory lipopeptides block SARS-CoV-2 infection in mice and enable long-term protective immunity.Communications biology · 2025Article
- How a paramyxovirus fusion/entry complex adapts to escape a neutralizing antibody.Nature communications · 2024Article
- Antiviral activity of the host defense peptide piscidin 1: investigating a membrane-mediated mode of action.Frontiers in chemistry · 2024Article
- Stimuli-Responsive Membrane Anchor Peptide Nanofoils for Tunable Membrane Association and Lipid Bilayer Fusion.ACS applied materials & interfaces · 2022Article
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- Leveraging the therapeutic, biological, and self-assembling potential of peptides for the treatment of viral infections.Journal of controlled release : official journal of the Controlled Release Society · 2022Review
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- Computational methods to study enveloped viral entry.Biochemical Society transactions · 2021Review
- Inhibition of Viral Membrane Fusion by Peptides and Approaches to Peptide Design.Pathogens (Basel, Switzerland) · 2021Review
- Structure-based design and characterization of novel fusion-inhibitory lipopeptides against SARS-CoV-2 and emerging variants.Emerging microbes & infections · 2021Article
- Antivirals targeting paramyxovirus membrane fusion.Current opinion in virology · 2021Review
- The pH-sensitive action of cholesterol-conjugated peptide inhibitors of influenza virus.Biochimica et biophysica acta. Biomembranes · 2021Article
- Inhibition of Measles Viral Fusion Is Enhanced by Targeting Multiple Domains of the Fusion Protein.ACS nano · 2021Article
- Engineering Protease-Resistant Peptides to Inhibit Human Parainfluenza Viral Respiratory Infection.Journal of the American Chemical Society · 2021Article
11 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 3 countries.
Funding
Abstract
The fusion of enveloped viruses with the host cell is driven by specialized fusion proteins to initiate infection. The "class I" fusion proteins harbor two regions, typically two heptad repeat (HR) domains, which are central to the complex conformational changes leading to fusion: the first heptad repeat (HRN) is adjacent to the fusion peptide, while the second (HRC) immediately precedes the transmembrane domain. Peptides derived from the HR regions can inhibit fusion, and one HR peptide, T20 (enfuvirtide), is in clinical use for HIV-1. For paramyxoviruses, the activities of two membrane proteins, the receptor-binding protein (hemagglutinin-neuraminidase [HN] or G) and the fusion protein (F), initiate viral entry. The binding of HN or G to its receptor on a target cell triggers the activation of F, which then inserts into the target cell and mediates the membrane fusion that initiates infection. We have shown that for paramyxoviruses, the inhibitory efficacy of HR peptides is inversely proportional to the rate of F activation. For HIV-1, the antiviral potency of an HRC-derived peptide can be dramatically increased by targeting it to the membrane microdomains where fusion occurs, via the addition of a cholesterol group. We report here that for three paramyxoviruses-human parainfluenza virus type 3 (HPIV3), a major cause of lower respiratory tract diseases in infants, and the emerging zoonotic viruses Hendra virus (HeV) and Nipah virus (NiV), which cause lethal central nervous system diseases-the addition of cholesterol to a paramyxovirus HRC-derived peptide increased antiviral potency by 2 log units. Our data suggest that this enhanced activity is indeed the result of the targeting of the peptide to the plasma membrane, where fusion occurs. The cholesterol-tagged peptides on the cell surface create a protective antiviral shield, target the F protein directly at its site of action, and expand the potential utility of inhibitory peptides for paramyxoviruses.
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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.