ArticlePloS one2012
Ezrin interacts with the SARS coronavirus Spike protein and restrains infection at the entry stage.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04627233 (The Clinical Trial of Application of Ezrin Peptide), which is not on this map. Cited by 39 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.
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.
The Clinical Trial of Application of Ezrin Peptide (HEP-1) for Treatment of Coronavirus Disease (COVID-19) Infection
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Prior and novel coronaviruses, Coronavirus Disease 2019 (COVID-19), and human reproduction: what is known?Fertility and sterility · 2020Pooled it
- SARS-CoV-2 S assembly into virions facilitated by host ERM proteins.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- ICAM-1-mediated Src signaling pathway plays a pivotal role in encephalomyocarditis virus entry.Journal of virology · 2025Article
- Mucormycosis and COVID-19: Unraveling the Interplay of Fungal Infection in a Global Health Crisis: An Overview.Infectious disorders drug targets · 2025Review
- Article
- Coronavirus and the Cytoskeleton of Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Docking and molecular dynamics studies of human ezrin protein with a modelled SARS-CoV-2 endodomain and their interaction with potential invasion inhibitors.Journal of King Saud University. Science · 2022Article
- The serum of COVID-19 asymptomatic patients up-regulates proteins related to endothelial dysfunction and viral response in circulating angiogenic cells ex-vivo.Molecular medicine (Cambridge, Mass.) · 2022Article
- Modeling of the thermal properties of SARS-CoV-2 S-protein.Frontiers in molecular biosciences · 2022Article
- Ezrin Peptide Therapy from HIV to COVID: Inhibition of Inflammation and Amplification of Adaptive Anti-Viral Immunity.International journal of molecular sciences · 2021Review
- Cell Entry of Animal Coronaviruses.Viruses · 2021Review
- Sequences in the cytoplasmic tail of SARS-CoV-2 Spike facilitate expression at the cell surface and syncytia formation.Nature communications · 2021Article
- Dysbalance of ACE2 levels - a possible cause for severe COVID-19 outcome in COPD.The journal of pathology. Clinical research · 2021Article
- An optimized and robust SARS-CoV-2 pseudovirus system for viral entry research.Journal of virological methods · 2021Article
- Review
- Potential therapeutic agents to COVID-19: An update review on antiviral therapy, immunotherapy, and cell therapy.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Coronavirus entry: how we arrived at SARS-CoV-2.Current opinion in virology · 2021Review
- Serial co-expression analysis of host factors from SARS-CoV viruses highly converges with former high-throughput screenings and proposes key regulators.Briefings in bioinformatics · 2021Article
- Identification of potential inhibitors of coronavirus hemagglutinin-esterase using molecular docking, molecular dynamics simulation and binding free energy calculation.Molecular diversity · 2021Article
- The chemical biology of coronavirus host-cell interactions.RSC chemical biology · 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
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEntry of Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) and its envelope fusion with host cell membrane are controlled by a series of complex molecular mechanisms, largely dependent on the viral envelope glycoprotein Spike (S). There are still many unknowns on the implication of cellular factors that regulate the entry process. METHODOLOGY/PRINCIPAL
findingsWe performed a yeast two-hybrid screen using as bait the carboxy-terminal endodomain of S, which faces the cytosol during and after opening of the fusion pore at early stages of the virus life cycle. Here we show that the ezrin membrane-actin linker interacts with S endodomain through the F1 lobe of its FERM domain and that both the eight carboxy-terminal amino-acids and a membrane-proximal cysteine cluster of S endodomain are important for this interaction in vitro. Interestingly, we found that ezrin is present at the site of entry of S-pseudotyped lentiviral particles in Vero E6 cells. Targeting ezrin function by small interfering RNA increased S-mediated entry of pseudotyped particles in epithelial cells. Furthermore, deletion of the eight carboxy-terminal amino acids of S enhanced S-pseudotyped particles infection. Expression of the ezrin dominant negative FERM domain enhanced cell susceptibility to infection by SARS-CoV and S-pseudotyped particles and potentiated S-dependent membrane fusion. CONCLUSIONS/SIGNIFICANCE: Ezrin interacts with SARS-CoV S endodomain and limits virus entry and fusion. Our data present a novel mechanism involving a cellular factor in the regulation of S-dependent early events of 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.