ArticleJournal of medical virology2020
The anti-HIV drug nelfinavir mesylate (Viracept) is a potent inhibitor of cell fusion caused by the SARSCoV-2 spike (S) glycoprotein warranting further evaluation as an antiviral against COVID-19 infections.
Article in Journal of medical virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
104 citing papers in PubMed, 2 syntheses or guidelines pooled it, 159 citations in OpenAlex.
- Human Immunodeficiency Virus and Severe Acute Respiratory Syndrome Coronavirus 2 Coinfection: A Systematic Review of the Literature and Challenges.AIDS research and human retroviruses · 2021Pooled it
- Treatment of severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and coronavirus disease 2019 (COVID-19): a systematic review ofTheranostics · 2021Pooled it
- Preventive and therapeutic benefits of nelfinavir in rhesus macaques and human beings infected with SARS-CoV-2.Signal transduction and targeted therapy · 2023Trial
- Antiviral drug discovery and development: challenges and future directions.Signal transduction and targeted therapy · 2026Review
- Harnessing Antiviral Peptides: From Molecular Mechanisms to Clinical Translation.Current research in pharmacology and drug discovery · 2025Review
- Advances and Challenges in Antiviral Development for Respiratory Viruses.Pathogens (Basel, Switzerland) · 2024Review
- Research Progress on Spike-Dependent SARS-CoV-2 Fusion Inhibitors and Small Molecules Targeting the S2 Subunit of Spike.Viruses · 2024Review
- Review
- Exploring Scoring Function Space: Developing Computational Models for Drug Discovery.Current medicinal chemistry · 2024Review
- Expression and fusogenic activity of SARS CoV-2 Spike protein displayed in the HSV-1 Virion.bioRxiv : the preprint server for biology · 2023Article
- Article
- Potential Target Discovery and Drug Repurposing for Coronaviruses: Study Involving a Knowledge Graph-Based Approach.Journal of medical Internet research · 2023Article
- Article
- SARS-CoV-2 Syncytium under the Radar: Molecular Insights of the Spike-Induced Syncytia and Potential Strategies to Limit SARS-CoV-2 Replication.Journal of clinical medicine · 2023Review
- Montelukast and Telmisartan as Inhibitors of SARS-CoV-2 Omicron Variant.Pharmaceutics · 2023Article
- Metabolic alterations upon SARS-CoV-2 infection and potential therapeutic targets against coronavirus infection.Signal transduction and targeted therapy · 2023Review
- Review
- Review
- Potential antiviral effects of pantethine against SARS-CoV-2.Scientific reports · 2023Article
- Polymer modification of SARS-CoV-2 spike protein impacts its ability to bind key receptor.European polymer journal · 2023Article
44 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
7 authors at 3 institutions in 1 country.
Funding
Abstract
Severe acute respiratory syndrome coronavirus-2 (SARS CoV-2) is the causative agent of the coronavirus disease-2019 (COVID-19) pandemic. Coronaviruses enter cells via fusion of the viral envelope with the plasma membrane and/or via fusion of the viral envelope with endosomal membranes after virion endocytosis. The spike (S) glycoprotein is a major determinant of virus infectivity. Herein, we show that the transient expression of the SARS CoV-2 S glycoprotein in Vero cells caused extensive cell fusion (formation of syncytia) in comparison to limited cell fusion caused by the SARS S glycoprotein. Both S glycoproteins were detected intracellularly and on transfected Vero cell surfaces. These results are in agreement with published pathology observations of extensive syncytia formation in lung tissues of patients with COVID-19. These results suggest that SARS CoV-2 is able to spread from cell-to-cell much more efficiently than SARS effectively avoiding extracellular neutralizing antibodies. A systematic screening of several drugs including cardiac glycosides and kinase inhibitors and inhibitors of human immunodeficiency virus (HIV) entry revealed that only the FDA-approved HIV protease inhibitor, nelfinavir mesylate (Viracept) drastically inhibited S-n- and S-o-mediated cell fusion with complete inhibition at a 10-μM concentration. In-silico docking experiments suggested the possibility that nelfinavir may bind inside the S trimer structure, proximal to the S2 amino terminus directly inhibiting S-n- and S-o-mediated membrane fusion. Also, it is possible that nelfinavir may act to inhibit S proteolytic processing within cells. These results warrant further investigations of the potential of nelfinavir mesylate to inhibit virus spread at early times after SARS CoV-2 symptoms appear.
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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.