ArticleeLife2021
SARS-CoV-2 requires cholesterol for viral entry and pathological syncytia formation.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
140 citing papers in PubMed, 1 synthesis or guideline pooled it, 216 citations in OpenAlex.
- The rationale for the treatment of long-Covid symptoms - A cardiologist's view.Frontiers in cardiovascular medicine · 2022Pooled it
- Circulating cholesterol fuels SARS-CoV-2 replication via ORF3a.EMBO reports · 2026Article
- Brain corticogenesis promotes SARS-CoV-2 neuro-glial tropism through lipid-dependent viral replication.Stem cell reports · 2026Article
- Ondansetron exhibits potent antiviral activity against enterovirus 71 infection in vitro and in vivo.Virus research · 2026Article
- Viral syncytia evolve to resist interferon.Nature communications · 2026Article
- SARS-CoV-2 ORF3a blocks lysosomal cholesterol egress by disrupting VPS39-regulated NPC2 trafficking and BMP metabolism.Cell reports · 2026Article
- Tailoring virus-inspired nanoparticles for advanced drug and gene delivery.Materials today. Bio · 2026Review
- Molecular mechanism of cholesterol-dependent membrane fusion in SARS-CoV-2 entry.Signal transduction and targeted therapy · 2026Article
- STAT1 signaling controls cholesterol metabolism in epithelial cells and RSV-induced syncytia formation.Npj viruses · 2026Article
- Tetrandrine-driven autophagy suppresses SARS-CoV-2 replication by modulating cholesterol and IGF signaling pathways.Cell death discovery · 2026Article
- Mathematical Modeling of Cell-Cell Fusion Assays to Characterize Virus-Mediated Cell Fusion.Advances in experimental medicine and biology · 2026Review
- Discovery of Cetaben as a Novel Antiviral Agent Against Porcine Epidemic Diarrhea Virus From a Cholesterol-Lowering Compound Library.Transboundary and emerging diseases · 2026Article
- Glycocalyx at the host-virus interface: a double-edged sword in virus infection and tissue damage.Frontiers in molecular biosciences · 2026Review
- The Selective DHCR24 Blocker SH42 Inhibits ACE2 Binding and Cellular Entry of SARS-CoV-2 Spike Proteins More Efficiently Than Atorvastatin.Research (Washington, D.C.) · 2026Article
- Nanostructured surfaces for enveloped virus inactivation: mechanisms and fabrication strategies.Frontiers in bioengineering and biotechnology · 2026Review
- Mechanisms of Cell-Cell Fusion in SARS-CoV-2: An Evolving Strategy for Transmission and Immune Evasion.Viruses · 2025Review
- SARS-CoV-2 ORF3a blocks lysosomal cholesterol egress by disrupting VPS39-regulated NPC2 trafficking and BMP metabolism.bioRxiv : the preprint server for biology · 2025Article
- Cholesterol-rich lipid rafts mediate endocytosis as a common pathway for respiratory syncytial virus entry into different host cells.Microbiology spectrum · 2025Article
- Article
- Entry Inhibitors of SARS-CoV-2 Targeting the Transmembrane Domain of the Spike Protein.Viruses · 2025Article
80 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
19 authors at 6 institutions in 1 country.
Funding
Abstract
Many enveloped viruses induce multinucleated cells (syncytia), reflective of membrane fusion events caused by the same machinery that underlies viral entry. These syncytia are thought to facilitate replication and evasion of the host immune response. Here, we report that co-culture of human cells expressing the receptor ACE2 with cells expressing SARS-CoV-2 spike, results in synapse-like intercellular contacts that initiate cell-cell fusion, producing syncytia resembling those we identify in lungs of COVID-19 patients. To assess the mechanism of spike/ACE2-driven membrane fusion, we developed a microscopy-based, cell-cell fusion assay to screen ~6000 drugs and >30 spike variants. Together with quantitative cell biology approaches, the screen reveals an essential role for biophysical aspects of the membrane, particularly cholesterol-rich regions, in spike-mediated fusion, which extends to replication-competent SARS-CoV-2 isolates. Our findings potentially provide a molecular basis for positive outcomes reported in COVID-19 patients taking statins and suggest new strategies for therapeutics targeting the membrane of SARS-CoV-2 and other fusogenic viruses.
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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.