ArticleNature biomedical engineering2024
High-throughput screening of genetic and cellular drivers of syncytium formation induced by the spike protein of SARS-CoV-2.
Article in Nature biomedical engineering, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- CELLISA - a cell-cell binding assay for evaluation of nanovesicle targeting proteins.bioRxiv : the preprint server for biology · 2026Article
- Single-Target Pairing System (StarPair) for Large-Scale Interrogation of Cell-Cell Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Droplet-based single-cell pairing for high-throughput interaction mapping of antigen-receptor combinations.Science advances · 2025Article
- A Machine Vision Perspective on Droplet-Based Microfluidics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Genome-wide CRISPR screens identify CLC-2 as a drug target for anti-herpesvirus therapy: tackling herpesvirus drug resistance.Science China. Life sciences · 2025Article
- SARS-CoV-2 S-protein expression drives syncytia formation in endothelial cells.Scientific reports · 2025Article
- Mesenchymal Stem Cells Carrying Viral Fusogenic Protein p14 to Treat Solid Tumors by Inducing Cell-Cell Fusion and Immune Activation.Research (Washington, D.C.) · 2025Article
- Screening for drivers of SARS-CoV-2 uptake.Nature biomedical engineering · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Mapping mutations and discovering cellular determinants that cause the spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to induce infected cells to form syncytia would facilitate the development of strategies for blocking the formation of such cell-cell fusion. Here we describe high-throughput screening methods based on droplet microfluidics and the size-exclusion selection of syncytia, coupled with large-scale mutagenesis and genome-wide knockout screening via clustered regularly interspaced short palindromic repeats (CRISPR), for the large-scale identification of determinants of cell-cell fusion. We used the methods to perform deep mutational scans in spike-presenting cells to pinpoint mutable syncytium-enhancing substitutions in two regions of the spike protein (the fusion peptide proximal region and the furin-cleavage site). We also used a genome-wide CRISPR screen in cells expressing the receptor angiotensin-converting enzyme 2 to identify inhibitors of clathrin-mediated endocytosis that impede syncytium formation, which we validated in hamsters infected with SARS-CoV-2. Finding genetic and cellular determinants of the formation of syncytia may reveal insights into the physiological and pathological consequences of cell-cell fusion.
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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.