The Mechanism and Consequences of SARS-CoV-2 Spike-Mediated Fusion and Syncytia Formation
Copyright © 2021 Elsevier Ltd. All rights reserved..
Syncytia are formed when individual cells fuse. SARS-CoV-2 induces syncytia when the viral spike (S) protein on the surface of an infected cell interacts with receptors on neighboring cells. Syncytia may potentially contribute to pathology by facilitating viral dissemination, cytopathicity, immune evasion, and inflammatory response. SARS-CoV-2 variants of concern possess several mutations within the S protein that enhance receptor interaction, fusogenicity and antibody binding. In this review, we discuss the molecular determinants of S mediated fusion and the antiviral innate immunity components that counteract syncytia formation. Several interferon-stimulated genes, including IFITMs and LY6E act as barriers to S protein-mediated fusion by altering the composition or biophysical properties of the target membrane. We also summarize the effect that the mutations associated with the variants of concern have on S protein fusogenicity. Altogether, this review contextualizes the current understanding of Spike fusogenicity and the role of syncytia during SARS-CoV-2 infection and pathology.
| Errataetall: |
CommentIn: EMBO J. 2021 Dec 15;40(24):e110041. - PMID 34779518 |
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| Medienart: |
E-Artikel |
| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:434 |
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| Enthalten in: |
Journal of molecular biology - 434(2022), 6 vom: 30. März, Seite 167280 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Rajah, Maaran Michael [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 15.04.2022 Date Revised 08.12.2022 published: Print-Electronic CommentIn: EMBO J. 2021 Dec 15;40(24):e110041. - PMID 34779518 Citation Status MEDLINE |
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| doi: |
10.1016/j.jmb.2021.167280 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM331480891 |
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| 520 | |a Copyright © 2021 Elsevier Ltd. All rights reserved. | ||
| 520 | |a Syncytia are formed when individual cells fuse. SARS-CoV-2 induces syncytia when the viral spike (S) protein on the surface of an infected cell interacts with receptors on neighboring cells. Syncytia may potentially contribute to pathology by facilitating viral dissemination, cytopathicity, immune evasion, and inflammatory response. SARS-CoV-2 variants of concern possess several mutations within the S protein that enhance receptor interaction, fusogenicity and antibody binding. In this review, we discuss the molecular determinants of S mediated fusion and the antiviral innate immunity components that counteract syncytia formation. Several interferon-stimulated genes, including IFITMs and LY6E act as barriers to S protein-mediated fusion by altering the composition or biophysical properties of the target membrane. We also summarize the effect that the mutations associated with the variants of concern have on S protein fusogenicity. Altogether, this review contextualizes the current understanding of Spike fusogenicity and the role of syncytia during SARS-CoV-2 infection and pathology | ||
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| 650 | 4 | |a spike | |
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| 700 | 1 | |a Buchrieser, Julian |e verfasserin |4 aut | |
| 700 | 1 | |a Schwartz, Olivier |e verfasserin |4 aut | |
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