ArticlemBio2023
Determinants and Mechanisms of the Low Fusogenicity and High Dependence on Endosomal Entry of Omicron Subvariants.
Article in mBio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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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
29 citing papers in PubMed, 38 citations in OpenAlex.
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- Dose-dependent effects of recombinant spike protein-based vaccination on SARS-CoV-2 evolutionary dynamics and the emergence of variants in hamster models.The Journal of general virology · 2026Article
- Altered infectivity, cell-cell fusion, and immune evasion of SARS-CoV-2 BA.3.2 and LP.8.1 variants.Journal of virology · 2026Article
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- Spike destabilization attenuates Mink Cluster 5 SARS-CoV-2.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Tetrandrine-driven autophagy suppresses SARS-CoV-2 replication by modulating cholesterol and IGF signaling pathways.Cell death discovery · 2026Article
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- A public health perspective of SARS-CoV-2 evolution and surveillance strategies in Germany from 2020 to 2023.Communications medicine · 2025Review
- An Italian Single-Center Genomic Surveillance Study: Two-Year Analysis of SARS-CoV-2 Spike Protein Mutations.International journal of molecular sciences · 2025Article
- SARS-CoV-2 evolution enhances endocytic uptake while preserving TMPRSS2-dependent fusion.Frontiers in immunology · 2025Article
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- SARS-CoV-2 Omicron variations reveal mechanisms controlling cell entry dynamics and antibody neutralization.PLoS pathogens · 2024Article
- Insights into the Replication Kinetics Profiles of Malaysian SARS-CoV-2 Variant Alpha, Beta, Delta, and Omicron in Vero E6 Cell Line.International journal of molecular sciences · 2024Article
- Functional and antigenic characterization of SARS-CoV-2 spike fusion peptide by deep mutational scanning.Nature communications · 2024Article
- The Antiviral Activity of Interferon-Induced Transmembrane Proteins and Virus Evasion Strategies.Viruses · 2024Review
- The SARS-CoV-2 Spike is a virulence determinant and plays a major role on the attenuated phenotype of Omicron virus in a feline model of infection.Journal of virology · 2024Article
- Differentiating Cell Entry Potentials of SARS-CoV-2 Omicron Subvariants on Human Lung Epithelium Cells.Viruses · 2024Article
- Omicron Spike confers enhanced infectivity and interferon resistance to SARS-CoV-2 in human nasal tissue.Nature communications · 2024Article
- Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The rapid spread and strong immune evasion of the SARS-CoV-2 Omicron subvariants has raised serious concerns for the global COVID-19 pandemic. These new variants exhibit generally reduced fusogenicity and increased endosomal entry pathway utilization compared to the ancestral D614G variant, the underlying mechanisms of which remain elusive. Here, we show that the C-terminal S1 mutations of the BA.1.1 subvariant, H655Y and T547K, critically govern the low fusogenicity of Omicron. Notably, H655Y also dictates the enhanced endosome entry pathway utilization. Mechanistically, T547K and H655Y likely stabilize the spike trimer conformation as suggested by increased molecular interactions in structural modeling and enhanced S1 shedding of their reversion mutants K547T and Y655H in viral producer cells. Importantly, the H655Y mutation also determines the low fusogenicity and enhanced dependence on the endosomal entry pathway of other Omicron subvariants, including BA.2, BA.2.12.1, BA.4/5, and BA.2.75. Together, these results uncover mechanisms governing Omicron subvariant entry and provide insights into altered Omicron tissue tropism and pathogenesis.
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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.