ArticlePLoS pathogens2023
Spike substitution T813S increases Sarbecovirus fusogenicity by enhancing the usage of TMPRSS2.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- A potent Gc neutralizing antibody reveals architecture-dependent bispecific protection against SFTSV.Emerging microbes & infections · 2026Article
- Structural basis for sarbecovirus Rc-o319 spike adaptation to Rhinolophus cornutus Bat ACE2 and constraints on switching to human ACE2.PLoS pathogens · 2026Article
- Designing a novel vaccine against COVID-19 based on spike SARS-Cov-2 notable mutations using immunoinformatics approaches.PloS one · 2026Article
- Structures and receptor binding activities of merbecovirus spike proteins reveal key signatures for human DPP4 adaptation.Science advances · 2025Article
- SARS-related coronavirus S-protein structures reveal synergistic RBM interactions underpinning high-affinity human ACE2 binding.Science advances · 2025Article
- Spike substitutions E484D, P812R and Q954H mediate ACE2-independent entry of SARS-CoV-2 across different cell lines.PloS one · 2025Article
- Antibodies utilizing VL6-57 light chains target a convergent cryptic epitope on SARS-CoV-2 spike protein and potentially drive the genesis of Omicron variants.Nature communications · 2024Article
- Functional and antigenic characterization of SARS-CoV-2 spike fusion peptide by deep mutational scanning.Nature communications · 2024Article
- Functional and antigenic characterization of SARS-CoV-2 spike fusion peptide by deep mutational scanning.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
30 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV Spike (S) protein shares considerable homology with SARS-CoV-2 S, especially in the conserved S2 subunit (S2). S protein mediates coronavirus receptor binding and membrane fusion, and the latter activity can greatly influence coronavirus infection. We observed that SARS-CoV S is less effective in inducing membrane fusion compared with SARS-CoV-2 S. We identify that S813T mutation is sufficient in S2 interfering with the cleavage of SARS-CoV-2 S by TMPRSS2, reducing spike fusogenicity and pseudoparticle entry. Conversely, the mutation of T813S in SARS-CoV S increased fusion ability and viral replication. Our data suggested that residue 813 in the S was critical for the proteolytic activation, and the change from threonine to serine at 813 position might be an evolutionary feature adopted by SARS-2-related viruses. This finding deepened the understanding of Spike fusogenicity and could provide a new perspective for exploring Sarbecovirus' evolution.
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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.