ArticleLife science alliance2022
SARS-CoV-2 spike E156G/Δ157-158 mutations contribute to increased infectivity and immune escape.
Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- A SARS-CoV-2 variant-induced NTD-targeting antibody enhances viral infection via a distinctive binding mode.PLoS pathogens · 2026Article
- Genome data artifacts and functional studies of deletion repair in the BA.1 SARS-CoV-2 spike protein.Virus evolution · 2025Article
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- T Cell Peptide Prediction, Immune Response, and Host-Pathogen Relationship in Vaccinated and Recovered from Mild COVID-19 Subjects.Biomolecules · 2024Article
- Whole-Genome Sequencing and Mutation Analyses of SARS-CoV-2 Isolates from Indonesia.Pathogens (Basel, Switzerland) · 2024Article
- Article
- Unlocking the puzzle: non-defining mutations in SARS-CoV-2 proteome may affect vaccine effectiveness.Frontiers in public health · 2024Article
- Immunogenicity of the CoronaVac vaccine in children: a real-world study.Frontiers in immunology · 2024Article
- Editorial: Exploring genetic characteristics and molecular mechanisms of host adaptation of viruses with artificial intelligence (AI) or (and) biological (BIO) approaches.Frontiers in cellular and infection microbiology · 2024Article
- Introduction, Dispersal, and Predominance of SARS-CoV-2 Delta Variant in Rio Grande do Sul, Brazil: A Retrospective Analysis.Microorganisms · 2023Article
- Dynamics of water-mediated interaction effects on the stability and transmission of Omicron.Scientific reports · 2023Article
- Characterization of SARS-CoV-2 Variants in Military and Civilian Personnel of an Air Force Airport during Three Pandemic Waves in Italy.Microorganisms · 2023Article
- Rational Use of Monoclonal Antibodies as Therapeutic Treatment in an Oncologic Patient with Long COVID.Viruses · 2023Article
- Taking stock of the mutations in human SARS-CoV-2 spike proteins: From early days to nearly the end of COVID-19 pandemic.Current research in structural biology · 2023Article
- Article
- Neutralizing and enhancing antibodies against SARS-CoV-2.Inflammation and regeneration · 2022Review
- Review
- SARS-CoV-2 variants and spike mutations involved in second wave of COVID-19 pandemic in India.Transboundary and emerging diseases · 2022Article
- Development of a simple genotyping method based on indel mutations to rapidly screen SARS-CoV-2 circulating variants: Delta, Omicron BA.1 and BA.2.Journal of virological methods · 2022Article
- SARS-CoV-2 spike N-terminal domain modulates TMPRSS2-dependent viral entry and fusogenicity.Cell reports · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Breakthrough infections by emerging SARS-CoV-2 variants raise significant concerns. Here, we sequence-characterized the spike gene from breakthrough infections that corresponded to B.1.617 sublineage. Delineating the functional impact of spike mutations revealed that N-terminal domain (NTD)-specific E156G/Δ157-158 contributed to increased infectivity and reduced sensitivity to vaccine-induced antibodies. A six-nucleotide deletion (467-472) in the spike-coding region introduced this change in the NTD. We confirmed the presence of E156G/Δ157-158 from cases concurrently screened, in addition to other circulating spike (S1) mutations such as T19R, T95I, L452R, E484Q, and D614G. Notably, E156G/Δ157-158 was present in more than 90% of the sequences reported from the USA and UK in October 2021. The spike-pseudotyped viruses bearing a combination of E156G/Δ157-158 and L452R exhibited higher infectivity and reduced sensitivity to neutralization. Notwithstanding, the post-recovery plasma robustly neutralized viral particles bearing the mutant spike. When the spike harbored E156G/Δ157-158 along with L452R and E484Q, increased cell-to-cell fusion was also observed, suggesting a combinatorial effect of these mutations. Our study underscores the importance of non-RBD changes in determining infectivity and immune escape.
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Registered trials
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