ArticleNature communications2022
Compensatory epistasis maintains ACE2 affinity in SARS-CoV-2 Omicron BA.1.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 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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Who cites it
107 citing papers in PubMed, 167 citations in OpenAlex.
- From sites to structure to serology: a roadmap for structure-aware molecular evolution of antigenically evolving viruses.Journal of virology · 2026Review
- Different mechanisms for human rhinovirus survival in the presence of deleterious amino acid substitutions at virion protein-protein or RNA-protein interfaces.Journal of virology · 2026Article
- Deep mutational scanning of recent SARS-CoV-2 variants highlights changing amino acid preferences within epistatic hotspot residues.PLoS pathogens · 2026Article
- Epistasis and background dependence in the evolution of Omicron variants of the SARS-CoV-2 spike protein.Molecular biology and evolution · 2026Article
- Genomic-epidemiological analysis of 15 million SARS-CoV-2 genomes reveals accelerated fitness gain of JN.1 lineage.Virologica Sinica · 2026Article
- Determinants of metal import and specificity in a bacterial transporter.bioRxiv : the preprint server for biology · 2026Article
- The role of receptor binding and immunity in SARS-CoV-2 fitness landscape: A modeling study.iScience · 2026Article
- Influenza hemagglutinin subtypes have different sequence constraints despite sharing extremely similar structures.bioRxiv : the preprint server for biology · 2026Article
- Beyond the Mutation Abyss: Revisiting SARS-CoV-2 Receptor-Binding Domain Evolution from ACE2 Binding Optimization to Immune Epitope Remodeling.Pathogens (Basel, Switzerland) · 2026Article
- Structural Constraints Acting on the SARS-CoV-2 Spike Protein Reveal Limited Space for Viral Adaptation.Genome biology and evolution · 2026Article
- Predicting viral sensitivity to antibodies using genetic sequences and antibody similarities.PLoS computational biology · 2026Article
- Article
- From single-sequences to evolutionary trajectories: protein language models capture the evolutionary potential of SARS-CoV-2.Nature communications · 2026Article
- Functional and antigenic constraints on the Nipah virus fusion protein.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Clonal interference and changing selective pressures shape the escape of SARS-CoV-2 from hundreds of antibodies.Virus evolution · 2026Article
- Experimental evolution in an era of molecular manipulation.Nature reviews. Genetics · 2026Review
- Functional and antigenic constraints on the Nipah virus fusion protein.bioRxiv : the preprint server for biology · 2026Article
- Characterization of the heterogeneity in SARS-CoV-2 fitness dynamics via graph representation learning.PLoS computational biology · 2026Article
- Influenza hemagglutinin subtypes have different sequence constraints despite sharing extremely similar structures.Virus evolution · 2026Article
- Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
The Omicron BA.1 variant emerged in late 2021 and quickly spread across the world. Compared to the earlier SARS-CoV-2 variants, BA.1 has many mutations, some of which are known to enable antibody escape. Many of these antibody-escape mutations individually decrease the spike receptor-binding domain (RBD) affinity for ACE2, but BA.1 still binds ACE2 with high affinity. The fitness and evolution of the BA.1 lineage is therefore driven by the combined effects of numerous mutations. Here, we systematically map the epistatic interactions between the 15 mutations in the RBD of BA.1 relative to the Wuhan Hu-1 strain. Specifically, we measure the ACE2 affinity of all possible combinations of these 15 mutations (2
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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.