ArticleFrontiers in immunology2022
A Coarse-Grained Model of Affinity Maturation Indicates the Importance of B-Cell Receptor Avidity in Epitope Subdominance.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Computational Design and Expression of Headless Influenza Hemagglutinin Antigens Toward a Modular Universal Nanoparticle Vaccine.Antibodies (Basel, Switzerland) · 2026Article
- Phenomenological Modeling of Antibody Response from Vaccine Strain Composition.Antibodies (Basel, Switzerland) · 2025Article
- A paradigm shift in simulating affinity maturation to elicit broadly neutralizing antibodies.Frontiers in immunology · 2025Review
- Antibody accessibility determines location of spike surface mutations in SARS-CoV-2 variants.PLoS computational biology · 2023Article
- Moving the needle: Employing deep reinforcement learning to push the boundaries of coarse-grained vaccine models.Frontiers in immunology · 2022Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The elicitation of broadly neutralizing antibodies (bnAbs) is a major goal in the design of vaccines against rapidly-mutating viruses. In the case of influenza, many bnAbs that target conserved epitopes on the stem of the hemagglutinin protein (HA) have been discovered. However, these antibodies are rare, are not boosted well upon reinfection, and often have low neutralization potency, compared to strain-specific antibodies directed to the HA head. Different hypotheses have been proposed to explain this phenomenon. We use a coarse-grained computational model of the germinal center reaction to investigate how B-cell receptor binding valency affects the growth and affinity maturation of competing B-cells. We find that receptors that are unable to bind antigen bivalently, and also those that do not bind antigen cooperatively, have significantly slower rates of growth, memory B-cell production, and, under certain conditions, rates of affinity maturation. The corresponding B-cells are predicted to be outcompeted by B-cells that bind bivalently and cooperatively. We use the model to explore strategies for a universal influenza vaccine,
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