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Host-Pathogen Coevolution and the Emergence of Broadly Neutralizing Antibodies in Chronic Infections

Fig 1

coevolution of antibodies and viruses.

(A) Schematic of affinity maturation in a germinal center. A naive, germline B-cell receptor (black) with marginal binding affinity for the circulating antigen (red pentagon) enters the process of affinity maturation in a germinal center. Hypermutations produce a diverse set of B-cell receptors (colors), the majority of which do not increase the neutralization efficacy of B-cells, except for some beneficial mutations that increase binding affinity (dark blue and green) to the presented antigen. The selected B-cells may enter the blood and secrete antibodies, or enter further rounds of hypermutations to enhance their neutralization ability. Antigens mutate and are selected (yellow pentagon) based on their ability to escape the current immune challenge. (B) We model the interaction between the genotype of a B-cell receptor and its secreted antibody (blue) with a viral genotype (red) in both variable and conserved regions of the viral genome. The black and white circles indicate the state of the interacting loci with values ±1. Loci in the conserved region of the virus are fixed at +1. The length of the arrows indicate the contribution of each locus to the binding affinity, κi, which is a measure of the accessibility of an antibody lineage to viral epitopes. The blue arrows indicate the interactions that increase binding affinity (i.e., loci with same signs in antibody and viral genotype), whereas red arrows indicate interaction that decrease the affinity (i.e., loci with opposite signs in antibody and viral genotype.)

Fig 1