Although mice are generally unable to elicit HIV bnAb-lineage B cell responses due to their short CDR3 domains (65), we found that this combination adjuvant strategy recruited a more clonally expanded and diverse B cell response and resulted in GCs that included increased numbers of antigen-specific BCR clones elicited across animals, all features expected in humans to promote more reliable priming of rare precursor B cells that are needed for bnAb responses against HIV and other infectious diseases. This evidence concerns the gene BCR and infectious disease.