Respiratory syncytial virus (RSV) is a common pathogen that causes lower respiratory tract infections leading to significant morbidity and mortality at the extremes of age. Although vaccines have recently been approved for use in adults over 60, a vaccine that can prevent infection in the infant population is lacking. Current strategies to protect infants from RSV rely on passive immunity, either by the transfer of neutralizing monoclonal antibodies (mAbs) or maternal vaccination and transplacental antibody transfer. A vaccine that can rapidly elicit protective neutralizing antibodies and establish immunological memory in the infant population would fulfill a critical unmet need. A subset of antibodies that arise from the chromosomally encoded VH3-21/VL1-40 gene pairing are unique in that they are structurally pre-configured to bind to and neutralize RSV without the need to undergo affinity maturation, making them ideal candidates to be elicited through vaccination. Here, I describe a vaccine immunogen derived from anti-idiotypic monoclonal antibodies (ai-mAbs) that can recognize RSV-neutralizing VH3- 21/VL1-40 B cell receptors from diverse pools of PBMCs. Additionally, I describe the characterization of a novel knock-in mouse model that expresses a bona fide germline VH3- 21/VL1-40 RSV-neutralizing B cell receptor, ADI-19425, and demonstrate the utility of this model to evaluate the immunogenicity of the ai-mAb in pre-clinical vaccine/challenge studies. I found that immunization with the ai-mAb vaccine elicited robust on-target B cell activation and a durable neutralizing serum response that functioned to reduce RSV lung titers upon viral challenge. Collectively, this data illustrates the efficacy of the ai-mAb as a novel infant RSV vaccine candidate and supports its further evaluation in preclinical studies.