Respiratory syncytial virus (RSV) is the top cause of severe lower respiratory disease in infants and children and causes over 100,000 deaths in children worldwide each year. RSV is also a leading cause of respiratory disease in immunocompromisedand elderly populations. However, no FDA approved vaccine exists to protect against RSV infection. RSV contains two immunogenic proteins on its envelope, RSV F and RSV G, that have been the targets of vaccine developmental strategies. Most current efforts to create a vaccine against RSV focus on RSV F, and several candidates are in phase III clinical trials. The only current prophylaxis available for RSV is a monoclonal antibody against RSV F, yet it does not prevent infection. RSV G as a vaccine immunogen is linked to vaccine enhanced disease and is poorly immunogenic, however anti-RSV G antibodies have been shown to be protective in animal models of RSV disease and correlate with protection in humans. In this thesis, I present the history of an inactivated RSV vaccine that caused vaccine enhanced disease in children, a summary of studies using RSV G as a vaccine antigen, and an overview of the RSV G vaccine antigens currently in clinical trials. I present data showing that the structure-based design of an RSV G immunogen with a mutation in the central conserved domain is a promising vaccine candidate. Finally, I present studies to investigate RSV G binding and activation of the human chemokine receptor CX3CR1 on mammalian cells. Overall, these studies provide a foundation for the further development of the RSV G immunogen as a vaccine candidate to protect against RSV disease.