| dc.description.abstract | The reemergence of whooping cough, or pertussis, in the past 30 years can be explained in part by two factors: the imperfect, waning immunity of acellular pertussis (aP) subunit vaccines and the likely vaccine-driven evolution observed in circulating Bordetella pertussis strains. The high transmission rate and disease burden among infants has led to global efforts to make improvements on aP vaccines. Despite an unclear mechanism of protection, the humoral response and B-cell memory remain critical in the clearance of B. pertussis. The five canonical aP vaccine antigens (pertussis toxin (PT), pertactin (Prn), filamentous hemagglutnin (FHA), fimbriae serotype 2 (Fim2), and fimbriae serotype 3 (Fim3)) have been investigated for their immunodominant B-cell epitopes, which guides vaccine improvement as well as the development of correlates of protection. aP vaccines have resulted in mutations in the five aP vaccine antigens and deficiencies in Prn and FHA, with the potential to hinder the ability of the vaccine-induced humoral immunity to prevent re-infection. In fact, mutations in Prn, Fim2, and Fim3 have already been reported in their immunodominant regions. Further characterization of the immunodominant epitopes of the traditional and new pertussis antigens and evolutionary conservation thereof could help combat the resurgence of pertussis cases through the development of a stronger vaccine. The application of newer vaccine technologies, such as mRNA or recombinant protein, as well as the addition of pertussis-derived adjuvants could result in highly protective vaccine-induced immunity. | |
