It will be interesting to test in future studies whether SNP cluster I strains have any advantage in hosts immunised with WCV. The WCV imposes a different selection pressure as the WCV contains hundreds of antigens. In addition, WCV stimulates different types of immunity. WCV resembles the natural pertussis infection and induces T helper type 1 (Th1) response and to a lesser extent, Th17 response, while ACV stimulates more Th2 responses than Th1 and Th17 responses [31]. In the baboon model, WCV-immunised animals were able to clear the infection much faster and were less infectious [22].
Increased Aurora A Inhibitor I of the cluster I strain to the ACV may be contributed by genetic changes in the vaccine antigen genes. SNP cluster I strains carry pxtP3 and prn2 as well as ptxA1 [11], [12] and [19]. The study by Komatsu et al. [32] examined the effect of replacing either or both of ptxA and prn alleles in the Tohama I background and found that isogenic mutants carrying double mutations (by replacing ptxA2 with ptxA1 and prn1 with prn2) had a synergistic effect. The pxtA1-prn2 double mutant colonised better than the wild type Tohama I strain in immunised mice while single mutants of either pxtA1 or prn2 performed no better than the wild type. These findings are consistent with our results and support that the genetic changes in the vaccine antigen genes occurred in SNP cluster I strains may have provided a selective advantage in the ACV immunised environment.
Increased Aurora A Inhibitor I of the cluster I strain to the ACV may be contributed by genetic changes in the vaccine antigen genes. SNP cluster I strains carry pxtP3 and prn2 as well as ptxA1 [11], [12] and [19]. The study by Komatsu et al. [32] examined the effect of replacing either or both of ptxA and prn alleles in the Tohama I background and found that isogenic mutants carrying double mutations (by replacing ptxA2 with ptxA1 and prn1 with prn2) had a synergistic effect. The pxtA1-prn2 double mutant colonised better than the wild type Tohama I strain in immunised mice while single mutants of either pxtA1 or prn2 performed no better than the wild type. These findings are consistent with our results and support that the genetic changes in the vaccine antigen genes occurred in SNP cluster I strains may have provided a selective advantage in the ACV immunised environment.
