In the search for potential vaccine targets for Yersina pestis (the organism that causes the bubonic or pneumonic plague), Dr. Eric Weening and collaborators from the Virginia Miller lab have demonstrated that differences in the mouse genetic background can influence pathogenicity and virulence. They were investigating the roles of two fimbrial proteins PsaA and Caf1 (also known as the F1 capsule) during Yersinia pestis pathogenesis. PsaA and Caf1 both are potential vaccine targets.
During their studies they found that Y. pestis defective in its ability to produce Psa fimbriae were attenuated to equal degrees in two genetically different mouse strains (C57BL/6J and BALB/cJ). However, when they investigated Yersinia pestis deficient in its ability to produce the F1 capsule /Caf1 fimbriae, the bacteria were only slightly attenuated in its ability to cause bubonic plague in BALB/cJ mice, but were severely attenuated in the C57BL/6J strain.
The role of the F1 capsule has been confusing over the last 20 years due to the fact that varying results have been documented for the requirement of Caf1 in Y. pestis pathogenesis. With this research, the Miller lab hypothesizes that these varying results potentially could be due to the differences in the strains of mice used in previous experiments and that the F1 capsule may be more important for virulence in some mouse backgrounds than others. The Miller lab is currently investigating the mechanism behind the differences in attenuation for the F1 capsule mutants in the different mouse backgrounds.