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Current efforts to develop plague vaccines focus on LcrV, a polypeptide that resides at the tip of type III secretion needles. LcrV-specific antibodies blockYersinia pestis type III injection of Yop effectors into host immune cells, thereby enabling phagocytes to kill the invading pathogen. Earlier work reported that antibodies againstY. pestis LcrV cannot block type III injection byYersinia enterocolitica strains and suggested thatlcrV polymorphisms may provide for escape from LcrV-mediated plague immunity. We show here that polyclonal or monoclonal antibodies raised againstY. pestis KIM D27 LcrV (LcrVD27 ) bind LcrV fromY. enterocolitica O:9 strain W22703 (LcrVW22703 ) or O:8 strain WA-314 (LcrVWA-314 ) but are otherwise unable to block type III injection byY. enterocolitica strains. Replacing thelcrV gene on the pCD1 virulence plasmid ofY. pestis KIM D27 with eitherlcrVW22703 orlcrVWA-314 does not affect the ability of plague bacteria to secrete proteins via the type III pathway, to inject Yops into macrophages, or to cause lethal plague infections in mice. LcrVD27 -specific antibodies blocked type III injection byY. pestis expressinglcrVW22703 orlcrVWA-314 and protected mice against intravenous lethal plague challenge with these strains. Thus, although antibodies raised against LcrVD27 are unable to block the type III injection ofY. enterocolitica strains, expression oflcrVW22703 orlcrVWA-314 inY. pestis did not allow these strains to escape LcrV-mediated plague protective immunity in the intravenous challenge model.

Polymorphisms in the lcrV Gene of Yersinia enterocolitica and Their Effect on Plague Protective Immunity