Virulent strains of Yersinia pestis, Y. pseudotuberculosis and Yersinia enterocolitica invariably autoagglutinated in tissue culture media when grown at 36 degrees C. Avirulent strains did not possess this property.

Correlation of autoagglutination and virulence of yersiniae.

Protection against experimental bubonic and pneumonic plague by a recombinant capsular F1-V antigen fusion protein vaccine

Type III-mediated translocation of Yop effectors is an essential virulence mechanism of pathogenic Yersinia. LcrV is the only protein secreted by the type III secretion system that induces protective immunity. LcrV also plays a significant role in the regulation of Yop expression and secretion. The role of LcrV in the virulence process has, however, remained elusive on account of its pleiotropic effects. Here, we show that anti-LcrV antibodies can block the delivery of Yop effectors into the target cell cytosol. This argues strongly for a critical role of LcrV in the Yop translocation process. Additional evidence supporting this role was obtained by genetic analysis. LcrV was found to be present on the bacterial surface before the establishment of bacteria target cell contact. These findings suggest that LcrV serves an important role in the initiation of the translocation process and provides one possible explanation for the mechanism of LcrV-induced protective immunity.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2958.1999.01408.x

The V-antigen of Yersinia is surface exposed before target cell contact and involved in virulence protein translocation :

Plague, caused by Yersinia pestis , is recognized as the most devastating acute infectious disease experienced by humankind. This notoriety is based upon the high rate of mortality, the rapid onset, and the appalling pathology associated with both the bubonic and pneumonic forms of the infection.

/pdf/interleukin-10-and-inhibition-of-innate-immunity-to-2of78ucaj0.pdf

Interleukin-10 and inhibition of innate immunity to Yersiniae: roles of Yops and LcrV (V antigen).

It is established that an approximately 70-kb Lcr plasmid enables Yersinia pestis, the causative agent of bubonic plague, to multiply in focal necrotic lesions within visceral organs of mice by preventing net synthesis of the cytokines tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma), thereby minimizing inflammation (Lcr+) Rabbit antiserum raised against cloned staphylococcal protein A-V antigen fusion peptide (PAV) is known to passively immunize mice against 10 minimum lethal doses of intravenously injected Lcr+ cells of Y pestis In this study, injected PAV suppressed TNF-alpha and IFN-gamma in mice challenged with avirulent V antigen-deficient Y pestis (lcrV or Lcr-) and promoted survival in vivo of these isolates as well as salmonellae and Listeria monocytogenes (with which the outcome was lethal) Active immunization of mice with PAV protected against 1,000 minimum lethal doses of intravenously injected Lcr+ cells of Y pestis and Yersinia pseudotuberculosis but not Yersinia enterocolitica The progressive necrosis provoked by Lcr+ cells of Y pestis in visceral organs of nonimmunized mice was replaced after active immunization with PAV by massive infiltration of neutrophils and mononuclear cells (which generated protective granulomas indistinguishable from those formed against avirulent Lcr- mutants in nonimmunized mice) Distinct multiple abscesses typical of Lcr+ cells of Y pseudotuberculosis were prevented by similar immunization Significant synthesis of TNF-alpha and IFN-gamma occurred in spleens of mice actively immunized with PAV after challenge with Lcr+ cells of Y pestis These findings suggest that V antigen contributes to disease by suppressing the normal inflammatory response

Suppression of cytokines in mice by protein A-V antigen fusion peptide and restoration of synthesis by active immunization.

The effects of loss of different virulence determinants on the virulence and immunogenicity of strains of Pasteurella pestis.

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The effects of loss of different virulence determinants on the virulence and immunogenicity of strains of Pasteurella pestis.