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The **V-antigen** (canonical: Yersinia type III secretion protein; also known as LcrV or PcrV in Yersinia and Pseudomonas, respectively) is a multifunctional bacterial virulence protein essential for the activity of the type III secretion system (T3SS) in several pathogenic Gram-negative bacteria including Yersinia pestis, Yersinia pseudotuberculosis, and Pseudomonas aeruginosa[4][10]. It forms a pentameric cap at the tip of the T3SS needle complex, evolving from the bacterial flagellar cap, and is critical for the direct translocation of bacterial toxins (effectors) into eukaryotic host cells[4]. Inhibition or immunization against the V-antigen has shown prophylactic and therapeutic efficacy in animal models, and vaccine and antibody-based therapies targeting this antigen are being developed and trialed for the prevention or treatment of severe infections by these organisms[4][10]. The V-antigen is not a human molecule, but a microbial protein target considered highly important for anti-virulence therapy, particularly in the context of emerging antibiotic resistance. Multiple closely related proteins (homologs) exist in other Gram-negative pathogens, although structural differences may affect cross-protection and targeting[4].
Blocking V-antigen with antibody or antisera prevents effective function of bacterial type III secretion systems and blocks translocation of bacterial cytotoxins into host cells, thereby reducing virulence and enabling immune clearance[4][10].
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