The minor pilin PilV provides a conserved adhesion site throughout the antigenically variable meningococcal type IV pilus
Jean‐Philippe Barnier, Julie Meyer, Subramania Kolappan, Haniaa Bouzinba-Ségard, Gaël Gesbert, Anne Jamet, Eric Frapy, Sophia Schönherr-Hellec, Elena Capel, Zoé Virion, Marion Dupuis, Emmanuelle Bille, P. Morand, Taliah Schmitt, Sandrine Bourdoulous, Xavier Nassif, Lisa Craig, Mathieu Coureuil
Abstract
Significance Type IV pili (T4P) are among the most widespread adhesive factors in prokaryotes. In pathogenic Neisseria , the major pilin, which provides the structural framework for the filamentous T4P, undergoes antigenic variation allowing the bacteria to evade the humoral immune response without impacting host-cell adhesion. Here, we show that a minor pilin, PilV, is distributed throughout the pilus and contributes to Neisseria meningitidis adhesion and that antibodies to PilV block meningococcal adhesion in vivo. Our results provide a mechanism whereby N. meningitidis varies its immunodominant major pilin to escape antibody recognition while maintaining conserved sites throughout the pilus for host receptor binding. They further suggest a strategy to prevent or block deadly N. meningitidis infections by targeting this minor pilin.