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Pertussis toxin (PT), filamentous haemagglutinin (FHA), and pertactin (PRN) are the primary virulence factors of Bordetella pertussis, the causative agent of whooping cough. PT is a complex AB5-type exotoxin that ADP-ribosylates inhibitory G-proteins, leading to increased cAMP levels and interference with immune cell signaling and recruitment [1]. FHA and PRN are essential adhesins; FHA is a large secreted protein that mediates binding to host cells and macrophages, while PRN is an autotransporter protein that aids in attachment to the respiratory epithelium [2]. These three components serve as the principal antigens in modern acellular pertussis (aP) vaccines, where they are used to induce protective neutralizing antibodies [3]. Despite their success in reducing disease severity, the reliance on these specific antigens has been linked to the emergence of 'vaccine-escape' strains, particularly those lacking pertactin, and a noted faster waning of immunity compared to older whole-cell vaccines [4]. Understanding the interplay of these proteins is critical for the development of next-generation vaccines that provide more durable protection [5]. (Citations: [1] Carbonetti, N.H., 2010, Pathog Dis; [2] Locht, C., et al., 2001, Int J Med Microbiol; [3] CDC Pink Book, 2021; [4] Mooi, F.R., et al., 2009, Emerg Infect Dis; [5] UniProt P04977, P12255, P14283)
Induction of active immunity through the production of neutralizing antibodies (anti-PT, anti-FHA, and anti-PRN) and memory B and T cell responses to prevent bacterial colonization and toxin-mediated systemic effects.
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