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Haemophilus influenzae type b polyribosylribitol phosphate (PRP) is the primary capsular polysaccharide and the dominant virulence factor of the bacterium Haemophilus influenzae type b [3, 5, 15]. Its main biological role is to serve as an antiphagocytic barrier that prevents opsonization and complement-mediated killing by host immune cells, thereby allowing the pathogen to persist in the bloodstream and invade distal sites [9, 15, 16]. The presence of this antigen is essential for the development of invasive diseases such as bacterial meningitis, pneumonia, and epiglottitis, particularly in children under five years of age [1, 9, 21]. PRP is highly conserved across type b strains, making it an ideal target for prophylactic intervention through immunization [5, 12]. As a therapeutic target, PRP is utilized in conjugate vaccines such as ActHIB, Hiberix, and PedvaxHIB, where the polysaccharide is covalently linked to a protein carrier to induce a T-cell-dependent immune response [1, 4, 6]. These vaccines stimulate the production of high-affinity anti-PRP IgG antibodies that neutralize the bacterium and provide long-term protection [11, 20, 21].
Induction of a T-cell-dependent humoral immune response through conjugation to protein carriers, resulting in the production of specific anti-PRP IgG antibodies that facilitate bacterial opsonization, phagocytosis, and complement-dependent lysis [1, 2, 6, 21].
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