Authors
Yasmina Drissi-El Boukili, Vera Kühne, H Magloire Natama, Pieter Moris, Elisabet Tintó-Font, Antonia Windkouni Bere, Odin Goovaerts, Pieter Guetens, Ana Moreno-Murillo, Yarno Valgaerts, T Edwig Traoré, D Florence Ouedraogo, Halidou Tinto, Ann Van de Velde, Alfred Cortés, Guy Caljon, Anna Rosanas-Urgell
Published in
PLoS pathogens. Volume 22. Issue 9. Pages e1014542. Epub Sep 29, 2026.
Abstract
Malaria transmission relies on the differentiation of asexual parasites into gametocytes, a process initiated by sexual conversion (SC). Mutations in the host hemoglobin beta (HBB) gene are known to influence parasite growth and disease outcome, yet their impact on SC remains unclear. We investigated the effect of HBB mutant genotypes on Plasmodium falciparum (P. falciparum) SC and humoral immunity in individuals from Nanoro, Burkina Faso. To measure SC rates in natural human malaria infections, we developed a new ex vivo SC assay (evSCA). We found that in human natural P. falciparum infections, SC rates were higher in individuals with HbAS or HbAC than in individuals with wild-type HBB (HbAA). Consistently, using an in vitro SC assay (ivSCA) based on the NF54-gexp02-Tom reporter line we found that cultures grown in HbAS red blood cells (RBCs) had higher SC rates than those grown in HbAA RBCs. Furthermore, IgG and IgM responses against trophozoite- and stage I gametocyte-infected RBC antigens, quantified by flow cytometry, did not differ between plasma from individuals with different HBB genotypes. These results demonstrate that exposure to RBCs with HBB mutations enhances SC, highlighting a host-genetic factor that may influence malaria transmission potential.
PMID:
42809541
Bibliographic data and abstract were imported from PubMed on 30 Sep 2026.
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