Tay M.Z.Tang W.Lee W.C.Ong A.S.M.Novera W.Malleret B.Carissimo G.Chacko A.M.El-Sahili A.Lescar J.Fan Y.McGready R.M.Chu C.S.Chan J.K.Y.Ng L.F.P.Russell B.Nosten F.Rénia L.Mahidol University2024-10-012024-10-012024-09-23The Journal of infectious diseases Vol.230 No.3 (2024) , e737-e742https://repository.li.mahidol.ac.th/handle/123456789/101433We previously described a novel Plasmodium vivax invasion mechanism into human reticulocytes via the PvRBP2a-CD98 receptor-ligand pair. Using linear epitope mapping, we assessed the PvRBP2a epitopes involved in CD98 binding and recognized by antibodies from patients who were infected. We identified 2 epitope clusters mediating PvRBP2a-CD98 interaction. Cluster B (PvRBP2a431-448, TAALKEKGKLLANLYNKL) was the target of antibody responses in humans infected by P vivax. Peptides from each cluster were able to prevent live parasite invasion of human reticulocytes. These results provide new insights for development of a malaria blood-stage vaccine against P vivax.MedicineArticleSCOPUS10.1093/infdis/jiae1112-s2.0-852048192071537661338441336