journal contribution
posted on 2024-09-30, 03:45 authored by Dimuthu AngageDimuthu Angage, J Chmielewski, Janesha Chandimali MaddumageJanesha Chandimali Maddumage, E Hesping, S Caiazzo, KH Lai, LM Yeoh, Joseph MenassaJoseph Menassa, DH Opi, Callum CairnsCallum Cairns, Hamsa PuthalakathHamsa Puthalakath, JG Beeson, Marc KvansakulMarc Kvansakul, JA Boddey, DW Wilson, Robin AndersRobin Anders, Michael FoleyMichael Foley Apical membrane antigen-1 (AMA1) is a conserved malarial vaccine candidate essential for the formation of tight junctions with the rhoptry neck protein (RON) complex, enabling Plasmodium parasites to invade human erythrocytes, hepatocytes, and mosquito salivary glands. Despite its critical role, extensive surface polymorphisms in AMA1 have led to strain-specific protection, limiting the success of AMA1-based interventions beyond initial clinical trials. Here, we identify an i-body, a humanised single-domain antibody-like molecule that recognises a conserved pan-species conformational epitope in AMA1 with low nanomolar affinity and inhibits the binding of the RON2 ligand to AMA1. Structural characterisation indicates that the WD34 i-body epitope spans the centre of the conserved hydrophobic cleft in AMA1, where interacting residues are highly conserved among all Plasmodium species. Furthermore, we show that WD34 inhibits merozoite invasion of erythrocytes by multiple Plasmodium species and hepatocyte invasion by P. falciparum sporozoites. Despite a short half-life in mouse serum, we demonstrate that WD34 transiently suppressed P. berghei infections in female BALB/c mice. Our work describes the first pan-species AMA1 biologic with inhibitory activity against multiple life-cycle stages of Plasmodium. With improved pharmacokinetic characteristics, WD34 could be a potential immunotherapy against multiple species of Plasmodium.
Funding
D.A. was supported by La Trobe University Graduate Research Scholarship (LTGRS), and La Trobe University Full Fee Research Scholarship (LTUFFRS). J.C. and K.H.L. were supported by ARC-RTP Scholarships. D.W.W. acknowledges Hospital Research Foundation Fellowship and collaborative research grant. J.A.B. and J.G.B. acknowledge NHMRC Investigator Grants 1176955 and 1173046, respectively. The Burnet Institute is supported by NHMRC and Victorian State Government infrastructure grants.
History
Publication Date
2024-12-01Journal
Nature CommunicationsVolume
15Issue
1Article Number
7206Pagination
17p.Publisher
Springer NatureISSN
2041-1723Rights Statement
© The Author(s) 2024. This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s licence, unless indicated otherwise in a credit line to the material.