Apical membrane antigen-1 (AMA1) and merozoite surface protein 2 (MSP2) are key malaria vaccine candidates, with AMA1 playing a critical role in host cell invasion by Plasmodium parasites. However, extensive polymorphisms in both proteins present challenges for their use as vaccine targets. Unlike AMA1, which is well-structured MSP2 is predominantly disordered, further complicating its use in a vaccine. We used phage display to screen an i-body library for binders to AMA1 and MSP2 from various P. falciparum strains. This led to the identification of 12 AMA1-specific i-bodies, including WD34, which binds with low nanomolar affinity to a conserved epitope in multiple Plasmodium species. WD34 inhibited binding of the AMA1 ligand RON2, and reduced growth of erythrocytic and pre-erythrocytic parasites. X-ray crystallography revealed that WD34 binds to the conserved hydrophobic groove of AMA1, with binding sites consistent across apicomplexan parasites. The inhibition of P. falciparum, P. knowlesi, and transgenic P. falciparum expressing P.vivax AMA1, along with its suppression of P. yoelii infection in mice, highlights the therapeutic potential of WD34.
In contrast, no MSP2 binders were isolated, likely due to its disordered structure. AlphaFold2 confirmed NMR data that 3D7 and FC27 are disordered, however other variants are predicted to contain Ī²-solenoid folds. Developing stable recombinant structures for these variants may enable the selection of MSP2-targeting i-bodies and further our understanding of the function of MSP2. This study underscores the utility of phage display for structured antigens like AMA1, while indicating the need for innovative approaches for disordered antigens such as MSP2.