Plasmodium falciparum kelch13 mutations that cause artemisinin resistant malaria in Southeast Asia show markedly different patterns of evolutionary selection in Africa.

CDPK4 is a pleiotropic regulator controlling initiation of DNA replication, mitotic spindle assembly and flagellar activation during the early stages of Plasmodium transmission.

Ribosome profiling has bridged the knowledge gap between transcription and translation during malaria blood stage development and provided a comprehensive gene expression resource for this parasite.

Plasmodium-specific atypical memory B cells generated to naturally (mosquito) transmitted rodent malaria infection are short-lived activated B cells, and do not prevent resolution of infection or generation of long-lived memory.

Exchange of the I domain in the Plasmodium surface protein TRAP against evolutionary distant I domains rescues infectivity of sporozoites.

A comprehensive structural analysis of inhibitory murine antibody 3D11 binding to Plasmodium berghei circumsporozoite protein reveals common mechanisms of antibody evolution in mammals against Plasmodium parasites.

This comprehensive transcriptomic resource of dormant and replicating malaria liver parasites highlights the dearth of pathways that operate in the hypnozoites and the need to investigate druggability (i.e. selectivity and safety) of core pathways in malaria parasites.

Controlled human malaria infection model allows the study of gametocyte biology and dynamics providing novel insights and tools in malaria transmission and elimination efforts.

Under sustained malaria control in PNG, the incidence of distinct blood-stage infections quantifies heterogeneity in transmission, significantly predicting risk of both P. falciparum and P. vivax malaria episodes at a population and individual scale.

Optimised genome editing in P. knowlesi enables transgenic expression of a lead P. vivax vaccine candidate, revealing roles in host cell tropisms and providing tools for scalable vaccine efficacy testing.