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

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

LISP2 expression marks the beginning of awakening of dormant hypnozoite to developing malaria liver stages, which are susceptible to a novel prophylactic drug, Plasmodium PI4K inhibitor.

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.

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

The first comprehensive analysis of antigenic switching in the malaria-causing parasite Plasmodium falciparum provides new insights into the process that prevents individuals from acquiring immunity to the disease.

Mathematical modeling shows that local populations of the malaria parasite self-organize into a limited number of transient but distinct strains through competition for hosts in immunity space.

Given sufficient population adherence, mass drug administration for falciparum malaria can provide group level benefits, also known as ‘herd effects’.

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.

A common chromosome inversion in African malaria mosquito (Anopheles gambiae) is associated with differences in malaria infection, adult resting behavior and ecology, and may aid the most efficient vectors to evade malaria control.