The timing of surveillance for pfhrp2/3-deletions within a transmission season impacts estimates of the proportion of false-negative RDTs due to deletions, which may cause premature decisions to change RDT.

The introduction of rapid diagnostic testing for Plasmodium falciparum infections can explain an increased emergence of diagnostic resistant pfhrp2-deleted parasites in sub-Saharan Africa.

Sequence analyses show a pfhrp3 deletion mechanism involves duplication of chromosome 11 segment, which is normally removed via negative selection, and specific conditions are needed for spread including low transmission.

A novel high-throughput method for Plasmodium falciparum genotyping will enable malaria control programs to make informed decisions about the best tool to use for the diagnosis of malaria.

We investigate how parasites adapt to environmental changes in the context of changing transmission patterns, for example by increasing investment in transmission stages at low endemicity such as elimination settings.

Complete blood count data can increase the accuracy of the diagnosis of severe malaria in children in high transmission settings.

The sickle cell trait strongly protects against not only retinopathy-positive cerebral malaria but also retinopathy-negative cerebral malaria, providing evidence that malarial parasites also contribute to retinopathy-negative cerebral malaria and are not innocent bystanders.

Defining the probability of bacterial disease among children with severe malaria allows the integration of bacteraemia and severe malaria genome-wide association study data, identifying a novel risk locus for invasive bacterial disease.

Parasite variants associated with severe malaria do not have an intrinsic growth or survival advantage in vivo, which indicates that a change in host environment is required for their selection.