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.

Comparative transcriptomics of whole blood can be used to evaluate the systemic host response and its concordance between human and mouse malaria and aid the selection of appropriate models for translational malaria research.

The structure of full-length myosin A provides some hints about its atypical mechanism, and reveals that the light chain PfELC is a target to block malaria pathogenesis.

The rhoptry protein RhopH3 is crucial for the invasion and growth of the malaria parasite and disruption of it provides insight into the binding of the parasite to the host red blood cell and into the formation of new import pathways.

Parasites with pathogenic variant surface antigens are common in adult malaria patients with a naive immune status.

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.

Malaria parasites avoid destruction by their host's immune response through systematic and coordinated expression switching between members of a network of variant antigen-encoding genes, a process that is mediated by a uniquely conserved gene called var2csa.

Plasmodium falciparum invasion protein EBA-175, once shed from the parasite surface post invasion, facilitates RBC clustering and enhances parasite growth while simultaneously enabling parasite immune evasion of host neutralizing antibodies.

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.

Data exploring host and parasite signatures in the peripheral blood indicate that total parasite biomass is a better predictor of P. vivax-induced host responses and pathogenesis than peripheral parasitemia.