Increasing levels of glucose-6-phosphate dehydrogenase deficiency are associated with decreasing risk of cerebral malaria, but with increased risk of severe malarial anaemia.

Analysis of a large Kenyan dataset may resolve previously conflicting studies by identifying polymorphisms which interact to modify the risk of cerebral malaria.

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.

Selection bias, also known as collider bias, likely explains the apparent protective effect of G6PD deficiency against cerebral falciparum malaria.

Clinical, clinicopathological and image data from Malawian children shows that sequestration in P. falciparum cerebral malaria is visible clinically in the eye as orange retinal vessels and is strongly associated with death.

The Mediterranean variant of glucose-6-phosphate dehydrogenase deficiency confers a strong gene-dose proportional protective effect against symptomatic Plasmodium vivax malaria in the Pashtun ethnic group.

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

Illustrating the impact of host metabolism on infection outcome, loss of the aryl hydrocarbon receptor in radioresistant cells leads to heme-mediated kidney toxicity during malaria.

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.

A conceptual and unifying framework with a critical appraisal of lipid hijacking by microbes cycling between an arthropod vector and a mammalian host is explored.