Evolution of virulence in malaria

The pathogenesis of severe malarial disease is not yet fully understood. It is clear that host immunopathology plays a central role, and a recent paper in BMC Evolutionary Biology suggests that the ability of the parasite to stimulate interleukin-10 production is a major factor and speculates on its impact on the coevolution of host and parasite.

Plasmodium falciparum malaria is responsible for over 1 million deaths each year, mostly in children under the age of 5 living in sub-Saharan Africa. And yet the number of malaria infections which go on to become life threatening is proportionally very small, as the majority of these infections either remain asymptomatic (due to the acquisition of clinical but non-sterile immunity after repeated exposure) or progress to disease without lethal complications [1]. Viewed in an evolutionary context, the existence of severe disease presents a population-level compromise for the parasite between the necessity of bearing factors that increase survival and transmission and the risk that these will stimulate a host immune response that will either curtail the infection or perversely cause the death of the host (thus also spelling the end for the parasite). With the aim of identifying factors that may be relevant in the evolution of this balance, Long et al. in a recent article in BMC Evolutionary Biology [2] have investigated the influence of the inflammatory response on the severity of disease in a rodent model of malaria, and we discuss here how their results may bear on the coevolution of parasite and host, in the context of what is known about the determinants of severe malarial disease in humans.