The protozoan parasite Trypanosoma brucei gambiense has undergone recent clonal evolution that reveals the theoretically predicted Meselson effect at a genome-wide level.

Common kidney disease risk variants in African populations are associated with reduced susceptibility to deadly African trypanosomes.

Two gene variants provide different levels of protection against sleeping sickness, but this comes with an increased risk of developing chronic kidney disease.

The parasite that causes African sleeping sickness can be transmitted from mammals to tsetse flies in two stages of its lifecycle, rather than one as was previously thought.

African trypanosomes residing within the skin of infected humans represent an important yet overlooked transmissible parasite population that may thwart efforts to eliminate African sleeping sickness.

African trypanosomes have a trypanothione-based mitochondrial thiol redox metabolism.

A structure derived from cryogenic electron microscopy shows how ISG65, an African trypanosome receptor that aids virulence, binds C3b and suggests mechanisms through which ISG65 might aid complement resistance.

The structure of the trypanosome haptoglobin-haemoglobin receptor bound to its ligand reveals the molecular basis for ligand recognition in innate immunity and identifies molecular determinants that aid efficient uptake.