Cytotoxicity associated with APOL1 renal-risk variants occurs through its plasma-membrane localization, where aberrant channel activity drives a sustained sodium and calcium influx leading to cell swelling and eventually cell death.

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

The ligand specificity and expression profile of the haptoglobin-haemoglobin receptor has diversified throughout the evolution of trypanosomes.

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.