As I have mentioned before, there are a couple of common mutations of the APOL1 gene ( (G1 and G2) that protect against one strain of sleeping sickness, but unfortunately greatly increase the risk of kidney failure. The story was unsimple because they didn’t seem to protect against the other strain of sleeping sickness, the one that’s currently common in populations carrying G1 and G2. The first guess was that the other strain used to be common there and was replaced by a different strain, somehing like what may have happened in central Africa, where almost everyone is immune to vivax malaria, but you don’t see much vivax there ( instead, falciparum).
A recent publication clarifies things a bit. First, the two strains of human sleeping sickness are Trypanosoma brucei rhodesiense, which causes the acute East African form, and T.b. gambiense, which causes the more chronic West African form.
G2 gives strong protection against infection by the East African strain, but appears to increase vulnerability to the West African strain. G1 doesn’t do much against the East African strain, but allow asymptomatic carriage of the West African strain – better survival, rather than resistance to infection.