Interestingly, it has been recently shown that mutations in the C-terminal region of APOL1 interfere with the interaction of the Serum Resistance-Associated (SRA) protein with APOL1, which is the mechanism by which Trypanosoma brucei rhodesiense evades the trypanolytic activity of APOL1 that normally confers resistance to the parasite [28,29]. This suggests a potential explanation for a selective sweep which would have taken place in those regions in Africa where the Trypanosoma brucei rhodesiense has evolved and human infection has become widespread. If this is indeed the case, such a sweep is probably no more than a few thousands years old, since it is believed that the SRA protein evolved in Trypanosoma brucei rhodesiense when humans had become more numerous [30]. It is possible that the association of the variants caught up in this selective sweep with increased risk of kidney disease is incidental, although there may be more subtle mechanisms awaiting elucidation.
