LDLR and schistosomiasis: We can speculate, therefore, that HDL-C increases in schistosomiasis are a multi-step process, promoted by low CETP activity and enhanced further by the ε2-allele: ApoE2 has a higher affinity than ApoE3 or ApoE4 for HDL [62], allowing the particles to expand in size [18], [63], while defective ApoE2 receptor binding delays their clearance from plasma via hepatic LDL-receptors [17], [60].