Malaria protection comes from all Except
High-Yield Explanation
The geographic distributions of sickle cell disease, hemoglobins C and E, hereditary ovalocytosis, the thalassemias, and glucose-6-phosphate dehydrogenase (G6PD) deficiency closely resemble that of falciparum malaria before the introduction of control measures.This similarity suggests that these genetic disorders confer protection against death from falciparum malaria. For example, HbA/S heterozygotes(sickle cell trait) have a sixfold reduction in the risk of dying from severe falciparum malaria. Hemoglobin S-containing RBCs impair parasite growth at low oxygen tensions, and P. falciparum-infected RBCs containing hemoglobins S and C exhibit reduced cytoadherence because of reduced surface presentation of the adhesin PfEMP1. Parasite multiplication in HbA/E heterozygotes is reduced at high. Ref: Harrison&;s Principles of Internal Medicine; 19th edition; Chapter 248 Malaria; Page no: 1371