This link does not necessarily provide us with evidence that a cultural behavior has caused alterations in the genetic material, unlike the lactose tolerance, malaria resistance, and thrifty metabolism examples in humans.
However, a few species, most notably the Hawaii amakihi (Hemignathus virens), can survive with chronic malaria infection, exhibiting tolerance or resistance to the disease [ 21– 23].
Different inbred mice strains display differences in tolerance against malaria Plasmodium chabaudi (Råberg et al. 2007).
Presumably, the mechanism via which Nrf2 confers tissue damage control and disease tolerance to malaria also involves the expression of Nrf2-responsive genes regulating haeme/iron metabolism [ 43].
The analysis of five inbred mice strains showed a strong genetic trade-off between resistance and tolerance to malaria (Råberg et al. 2007).
These include the iron storage protein Ferritin H chain (FtH) [ 44, 45], which can confer per se tissue damage control and disease tolerance to malaria in mice [ 10].
We found high malaria-attributable fractions for seizures in children >6 months and these attributable fractions decreased with age, which may reflect the increasing immunity and tolerance to malaria as children grow older.
Sickle haemoglobin induces the expression of HO-1 through a mechanism regulated by Nrf2 and leading to the production of CO, which confers tissue damage control and disease tolerance to malaria [ 38, 39].
Sexual partners of carriers of this allele are homozygotes with two normal alleles; and therefore, only heterozygotes with higher tolerance to malaria, and not homozygotes with two s alleles and therefore with the fatal form of sickle cells disease, will occur among their offspring.
Quinacrine has the advantage of a long history of clinical use in the treatment of malaria, so that human tolerances are well known.
