Sickle cell disease (also called sickle cell anemia) is a human genetic disorder

Question

Sickle cell disease (also called sickle cell anemia) is a human genetic disorder that causes red blood cells to have a rigid crescent shape that interferes with the cells’ function. Famously, the sickle cell allele provides some protection against malaria, which can explain why sickle cell is much more common in populations that currently live, or have historically lived, in geographic areas with high malaria prevalence. There are no known genetic differences among malaria parasites in their ability infect hosts with sickle cell disease (Durand & Coetzer 2008). For a long time, it was believed that the misshapen red blood cells interfered with the malaria parasite’s ability to survive within the host, but more recent evidence suggests instead that the parasite survives unimpeded in sickle cells. Instead, it appears that the product of an enzyme that is much more active in sickle cells than in normal cells confers protection from the severe symptoms of malaria infection (Ferreira et al. 2011). What is this narrative an example of: host-parasite co-evolution, the evolution of virulence in the malaria parasite, the evolution of host resistance against the malaria parasite, or the evolution of host tolerance to the malaria parasite? Please justify your answer.

Explanation / Answer

It is a classic example of evolution of host tolerance to the malaria parasite. The experimental results of Ferreira et al. 2011 showed that in a mice with HbSAD , protection against experimental cerebral malaria (ECM) is not associated with decrease in pathogen load as reflected by similar percentage of infected RBC and similar number of circulating infected RBC in both Hbwt and HbSAD mice. Therefore, the protection of HbSAD mice against malaria is related with host tolerance to malaria parasite. The tolerance was proved to be induced by expression of heme oxygenase (HO) which form carbon monoxide (CO). CO prevents the accumulation of heme after Plasmodium infects to sickle cell RBC. Additional evidence arrived with the finding that sickle Hb inhibit the activation of CD8+ cells that recognize the antigens expressed by Plasmodium.

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