Several studies have proposed that sickle cell trait individuals (HbAS) confer partial protection against Malaria. Even though the mechanism is not clear, various mechanisms have been proposed as a means of malaria resistance by HbAS individuals of which some are sickling of their RBCs and splenic Phagocytosis. Thinking deep into this, I was wondering why then do people with HbSS develop severe malaria because if these mechanisms contribute to people with the Sickle cell trait malaria resistance, then people who are homozygous to the sickle gene should be more resistant to malaria. Any contribution?
Are all the RBCs of individuals with HbAS morphologically deformed? If some RBCs are normal, these would be targeted by the malaria merozoites released from hepatocytes and thus the individual is likely to be severely affected leading to severe anemia and other symptoms of clinical malaria
Moses Mwajar Ngeiywa That’s what we are taught to believe historically; however as Nora Whittle asked, how is it then people who are homozygous ie HbSS are prone to severe disease unlike the heterozygotes?
On a similar vein, HbAS curiously are only protected vs malaria but not other mosquito borne infections eg Dengue.
I made some research and from the attachEd file which was a research conducted by Natasha Archer and some other scientists, they proposed that low oxygen HbS polymerization leads to stalled growth and replication of the Plasmodium parasite and this is my own understanding. So in this case, the level of parasitemia in HbAS Individuals may not be enough to cause virulent malaria. Now in the case of HbSS individual, even though HbS polymerization might not allow parasites to multiply, that process itself isn’t favorable for micro-circulation of important gases like oxygen which leads to some Vaso-occlusive crises, at least HbAS individuals have the normal gene to compensate for that. I would also like to point the fact that the sickle gene does not protect against being infected by the parasites, but it protects affected individuals from developing severe malaria as a result of the P. falciparum infection. Even though parasites may not be able to multiply in HbSS individuals, those parasites that have already infected also adds up to destruction of their red cells causing their anaemia to be worse, that’s why their affected more by the infection. Impaired spleen activities in people known to have the sickle cell disease doesn’t allow total clearacne of the parasites as well.
Raisonnement très logique, malheureusement en dehors de mon champs de recherche . Je vous encourage à poursuivre les recherches.
Richard Riziki please translate for us non French speaking folks thanks!
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