Malaria is big killer in Africa. According to the WHO, 91% of the 438,000 malaria deaths last year were in sub-Saharan Africa.
However, I remember our science book back in Grade 7, or perhaps earlier, having a blurb about sickle cell anemia, which can be deadly. As I recall, it was caused by inheriting a particular genetic mutation (which is common in Africa) from both parents, while someone inheriting the mutation from only one parent acquired immunity from malaria.
I see there has been a recent update in understanding the mutation:
Sickle-cell mystery solved: Researchers discover how carriers of the sickle-cell anaemia gene are protected from malaria
It has been a medical mystery for 67 years, ever since the British geneticist Anthony Allison established that carriers of one mutated copy of the gene that causes sickle-cell anaemia are protected from malaria. The finding wasn’t trivial: in equatorial Africa, where Allison did his work, up to 40% of people are carriers of this mutated gene. Since then, scientific sleuths have wondered how exactly the gene protects them.
Michael Lanzer and his colleagues at Heidelberg University in Germany and the Biomedical Research Center Pietro Annigoni in Ouagadougou, Burkina Faso, used powerful electron microscopy techniques to compare healthy red blood cells both with 'normal' cells infected with the malaria parasite Plasmodium falciparum and with infected cells from people carrying the mutated “S” gene that causes sickle-cell disease, as well as another mutation, dubbed “C,” which occurs at the same spot. Both mutations lead to the substitution of a single amino acid in the hemoglobin molecule, causing the haemoglobin to aggregate abnormally inside the cell. In people with two copies of the S mutation, they deform into a half-moon shape — the 'sickle cells' that give the disease its name.
The researchers saw that in healthy red cells, very short pieces of actin filament — threads of protein crucial to maintaining the pliable internal 'skeleton' that lets the red blood cell squeeze through tiny blood vessels — are clustered just under the cell's outer membrane. But in infected cells, they observed that the malaria parasite steals this actin and uses it to construct an intracellular bridge to transport a parasite-made protein to the cell surface. This protein, called adhesin, makes the infected red blood cells 'sticky', causing them to adhere to each other and to the vessel wall to cause the widespread microvascular inflammation characteristic of malaria.
The parasite doesn't get everything its own way, however. Enter the sickle-cell factor. In red blood cells containing the aberrant sickle-cell haemoglobin, Lanzer and his team observed that the hijacking of actin filaments by the parasite was hobbled. The actin bridge was cut off from the intracellular depot of adhesin, and the vesicles that would normally transport the adhesin to the cell surface were floating free in the cytoplasm.
Further experiments led the team to hypothesize that ferryl haemoglobin, produced when the mutant haemoglobin reacts with oxygen, subverts the parasites’ efforts to reorganize their host cells' actin by preventing the actin proteins polymerizing to form long filaments.
The take-home message, says Lanzer, “is that the parasite, in order to survive within the red blood cell, has to remodel the host actin — and that evolutionary pressure has resulted in mutations in human haemoglobin that prevent this remodelling.” People who carry just one mutated copy of the sickle-cell gene still make enough normal haemoglobin and so are largely asymptomatic. So being a carrier confers a survival advantage in countries where malaria is endemic.