Editing Malaria (section)

===Genetic resistance===
{{Main|Human genetic resistance to malaria}}
Due to the high levels of [[death|mortality]] and [[morbidity]] caused by malaria—especially the ''P.&nbsp;falciparum'' species—it has placed the greatest [[Selection (biology)|selective pressure]] on the [[human genome]] in recent history. Several genetic factors provide some resistance to it including [[sickle cell trait]], [[thalassaemia]] traits, [[glucose-6-phosphate dehydrogenase deficiency]], and the absence of [[Duffy antigen]]s on red blood cells.<ref>{{cite journal | vauthors = Pierron D, Heiske M, Razafindrazaka H, Pereda-Loth V, Sanchez J, Alva O, Arachiche A, Boland A, Olaso R, Deleuze JF, Ricaut FX, Rakotoarisoa JA, Radimilahy C, Stoneking M, Letellier TD| title = Strong selection during the last millennium for African ancestry in the admixed population of Madagascar | journal = Nature Communications | volume = 9 | issue = 1 | pages = 932 | date = March 2018 | pmid = 29500350 | pmc = 5834599 | doi = 10.1038/s41467-018-03342-5 | bibcode = 2018NatCo...9..932P }}</ref><ref name="Kwiatkowski-2005" /><ref name="Hedrick-2011" />

The effect of sickle cell trait on malaria immunity illustrates some evolutionary trade-offs that have occurred because of endemic malaria. Sickle cell trait causes a change in the haemoglobin molecule in the blood. Normally, red blood cells have a very flexible, biconcave shape that allows them to move through narrow [[capillaries]]; however, when the modified [[hemoglobin S|haemoglobin&nbsp;S]] molecules are exposed to low amounts of oxygen, or crowd together due to dehydration, they can stick together forming strands that cause the cell to distort into a curved sickle shape. In these strands, the molecule is not as effective in taking or releasing oxygen, and the cell is not flexible enough to circulate freely. In the early stages of malaria, the parasite can cause infected red cells to sickle, and so they are removed from circulation sooner. This reduces the frequency with which malaria parasites complete their life cycle in the cell. Individuals who are [[homozygous]] (with two copies of the abnormal haemoglobin beta [[allele]]) have [[sickle-cell anaemia]], while those who are heterozygous (with one abnormal allele and one normal allele) experience resistance to malaria without severe anaemia. Although the shorter life expectancy for those with the homozygous condition would tend to disfavour the trait's survival, the trait is preserved in malaria-prone regions because of the [[heterozygote advantage|benefits]] provided by the heterozygous form.<ref name="Hedrick-2011" /><ref name="Weatherall-2008" />