Why hasn't evolution got rid of the sickle cell gene?

The sickle cell gene survives because one copy of it protects against malaria. People who inherit two copies have sickle cell disease: their red blood cells can bend into stiff crescents that jam small blood vessels, causing pain and organ damage, and without treatment they rarely reach adulthood. But people with just one copy, called carriers, usually have no symptoms, and when they catch malaria they are less likely to get severely ill.

In places where malaria has killed for generations, that protection is a big deal. Carriers survive and have children more often than people with two normal copies, so the gene keeps being passed on, even though it causes disease in the children who inherit two copies. Biologists call this a trade-off of natural selection. It is why the gene is most common in regions where malaria was rife: across equatorial Africa, 10 to 40% of people are carriers.

The whole story turns on a single letter of DNA. One change in the gene for haemoglobin, the protein that carries oxygen, swaps one building block for another. The disease was first described in 1910, when a young doctor spotted "sickle-shaped" cells in the blood of a dental student from Grenada. Today gene-editing therapies, approved in 2023, can treat it.