The deadliest of the four human malaria parasites, Plasmodium falciparum, has left its imprint on the human genome in the form of malaria-protective mutations, including those that cause sickle-cell anaemia. Now, Lluis Quintana-Murci and Anavaj Sakuntabhai at the Pasteur Institute in Paris and their colleagues show that — in a similar trade-off — pressure from a neglected strain, P. vivax, may maintain a common enzyme deficiency in southeast Asia that can cause jaundice and anaemia.
The team found that the local gene variant associated with the enzyme deficiency was also associated with a 30–60% reduction in parasite density of P. vivax but not P. falciparum. People with two copies of the gene had the lowest parasite densities. The results suggest that P. vivax has had a larger effect on the human genome than previously thought.