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The mutation responsible for Duffy negativity, which impedes  Plasmodium vivax  infection, has reached high frequencies in certain human populations. Conversely, mutations capable of blocking the more lethal  P .  falciparum  have not succeeded in malarious zones. Here we present an evolutionary-epidemiological model of malaria which demonstrates that if adaptive immunity against the most virulent effects of malaria is gained rapidly by the host, mutations which prevent infection  per se  are unlikely to succeed. Our results (i) explain the rarity of strain-transcending  P .  falciparum  infection blocking adaptations in humans; (ii) make the surprising prediction that mutations which block  P .  falciparum  infection are most likely to be found in populations experiencing low or infrequent malaria transmission, and (iii) predict that immunity against some of the virulent effects of  P .  vivax  malaria may be built up over the course of many infections.

Adaptive immunity selects against malaria infection blocking mutations