Plasmodium falciparum: immune pressure in Saimiri sciureus monkeys can select for a parasite population inducing a protective immunity that is not controlled by antibody.

Protective immunity against a Plasmodium falciparum blood infection can be passively transferred by antibodies in humans and in the primate experimental malaria model Saimiri sciureus. We report here the emergence of a novel virulent parasite population after such passive transfer of hyperimmune serum in splenectomized monkeys. These FUP-2 parasites have been partially genotyped and phenotyped. Although no genotypic variation was detected for four polymorphic loci compared to the original FUP-1 parasite population, FUP-2-infected erythrocytes exhibit little or no detectable surface determinants, including those reacting with antibodies raised against FUP-1 surface antigens. In addition, FUP-2-infected erythrocytes exhibit no rosetting or autoagglutination. Interestingly, although Saimiri monkeys control efficiently FUP-2 parasites after repetitive infections, this protection cannot be passively transferred to naive recipients. Our results suggest that antibody-mediated and antibody-independent T-cell-mediated protective responses may cooperate in controlling P. falciparum infection in splenectomized Saimiri monkeys.