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The acquisition of malaria immunity is both remarkably slow and unpredictable. At present, we know little about the malaria parasite genes that influence the host's ability to mount a protective immune response. Here, we show that a single-nucleotide polymorphism (SNP) resulting in a single amino acid change (S to F) in an ApiAP2 transcription factor in the rodent malaria parasite  () NK65 allowed infected mice to mount a T helper cell 1 (T1)-type immune response that controlled subsequent infections. As compared to NK65, NK65 parasites differentially expressed 46 genes, most of which are predicted to play roles in immune evasion. NK65 infections resulted in an early interferon-γ response and a later expansion of germinal centers, resulting in high levels of infected red blood cell-specific T1-type immunoglobulin G2b (IgG2b) and IgG2c antibodies. Thus, the  ApiAP2 transcription factor functions as a critical parasite virulence factor in malaria infections.

A single-nucleotide polymorphism in a Plasmodium berghei ApiAP2 transcription factor alters the development of host immunity