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Significance Malaria infection causes a severe disease with diverse symptoms. The molecular mechanisms underlying the differences of malaria pathology remain unknown or controversial. Here we infected mice with two closely related strains of rodent malaria parasitePlasmodium yoelii and characterized host genome-wide responses to the infections. We found that in mice infected with parasite N67, type I interferon was produced to a high level, leading to suppression of parasitemia. We further characterized the molecular mechanisms and identified host receptors in recognizing parasite ligands. In contrast, mice infected with N67C parasite mounted a strong inflammatory response, leading to severe pathology and host death. This study reveals previously unrecognized mechanisms associated with strain-specific malaria infection and provides important information for studying human malaria pathogenesis.

Strain-specific innate immune signaling pathways determine malaria parasitemia dynamics and host mortality