Abstract
In a recent Opinion article [1], White and colleagues discuss the value of the murine Plasmodium berghei ANKA model in identifying pathological processes and therapeutic interventions in human cerebral malaria (HCM). This model involves P. berghei ANKA infection of inbred CBA or C57BL/6 strain mice, which develop clinical symptoms of cerebral complications including paralysis, fitting and coma with death around Day 8 post-infection [2]. Resistant mouse strains such as BALB/c mice develop hyperparasitemia and severe anemia with death occurring about 3 weeks after infection.
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