to involve the alternative complement pathway and the C3b receptor on rat erythrocytes. The parasite activates complement and fixes C3b to its surface, which in turn binds to the rat erythrocyte C3b receptor, leading to intracellular infection. Additionally, erythrocytes with C3 on their surface are infected, thus suggesting that complement facilitates the para-site-erythrocyte interaction. Following intracellular maturation, merozoites exit the erythrocyte, resulting in perforations and damage to the red cell membrane. The actual mechanism of hemolysis is unknown. Circadian hemolysis from synchronous schizogony, typified by the cyclic fevers of Plasmod-

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