Groups of mice were inoculated with either low or high intraperitoneal doses of Plasmodium berghei infected erythrocytes (PIE). The course of infection was observed daily by counting new PIE which appeared in the red blood cells (RBC) of infected mice. At the same time, circulating interferon (IF) was tested. When low doses of infecting PIE were used (400 per mouse), circulating IF was first detected on the 5th day after inoculation. It increased to a maximal rate, when 5% of RBC were affected. It disappeared on the 8th day despite of a continuous rise of PIE. With high doses of PIE (60,000 per mouse), IF was detected on the 3rd day, when only 0.5% of RBC were parasitized. The maximal rate was observed on the 5th day when 20% of the RBC were affected. It disappeared on the 7th day, though the PIE rate would continue to rise. Treatment of mice by chloroquine (0.01 per g), at the time of first PIE appearance after Plasmodium infection, rapidly reduced the amount of PIE. In this case, no IF production was observed. Splenectomy resulted in an increased resistance of mice to the lethal effect of Plasmodium infection. IF production in such splenectomized mice was less important than in control. It was concluded that P. berghei was a good inducer of circulating IF at the beginning of the active disease, soon after infection. The fact was proven by the striking lowering effect of chloroquine and splenectomy that both reduced Plasmodium development and IF production.

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