Complement does not facilitate plasmodial infections.
The influence of the complement (C) system on Plasmodial infections in vivo (Plasmodium berghei in rats) and in vitro (Plasmodium falciparum) has been determined. In rats C3 depletion by treatment of animals with the C3 inactivator isolated from cobra venom factor results in infection that develops more rapidly, reaches a higher peak of parasitemia and is associated with an increased mortality rate (60%), in contrast to a lower degree of parasitemia and lack of mortality in C3-intact rats. The infection of human red cells by P. falciparum is not affected when serum C is inactivated either by heat treatment or by incubation with preformed immune complexes. Furthermore, human sera genetically deficient in C2, C3, C4, or C5 are as effective in facilitating the infection of red cells as is C-intact serum. These data suggest that, in contrast to Babesia sp., the in vitro or the in vivo infection of red cells by Plasmodium sp is not facilitated by the availability of C.
D000818:Animals; D003176:Complement C3 / Q000172:deficiency; D003165:Complement System Proteins / Q000276:immunology*; D004912:Erythrocytes / Q000276:immunology; D008288:Malaria / Q000276:immunology*; D008297:Male; D010962:Plasmodium berghei / Q000276:immunology; D010963:Plasmodium falciparum / Q000276:immunology; D051381:Rats
D003176:Complement C3; D003165:Complement System Proteins