Parasitologic and Immunologic Studies of Experimental Plasmodium falciparum Infection in Nonsplenectomized Chimpanzees (Pan troglodytes)

Diane W. TaylorLaboratory of Microbial Immunity, National Institute of Allergy and Infectious Diseases, NIH

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Robert A. WellsDepartment of Immunology, Walter Reed Army Institute of Research (WRAIR)

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Alain VernesUnite 42, INSERM, Flers, 59249, France

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Yvonne J. RosenbergLaboratory of Microbial Immunity, National Institute of Allergy and Infectious Diseases, NIH

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Stefanie VogelNational Dental Institute, NIH, Bethesda, Maryland

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Carter L. DiggsDepartment of Immunology, Walter Reed Army Institute of Research (WRAIR)

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Parasitologic, hematologic, and immunologic parameters were monitored in intact (nonsplenectomized), adult chimpanzees infected with a “chimp-adapted” strain of Plasmodium falciparum. Following primary and secondary injections of 109 P. falciparum-infected erythrocytes, each chimpanzee developed a low grade parasitemia (up to 1,000/mm3) and maintained the infection without evidence of eliminating the parasites. Hematologic and serum biochemical values, as well as the majority of immunologic parameters tested, remained unaltered in infected chimpanzees. However, 2 weeks after infection T cells from infected chimpanzees demonstrated an enhanced response in vitro to stimulation with the mitogen PHA, and monocyte phagocytic activity for antibody-coated erythrocytes (Fc-mediated phagocytosis) increased significantly. During malarial infection, apes developed a strong T cell proliferative response to P. falciparum antigens and monocytes showed enhanced phagocytic activity for P. falciparum-infected erythrocytes in the absence of immune serum. These results suggest that cellular immune mechanisms, especially macrophage activation, may help control, but not eliminate, P. falciparum malaria in chimpanzees.

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