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Parasitologic and Immunologic Studies of Experimental Plasmodium falciparum Infection in Nonsplenectomized Chimpanzees (Pan troglodytes)
Diane W. Taylor
Diane W. Taylor
Laboratory of Microbial Immunity, National Institute of Allergy and Infectious Diseases, NIH
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Robert A. Wells
Robert A. Wells
Department of Immunology, Walter Reed Army Institute of Research (WRAIR)
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Alain Vernes
Alain Vernes
Unite 42, INSERM, Flers, 59249, France
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Yvonne J. Rosenberg
Yvonne J. Rosenberg
Laboratory of Microbial Immunity, National Institute of Allergy and Infectious Diseases, NIH
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Stefanie Vogel
Stefanie Vogel
National Dental Institute, NIH, Bethesda, Maryland
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Carter L. Diggs
Carter L. Diggs
Department 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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