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Immunization with radiation attenuated  Plasmodium  sporozoites (RAS) elicits sterile protective immunity against sporozoite challenge in murine models and in humans. Similarly to RAS, the genetically attenuated sporozoites (GAPs) named  uis3(-) ,  uis4(-)  and  P36p(-)  have arrested growth during the liver stage development, and generate a powerful protective immune response in mice. We compared the protective mechanisms in  P. yoelii  RAS,  uis3(-)  and  uis4(-)  in BALB/c mice. In RAS and GAPs, sterile immunity is only achieved after one or more booster injections. There were no differences in the immune responses to the circumsporozoite protein (CSP) generated by RAS and GAPs. To evaluate the role of non-CSP T-cell antigens we immunized antibody deficient, CSP-transgenic BALB/c mice, that are T cell tolerant to CSP, with  P. yoelii  RAS or with  uis3(-)  or  uis4(-)  GAPs, and challenged them with wild type sporozoites. In every instance the parasite liver stage burden was approximately 3 logs higher in antibody deficient CSP transgenic mice as compared to antibody deficient mice alone. We conclude that CSP is a powerful protective antigen in both RAS and GAPs viz.,  uis3(-)  and  uis4(-)  and that the protective mechanisms are similar independently of the method of sporozoite attenuation.

Conserved Protective Mechanisms in Radiation and Genetically Attenuated uis3(-) and uis4(-) Plasmodium Sporozoites