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Abstract

The present disclosure is directed to parasites that cause malaria, particularly Plasmodium-species parasites, and more particularly to Plasmodium-species parasites that have been genetically altered to develop normally only to the late liver stage but are completely inhibited in transition to blood stage or infection of erythrocytes. In particular, the inventors have identified genetic alterations that cause these parasites to arrest at the late liver stage of development, resulting from the disruption of the gene function of the liver stage nuclear protein (LINUP) gene. This complete late liver stage arrest allows for expression of an enhanced array of parasitic antigens throughout liver stage development, but prevents entry to blood stage, erythrocytic infection and the associated signs, symptoms and pathology of malaria disease.

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First Claim