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The Kilian lab investigates novel secretory organelles generated by malaria parasites to establish host-parasite interaction and methods to simplify the diagnosis of malaria.

The asexual replication of the malaria parasite Plasmodium falciparum occurs in the red blood cells of the human host and is responsible for the symptoms and disease severity experienced by patients suffering from malaria tropica.

To ensure survival and successful procreation within the organelle-deprived host red blood cells, Plasmodium falciparum commences to reorganize the cytoplasm of the host cell. This cumulates in the generation of a novel secretory organelle outside the parasite’s own cell within the cytoplasm of the red blood cell. The secretory organelle was named Maurer’s clefts in the honor of Georg Maurer who first discovered the structure in 1902. The importance of the Maurer’s clefts is undeniable and failure to properly generate this organelle hampers host-parasite interaction, which can culminate in the clearance of the infected red blood cell by the spleen. More than 100 years after their discovery, the Maurer’s clefts still remain mysterious. The Kilian lab aims to decipher this fascinating organelle.

The Kilian lab further strives to simplify the diagnosis of malaria at point-of-care settings in malaria endemic areas using different approaches.

(A) Merozoites infect the red blood cells where they develop into ring, trophozoite and schizont. During that time the parasite generates the Maurer’s clefts. During the ring stage the organelle has a vesicular shape. In the mature trophozoite and schizont stages the Maurer’s clefts are flattened single or stacked cisternae. The Maurer’s clefts are crucial for trafficking the parasite protein PfEMP1 (P. falciparum erythrocyte membrane protein 1) to the red blood cell surface (B). There the protein is presented on red blood cell plasma membrane protrusions, so called knobs, which are generated by the parasite as well (C). Proper presentation of PfEMP1 is crucial to enable cytoadherence of the infected red blood cell to endothelial cells which line the blood vessel wall. Cytoadherence removes the infected red blood cell from the peripheral blood to avoid the passage of the spleen, where deformed red blood cells infected with mature developmental stages of the parasite are removed from circulation. Hidden away in the vascular bed of inner organs such as the brain, the parasite is able to complete the erythrocytic schizogony by producing merozoites which commence and infect new red blood cells. E: red blood cell, PVM: parasitophorous vacuolar membrane, MC: Maurer’s clefts, K: knobs, PM: red blood cell plasma membrane,

CP: cytoplasm. Image credit: Kilian et al., 2020 (BioEssays).

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