Sleeping sickness affects more than 50,000 people around the world, mostly in Sub-Saharan Africa. It is caused by the Trypanosoma parasite, which is transmitted by the tsetse fly. A team of CNRS researchers has identified a new protein within the parasite, the absence of which prevents the parasite from being able to feed itself and causes it to die. This work is of considerable importance, as it offers the potential of promising therapeutic strategies to fight the disease.
Sleeping sickness is a major public health and economic issue in Sub-Saharan Africa, and is a potential threat to 60 million people in some 36 African countries. It is estimated that 50,000 to 70,000 people are currently infected. The disease, which is always fatal in the absence of treatment, is caused by a unicellular parasite called Trypanosoma, which is transmitted by the bite of the tsetse fly. Existing treatment is expensive, toxic and difficult to administer in the field.
Trypanosoma lives in the blood, marrow, and an area of the brain called cephalorachidian liquid. It has an original cell component, the flagellar pouch. Derrick Robinson, a CNRS researcher at the CNRS / Université Bordeaux 2 laboratory, says of it: "this pouch, which has several functions, is the Achilles tendon of the parasite.” This is the area from which the flagellum emerges, enabling the parasite to move. Moreover, this pouch is the only place where endocytosis and exocytosis occur, two processes which allow exchange of materials between the parasite and its environment. (During endocytosis, the membrane of the poche flagellaire envelops and absorbs a particle. During exocytosis, the opposite occurs: the particle is expelled from the membrane.)
Derrick Robinson’s team, working with the Trypanosoma brucei brucei form, which is specific to animals, has identified a new protein, BILBO1, which is essential to the formation of the parasite’s flagellar pouch.
Taking their work even further, the researchers showed that BILBO1 is responsible for forming a specific structure of the cytoskeleton, which supports the flagellar pouch. When the protein is not expressed in the parasite, the parent cell is incapable of forming a new pouch, something which is necessary for the production of daughter cells. This mutant Trypanosoma can then no longer exchange with its environment, and cannot take in the nutrients necessary to sustain its life. The accumulation of waste which cannot be expelled by exocytosis results in the cells’ swelling, then in their not moving correctly, and finally to their not dividing. The parasite can thus be stopped by blocking BILBO1.
These results raise the hope of promising therapeutic avenues, by pointing to the potential of BILBO1 as a new target for trypanocidal drugs.
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