The pathogenesis of the parasite African trypanosome (T. brucei) has been linked to a key protein switch, detailed in a new study by researchers at the University of Iowa and the Veterans Affairs Medical Center of Iowa City, led by Dr. John Donelson.
The study explains how two enzymes enable the cell's surface to remodel itself in order to thwart the immune system of carrier tsetse flies.
African trypanosomiasis has long been endemic in regions of Sub-Saharan Africa. The fatal parasitic disease is known to largely affect humans and livestock. The disease currently affects roughly 60 million people in 36 African nations. Bloodstream trypanosomes thwart their host's immune response by periodically switching their major surface protein, the variant surface glycoprotein (VSG).
In this study, researchers looked at how trypanosomes shed their VSG to survive within the tsetse fly's midgut. By experimenting with enzyme gene deletion, Grandgenett et al. could test the parasite's survival rate.
This study addresses a key issue in the pathogenesis of African Trypanosomiasis: how the surface coat of the parasite is "shed" to facilitate immune evasion. Much previous work has been aimed at addressing this question and this work is the clearest identification of molecules involved in this process.
Reference: Grandgenett PM, Otsu K, Wilson HR, Wilson ME, Donelson JE (2007) A function for a specific zinc metalloprotease of African trypanosomes. PLoS Pathog 3(10): e150.doi:10.1371/journal.ppat.0030150
This research was supported by National Institutes of Health and Veterans Affairs.
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