Abstract
African trypanosomes undergo a complex developmental process in their tsetse fly vector before transmission back to a vertebrate host. Typically, 90% of fly infections fail, most during initial establishment of the parasite in the fly midgut. The specific mechanism(s) underpinning this failure are unknown. We have previously shown that a Glossina-specific, immunoresponsive molecule, tsetse EP protein, is up regulated by the fly in response to gram-negative microbial challenge. Here we show by knockdown using RNA interference that this tsetse EP protein acts as a powerful antagonist of establishment in the fly midgut for both Trypanosoma brucei brucei and T. congolense. We demonstrate that this phenomenon exists in two species of tsetse, Glossina morsitans morsitans and G. palpalis palpalis, suggesting tsetse EP protein may be a major determinant of vector competence in all Glossina species. Tsetse EP protein levels also decline in response to starvation of the fly, providing a possible explanation for increased susceptibility of starved flies to trypanosome infection. As starvation is a common field event, this fact may be of considerable importance in the epidemiology of African trypanosomiasis.
Highlights
African trypanosomes are protozoan parasites that cause sleeping sickness in humans and nagana in domestic livestock in sub-Saharan Africa
We show that a particular, tsetsespecific immune responsive protein called tsetse EP acts as a powerful antagonist of trypanosome establishment in the fly midgut
It is known that starvation of flies leads to an increase in their susceptibility to trypanosomes and this may be a considerable factor in the epidemiology of the disease in Africa
Summary
Trypanosomes, by influencing food production, natural resource utilization and the pattern of human settlement, are seen by the African Union as one of the greatest constraints to Africa’s socio-economic development [4]. African trypanosomes are cyclically transmitted by tsetse flies (Glossina spp.). Trypanosoma brucei and T. congolense undergo a complex cycle of development in the tsetse beginning almost immediately after ingestion of an infected bloodmeal when trypanosome bloodstream forms (BSF) differentiate to the procyclic form in the fly midgut lumen [5,6,7]. Between days 4 and 5 trypanosome infections are eliminated from most flies [7] through a process we term self-cure. Most mature tsetse are resistant to trypanosome infection the mechanisms involved in elimination of trypanosomes from the fly midgut (self-cure) are not understood [13]
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