Abstract
Chagas disease results from infection with the parasiteTrypanosoma cruzi. This disease remains a significant cause of morbidity and mortality in central and south America. Chagas disease now exists and is detected worldwide because of human migration. Control of Chagas disease has relied mainly on vector eradication however, the development of insect resistance to pesticides, coupled with cost and adverse health effects of insecticide treatments, has prompted our group to investigate novel methods of transmission control. Our laboratory has been instrumental in the development of the paratransgenic strategy to control vectorial transmission ofT. cruzi. In this paper, we discuss various components of the paratransgenic approach. Specifically, we describe classes of molecules that can serve as effectors, including antimicrobial peptides, endoglucanases, and highly specific single chain antibodies that target surface glycoprotein tags on the surface ofT. cruzi. Furthermore, we address evolving concepts related to field dispersal of engineered bacteria as part of the paratransgenic control strategy and attendant risk assessment evaluation.
Highlights
Chagas DiseaseChagas disease, is caused by the protozoan Trypanosoma cruzi
American trypanosomiasis, or Chagas disease, is caused by the protozoan Trypanosoma cruzi
We evaluated the risks of horizontal gene transfer (HGT) between R. rhodnii and Gordona rubropertinctus, a closely related nontarget Grampositive actinomycete [46]
Summary
Chagas disease, is caused by the protozoan Trypanosoma cruzi. Parasite maturation, which involves metacyclogenesis of T. cruzi from noninfective epimastigotes to infective trypomastigotes, occurs in the gut of the triatomine bugs and is an important step in the transmission of Chagas disease [34] This maturation process is dependent on interactions between the surface epitopes of T. cruzi and the gut lumen of the insect vector [35] and would be the target of scFv effector activity. An effective paratransgenic strategy for field application would involve the delivery of these effector molecules in combination, for example: AMPs with scFvs or AMP’s with endoglucanases This strategy should reduce transmission of T. cruzi, and the development of resistance resulting from prolonged treatment with a single effector
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