Specific inhibition of the morphogenesis of Trypanosoma cruzi by a monoclonal antibody

Abstract

Trypanosoma cruzi, the causative agent of Chagas' disease, is transmitted primarily by blood-sucking reduviid bugs. The insects themselves are infected by ingesting trypomastigotes with the blood of infected mammals. On ingestion by the vector, the parasites convert to epimastigotes which multiply within the lumen of the crop and midgut. In the hindgut and rectum of the reduviid, the epimastigotes transform into non-dividing metacyclic trypomastigotes which can, when passed with the faeces, infect the vertebrate host¹. Lectins capable of binding T. cruzi have been isolated from different regions of the vector's intestinal tract^2,3. It has been proposed that the interaction of these lectins with the surface membrane of the parasite regulates the morphogenesis of T. cruzi in the gut of the vector^2,3. In the present study we describe the inhibition of epimastigote to trypomastigote differentiation in vitro by a monoclonal antibody specific for a 72,000 molecular weight cell-surface glyco-protein of T. cruzi and propose that this molecule may be a receptor controlling parasite differentiation in the vector.