<em>Trypanosoma cruzi</em>: Role of δ-Amastin on Extracellular Amastigote Cell Invasion and Differentiation

<div><p><em>Trypanosoma cruzi</em> is a protozoan parasite that comprises different phylogenetic groups and is the causative agent of Chagas’ disease. Different <em>T. cruzi</em> strains present differences in infectivity in <em>in vitro</em> and <em>in vivo</em> experimental models, which are likely related to the expression of different virulence factors. Amastin is a surface glycoprotein abundantly expressed on the intracellular mammalian amastigote form of the parasite. In this study, we showed that a highly infective strain (G strain) of extracellular amastigote (EA) invasive forms expressed reduced RNA levels of amastin compared to a less infective strain (CL). The treatment of HeLa cells with recombinant δ-amastin reduced infectivity of EA forms. However, the ectopic expression of δ-amastin accelerated amastigote differentiation into trypomastigotes. Corroborating the virulence behavior in association with amastin expression, the EAs overexpressing amastin were precociously and robustly observed in the liver of susceptible mouse strains (A/JUnib), whereas parasitemia was never detected in <em>in vivo</em> assays. This is the first report on the regulatory role of amastin in the course of both <em>in vitro</em> and <em>in vivo T. cruzi</em> infection.</p>