Effects of TcFLA-1BP and TcGP72 Deletion on the Infectivity and Survival of Trypanosoma cruzi in Cell Cultures.

Abstract

Chagas disease, caused by the protozoan Trypanosoma cruzi, is a neglected tropical disease with limited treatment options and no available vaccine. Understanding the role of proteins in the parasite's biological cycle is critical for advancing vaccine development and optimizing therapies. The flagellar attachment zone (FAZ) proteins play a pivotal role in motility, pathogenicity, and cell division in trypanosomatids, but their functions in T. cruzi are not as well-characterized as in Trypanosoma brucei and Leishmania spp. This study investigates the orthologous TcGP72 and TcFLA-1BP proteins in T. cruzi, focusing on their roles in the infective forms of the parasite. Our findings demonstrate that TcFLA-1BP is important for efficient host cell infection in vitro, indicating its critical role in the parasite's infectivity. Conversely, TcGP72 is nonessential for the infection process, but significantly contributes to cytoskeletal remodeling during the parasite's life cycle. These results provide new insights into the distinct functional roles of FAZ proteins in T. cruzi. Furthermore, the study underscores the importance of TcGP72 in maintaining cellular architecture, reinforcing the relevance of FAZ proteins in the parasite's pathogenesis and structural integrity.