Abstract

Trypanosoma cruzi is the etiologic agent of Chagas disease, a life-threatening disease that affects different tissues. Within its mammalian host, T. cruzi develops molecular strategies for successful invasion of different cell types and adaptation to the intracellular environment. Conversely, the host cell responds to the infection by activating intracellular pathways to control parasite replication. Here, we reviewed genome-wide expression studies based on microarray and RNA-seq data from both parasite and host genes generated from animal models of infection as well as from Chagas disease patients. As expected, analyses of T. cruzi genes highlighted changes related to parasite energy metabolism and cell surface molecules, whereas host cell transcriptome emphasized the role of immune response genes. Besides allowing a better understanding of mechanisms behind the pathogenesis of Chagas disease, these studies provide essential information for the development of new therapies as well as biomarkers for diagnosis and assessment of disease progression.

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