María Cristina Vanrell

TL;DR: A new model is proposed in which T. cruzi takes advantage of the upregulation of autophagy during starvation to increase its successful colonization of host cells.

TL;DR: Both polyamine metabolism and autophagy are key processes during T. cruzi metacyclogenesis that could be exploited as drug targets to avoid the parasite cycle progression.

TL;DR: The data showed that depleting intracellular polyamines by inhibiting the biosynthetic enzyme ornithine decarboxylase with difluoromethylornithine (DFMO) suppressed the induction of autophagy in response to starvation or rapamycin treatment in two cell lines, suggesting DFMO is an FDA-approved drug that may have value in limiting Autophagy and the spread of the infection in Chagas disease and possibly other pathological settings.

TL;DR: An overview on the limitations of the current available medications to treat African trypanosomiasis, Chagas disease and Leishmaniasis is presented, along with a review on drug candidates presently undergoing clinical trials and drug candidates identified through drug repositioning initiatives.

TL;DR: The data suggest that autophagy plays a protective role against T. cruzi infection in mice, xenophagy being one of the processes activated as part of the repertoire of immune responses generated by the host.