M. D. Lewis

This study establishes a hamster model of Trypanosoma cruzi infection using bioluminescence imaging, revealing chronic tissue pathology and motor dysfunction not seen in mice.

This study identifies benznidazole-treated Trypanosoma cruzi persisters as transient non-proliferative parasites, not localized to specific tissues, and suggests their survival may involve DNA damage response or pre-existing non-replicative states.

This study shows that curative treatment with benznidazole at 6 weeks post-infection reverses digestive Chagas disease symptoms in mice, while delayed treatment leads to irreversible damage.

This study experimentally evolves Trypanosoma cruzi hybrids, showing tetraploid formation, mutation accumulation, and genome erosion over generations, suggesting adaptive potential through genetic exchange.

The paper identifies chronic T. cruzi infection foci in the colon linked to enteric neuropathic lesions, suggesting chemotherapy could prevent chronic disease.

This study shows that incomplete T cell recruitment to infection sites in the mouse colon allows Trypanosoma cruzi to persist chronically despite systemic T cell immunity.

This study identifies skeletal muscle and skin as major sites of Trypanosoma cruzi persistence in chronic murine infections using high-sensitivity imaging.

This study uses genetically modified parasites to show that T. cruzi replication and differentiation are asynchronous within host cells throughout infection.

This study shows that drug-cured Trypanosoma cruzi infections in mice provide long-lasting, cross-strain immunity against re-infection, outperforming recombinant vaccines.