We aim to understand the exit strategy of Trypanosoma cruzi, a human pathogen causing Chagas disease. This work is a fundamental piece in our understanding of disease progression and in the challenging venture of new anti-chagasic drug discovery.
Egress is a critical step of the life cycle for many intracellular pathogens. While the cellular strategies adopted by different organisms are diverse (programmed cell-death, exit without host cell lysis or active lytic destruction), the host cell exit is intimately linked to pathogenesis, spread of the disease and transmission.
Life-long infection with the intracellular parasite Trypanosoma cruziunderlies the development of human chronic Chagas disease causing severe cardiac, digestive, or neurological alterations. During the acute and chronic phase of the infection, effective and timely regulated parasite egress is crucial for the parasite survival and persistence. Despite its importance in disease progression and symptoms, the molecular mechanisms of active T. cruzi exit from its host cell are unknown.
