Host cell invasion by Trypanosoma cruzi: a unique strategy that promotes persistence

The intracellular protozoan parasite Trypanosoma cruzi is the causative agent of Chagas disease, a serious disorder that affects millions of people in Latin America. Despite the development of lifelong immunity following infections, the immune system fails to completely clear the parasites, which persist for decades within host tissues. Cardiomyopathy is one of the most serious clinical manifestations of the disease, and a major cause of sudden death in endemic areas. Despite decades of study, there is still debate about the apparent preferential tropism of the parasites for cardiac muscle, and its role in the pathology of the disease. In this review, we discuss these issues in light of recent observations, which indicate that T.similar to cruzi invades host cells by subverting a highly conserved cellular pathway for the repair of plasma membrane lesions. Plasma membrane injury and repair is particularly prevalent in muscle cells, suggesting that the mechanism used by the parasites for cell invasion may be a primary determinant of tissue tropism, intracellular persistence, and Chagas disease pathology.