Volume 36, Issue 3 pp. 734-747
Review Article

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

Maria Cecilia Fernandes

Maria Cecilia Fernandes

Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD, USA

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Norma W. Andrews

Corresponding Author

Norma W. Andrews

Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD, USA

Correspondence: Norma W. Andrews, Department of Cell Biology and Molecular Genetics, 2134 Bioscience Research Building, University of Maryland, College Park, MD 20742-5815, USA. Tel.: +1 301 405 9601; fax: +1 301 314 1248; e-mail: [email protected]Search for more papers by this author
First published: 17 February 2012
Citations: 11

Abstract

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. 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.

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