Mechanisms of Trypanosoma cruzi persistence in Chagas disease

• Published in: Cellular microbiology Vol. 14; no. 5; pp. 634 - 643
• Main Authors: Nagajyothi, Fnu, Machado, Fabiana S., Burleigh, Barbara A., Jelicks, Linda A., Scherer, Philipp E., Mukherjee, Shankar, Lisanti, Michael P., Weiss, Louis M., Garg, Nisha J., Tanowitz, Herbert B.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.05.2012; Hindawi Limited
• Subjects: Animals; Chagas Disease - immunology; Chagas Disease - parasitology; Chronic Disease; Host-Pathogen Interactions; Humans; Immune Evasion; Models, Biological; Trypanosoma cruzi; Trypanosoma cruzi - immunology; Trypanosoma cruzi - pathogenicity
• ISSN: 1462-5814; 1462-5822
• DOI: 10.1111/j.1462-5822.2012.01764.x

Summary Trypanosoma cruzi infection leads to development of chronic Chagas disease. In this article, we provide an update on the current knowledge of the mechanisms employed by the parasite to gain entry into the host cells and establish persistent infection despite activation of a potent immune response by the host. Recent studies point to a number of T. cruzi molecules that interact with host cell receptors to promote parasite invasion of the diverse host cells. T. cruzi expresses an antioxidant system and thromboxane A2 to evade phagosomal oxidative assault and suppress the host's ability to clear parasites. Additional studies suggest that besides cardiac and smooth muscle cells that are the major target of T. cruzi infection, adipocytes and adipose tissue serve as reservoirs from where T. cruzi can recrudesce and cause disease decades later. Further, T. cruzi employs at least four strategies to maintain a symbiotic‐like relationship with the host, and ensure consistent supply of nutrients for its own survival and long‐term persistence. Ongoing and future research will continue to help refining the models of T. cruzi invasion and persistence in diverse tissues and organs in the host.