Chapter category: Infectious Disease

Host Cell Actin Remodeling in Response to Trypanosoma cruzi: Trypomastigote Versus Amastigote Entry

This chapter appears in the following book:

Molecular Mechanisms
of Parasite Invasion

Edited by: Barbara A. Burleigh and Dominique Soldati-Favre
ISBN: 978-0-387-78266-9
» Get more information about this book at landesbioscience.com «

Chapter authors:
Renato A. Mortara, Walter K. Andreoli , Maria Cecília D.C. Fernandes, Claudio V. da Silva, Adriana B. Fernandes, Carolina L'Abbate and Solange da Silva

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Trypanosoma cruzi is the protozoan parasite that causes Chagas’ disease, a highly prevalent vector-borne disease in Latin America. Chagas’ disease is a major public health problem in endemic regions with an estimated 18 million people are infected with T. cruzi and another 100 million at risk (http://www.who.int/ctd/chagas/disease.htm). During its life cycle, T. cruzi alternates between triatomine insect vectors and mammalian hosts. While feeding on host’s blood, infected triatomines release in their feces highly motile and infective metacyclic trypomastigotes that may initiate infection. Metacyclic trypomastigotes promptly invade host cells (including gastric mucosa) and once free in the cytoplasm, differentiate into amastigotes that replicate by binary fission. Just before disruption of the parasite-laden cell, amastigotes differentiate back into trypomastigotes which are then released into the tissue spaces and access the circulation. Circulating trypomastigotes that disseminate the infection in the mammalian host may be taken up by feeding triatomines and may also transform, extracellularly, into amastigote-like forms. Unlike their intracellular counterparts, these amastigote-like forms, henceforth called amastigotes, are capable of infecting host cells. Studies in which the mechanisms of amastigote invasion of host cells have been compared to metacyclic trypomastigote entry have revealed interesting differences regarding the involvement of the target cell actin microfilament system.

Renato A. Mortara
Disciplina de Parasitologia, Departamento de Microbiologia, Imunologia e Parasitologia, UNIFESP, Escola Paulista de Medicina

Walter K. Andreoli
Disciplina de Parasitologia, Departamento de Microbiologia, Imunologia e Parasitologia, UNIFESP, Escola Paulista de Medicina

Maria Cecília D.C. Fernandes
Disciplina de Parasitologia, Departamento de Microbiologia, Imunologia e Parasitologia, UNIFESP, Escola Paulista de Medicina

Claudio V. da Silva
Disciplina de Parasitologia, Departamento de Microbiologia, Imunologia e Parasitologia, UNIFESP, Escola Paulista de Medicina

Adriana B. Fernandes
Disciplina de Parasitologia, Departamento de Microbiologia, Imunologia e Parasitologia, UNIFESP, Escola Paulista de Medicina

Carolina L'Abbate
Disciplina de Parasitologia, Departamento de Microbiologia, Imunologia e Parasitologia, UNIFESP, Escola Paulista de Medicina

Solange da Silva
Disciplina de Parasitologia, Departamento de Microbiologia, Imunologia e Parasitologia, UNIFESP, Escola Paulista de Medicina

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Chapter category: Infectious Disease

Host Cell Actin Remodeling in Response to Trypanosoma cruzi: Trypomastigote Versus Amastigote Entry

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