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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Amastigote Synapse: The Tricks of Trypanosoma cruzi Extracellular Amastigotes

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Bonfim-Melo, Alexis [1] ; Ferreira, Eden R. [1] ; Florentino, Pilar T. V. [2] ; Mortara, Renato A. [1]
Total Authors: 4
[1] Univ Fed Sao Paulo, Dept Microbiol Imunol & Parasitol, Escola Paulista Med, Sao Paulo - Brazil
[2] Univ Sao Paulo, Biomed Sci Inst 2, DNA Repair Lab, Sao Paulo - Brazil
Total Affiliations: 2
Document type: Review article
Web of Science Citations: 3

To complete its life cycle within the mammalian host, Trypanosoma cruzi, the agent of Chagas' disease, must enter cells. Trypomastigotes originating from the insect vector (metacyclic) or from infected cells (bloodstream/tissue culture-derived) are the classical infective forms of the parasite and enter mammalian cells in an actin-independent manner. By contrast, amastigotes originating from the premature rupture of infected cells or transformed from swimming trypomastigotes (designated extracellular amastigotes, EAs) require functional intact microfilaments to invade non-phagocytic host cells. Earlier work disclosed the key features of EA-HeLa cell interplay: actin-rich protrusions called `cups' are formed at EA invasion sites on the host cell membrane that are also enriched in actin-binding proteins, integrins and extracellular matrix elements. In the past decades we described the participation of membrane components and secreted factors from EAs as well as the actin-regulating proteins of host cells involved in what we propose to be a phagocytic-like mechanism of parasite uptake. Thus, regarding this new perspective herein we present previously described EA-induced `cups' as parasitic synapse since they can play a role beyond its architecture function. In this review, we focus on recent findings that shed light on the intricate interaction between extracellular amastigotes and non-phagocytic HeLa cells. (AU)

FAPESP's process: 12/21335-8 - The Cdc42/N-WASP and Rac1/WAVE2 pathways regulation of actin dynamics during cellular invasion by extracellular amastigotes of Trypanosoma cruzi
Grantee:Alexis de Sá Ribeiro do Bonfim de Melo
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 12/25282-6 - The role of ezrin, radixin and moesin (ERM proteins) in cell invasion by extracellular amastigotes of Trypanosoma cruzi.
Grantee:Éden Ramalho de Araujo Ferreira
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 11/03357-1 - Characterization of the epitopes expression and infectivity of extracellular amastigotes from different Trypanosoma cruzi strains
Grantee:Pilar Sampaio Tavares Veras
Support Opportunities: Scholarships in Brazil - Master
FAPESP's process: 11/51475-3 - Molecular and cellular biology of the parasitism by Trypanosoma cruzi
Grantee:José Franco da Silveira Filho
Support Opportunities: Research Projects - Thematic Grants