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Dates Attended
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Institution Name
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City, State |
Degree/Area of Study |
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1972
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Cayetano Heredia University
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Lima, Peru
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B.S.
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1974
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Cayetano Heredia University
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Lima, Peru
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M.S.
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1981
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Federal University of Rio de Janeiro
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Rio de Janeiro, Brazil
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Ph.D.
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1981-86
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Michigan State University
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East Lansing, MI
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Post-Doc
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| Dr. Villalta and his colleagues focus on the molecular mechanisms of host cell invasion of mammalian cells by Trypanosoma cruzi, the causative agent of Chagas, heart disease or American trypanosomiasis. Currently, they are investigating the structure-function of trypanosome ligands and their host cell receptors that mediate trypanosome attachment relationships and entry, leading to disease. The team has also been elucidating the signaling pathways required for trypanosome entry mediated by T. cruzi ligands and their host cell receptors, as well as the trypanosome invasive genes and host cell receptor genes required for the early infection process. These studies will provide a comprehensive molecular analysis of the early process of T. cruzi invasion, and foster development of novel means for therapeutic intervention.
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- Villalta, F., and Kierszenbaum, F. 1985. Role of surface N-acetyl glucosamine residues on host cell invasion by Trypanosoma cruzi. Biochim Biophys Acta 845(2): 216-22.
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- Villalta, F., and Kierszenbaum, F. 1985. The effects of swinsonine on the association of Trypanosoma cruzi with host cells. Mol. Biochem. Parasitol. 16: 1-10.
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- Kierszenbaum, F., Villalta, F., and Tai, P.C. 1986. Kinetics of human eosinophil activation upon interaction with intracellular (amastigote) forms of Trypanosoma cruzi. J. Immunol. 138: 662-666.
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- Villalta, F., and Kierszenbaum, F. 1986. Effects of human colony stimulating factor on the uptake and destruction of a pathogenic parasite (T. cruzi) by human neutrophils. J. Immunol. 137: 1703-1707.
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- Villalta, F., and Kierszenbaum, F. 1987. Role of membrane N-linked oligosaccharides in host cell interactions with invasive forms of Trypanosoma cruzi. Mol. Biochem. Parasitol. 22: 109-114.
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