Biochemical Requirements for Intracellular Invasion by Trypanosoma cruzi: Protein Synthesis1

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Abstract
The effects of irreversible inhibition of protein synthesis by pactamycin in either infective forms of T. cruzi or mammalian host cells on cellular invasion by this human pathogen were investigated. Treatment of bloodstream forms of T. cruzi with pactamycin markedly reduced their ability to bind either fibroblast-like cells of monkey [African green monkey Vero cell] origin or myoblasts of rat [heart RHM origin]. The number of amastigote forms that could be established intracellularly was also significantly decreased with respect to control values obtained when mock-treated (medium alone) trypomastigotes were incubated with the cells. Pactamycin treatment also reduced the infectivity of T. cruzi trypomastigotes for mice as evidenced by both significantly reduced parasitemia levels and mortality rates when compared with those of control mice infected with mock-treated parasites. Inhibition of protein synthesis in the host cells neither prevented cell infection by untreated trypomastigotes nor altered the percentages of infected cells or the magnitude of the infection in vitro. Protein synthesis may be a requirement for cell invasion by T. cruzi and the parasite can establish itself and replicate within cells relying on its own protein synthesis ability.