作者: Jaime Costales , Edwin C Rowland , None
DOI: 10.1645/GE-1074.1
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摘要: The mechanism by which Trypanosoma cruzi egresses from infected cells at the end of intracellular replication cycle is not understood. This study explored role T. cruzi-derived proteases and host-cell membrane permeability during parasite's egress process. Treatment with a fluoromethyl ketone, known to inhibit major protease, significantly reduced parasite egress. In addition, in late stages infection, showed increased as evidenced dye exclusion tests. Furthermore, parasites could be antibody stained inside host without chemical permeabilization plasma membrane. These results suggest that advanced cruzi, lose integrity. Previous studies our laboratory have found antibodies present sera mice chronically (antiegressin) bind surface reduce agreement these reports, western blot analysis several proteins cell extracts reacted mouse serum. findings reported herein might implications process egress, well action antiegressin.