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Infect Immun, June 1998, p. 2460-2465, Vol. 66, No. 6
Department of Molecular Genetics and
Biochemistry, University of Pittsburgh School of Medicine,
Pittsburgh, Pennsylvania 15261
Received 8 January 1998/Returned for modification 19 February
1998/Accepted 24 March 1998
Trypanosoma cruzi blood stage trypomastigotes are
highly resistant to complement-mediated killing in normal
serum. A previously described trypomastigote surface glycoprotein was
shown to have binding affinity for human complement components C3b and
C4b and restrict activation of the complement cascade, thus
preventing lysis of the parasites. Insect stage epimastigotes do not
produce detectable levels of this 160-kDa complement regulatory protein (CRP) and are highly sensitive to the lytic effects of complement. Epimastigotes were stably transfected with a T. cruzi
expression vector carrying the trypomastigote CRP cDNA and produced
fully functional recombinant CRP. The recombinant CRP had binding
affinity for C3b, and the transfected epimastigotes were protected from complement-mediated lysis. These results demonstrate for the first time
that a developmentally regulated gene of T. cruzi
trypomastigotes can be expressed in noninfectious epimastigotes and
that production of CRP by epimastigotes is sufficient to confer a
virulence-associated trait. Furthermore, these studies
demonstrate the critical role that trypomastigote CRP plays in the
protection of parasites from the deleterious effects of complement,
thus establishing the protein as a virulence factor of
T. cruzi.
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Stable Transfection of Trypanosoma cruzi
Epimastigotes with the Trypomastigote-Specific Complement
Regulatory Protein cDNA Confers Complement Resistance
Infect Immun, June 1998, p. 2460-2465, Vol. 66, No. 6
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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