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The course of Plasmodium berghei, P. chabaudi and P. yoelii infections in β-thalassaemic mice

Published online by Cambridge University Press:  06 April 2009

G. Clarebout
Affiliation:
INSERM U42, 369 rue Jules Guesde, BP39, F-59651 Villeneuve d' Ascq cedex, France
B. Gamain
Affiliation:
INSERM U42, 369 rue Jules Guesde, BP39, F-59651 Villeneuve d' Ascq cedex, France
C. Slomianny
Affiliation:
INSERM U42, 369 rue Jules Guesde, BP39, F-59651 Villeneuve d' Ascq cedex, France
D. Camus
Affiliation:
INSERM U42, 369 rue Jules Guesde, BP39, F-59651 Villeneuve d' Ascq cedex, France
D. Dive
Affiliation:
INSERM U42, 369 rue Jules Guesde, BP39, F-59651 Villeneuve d' Ascq cedex, France

Summary

In order to study the effects of acclimatization of Plasmodium in β-thalassaemic mice, we used a mouse model of β-thalassaemia (DBA/2J/β-thal/β-thal), similar to that observed in humans. We acclimatized 3 rodent malarias (P. berghei, P. chabaudi and P. yoelii) in DBA/2J and DBA/2J/β-thal/β-thal mice lines, by 4 intraperitoneal serial transfers. All 3 rodent malarias developed in red blood cells of β-thalassaemic mice without losing their virulence. There was no delay in infection and peaks of parasitaemia were similar in β-thalassaemic and normal mice. The mortality occurred earlier in β-thalassaemic mice than in control mice for P. berghei and P. chabaudi. This difference was more pronounced for P. yoelii NS where normal mice did not die. These results could be explained by a failure of erythropoiesis in β-thalassaemic mice, which are unable to compensate for the destruction of red blood cells by the parasites, and the mice died of anaemia. Ultrastructural examination of the rodent malaria parasites in β-thalassaemic RBC showed a normal development even in the presence of Heinz bodies. In conclusion, no effective protection against malaria was provided by the β-thalassaemia in this mouse model.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1996

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