Clarebout G, Gamain B, Slomianny C, Camus D, Dive D
INSERM U42, Villeneuve d'Ascq, France.
Parasitology. 1996 Mar;112 ( Pt 3):269-76. doi: 10.1017/s0031182000065781.
In order to study the effects of acclimatization of Plasmodium in beta-thalassaemic mice, we used a mouse model of beta-thalassaemia (DBA/2J/beta-thal/beta-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/beta-thal mice lines, by 4 intraperitoneal serial transfers. All 3 rodent malarias developed in red blood cells of beta-thalassaemic mice without losing their virulence. There was no delay in infection and peaks of parasitaemia were similar in beta-thalassaemic and normal mice. The mortality occurred earlier in beta-thalassaemic mice than in control mice for P. berghei and P. chabaudi. The 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 beta-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 beta-thalassaemic RBC showed a normal development even in the presence of Heinz bodies. In conclusion, no effective protection against malaria was provided by the beta-thalassaemia in this mouse model.
为了研究疟原虫在β地中海贫血小鼠体内适应性变化的影响，我们使用了一种β地中海贫血小鼠模型（DBA/2J/beta-thal/beta-thal），该模型与人类中观察到的情况相似。我们通过4次腹腔连续传代，使3种啮齿动物疟原虫（伯氏疟原虫、查巴迪疟原虫和约氏疟原虫）在DBA/2J和DBA/2J/beta-thal小鼠品系中适应。所有3种啮齿动物疟原虫均在β地中海贫血小鼠的红细胞中发育，且未丧失其毒力。β地中海贫血小鼠的感染没有延迟，寄生虫血症峰值与正常小鼠相似。对于伯氏疟原虫和查巴迪疟原虫，β地中海贫血小鼠的死亡时间早于对照小鼠。对于约氏疟原虫NS，差异更为明显，正常小鼠未死亡。这些结果可以通过β地中海贫血小鼠红细胞生成失败来解释，这些小鼠无法补偿寄生虫对红细胞的破坏，最终死于贫血。对β地中海贫血红细胞中啮齿动物疟原虫的超微结构检查显示，即使存在海因茨小体，疟原虫也能正常发育。总之，在这个小鼠模型中，β地中海贫血并没有提供有效的疟疾防护。
