THE REGULATION OF MALARIA PARASITEMIA - PARAMETER ESTIMATES FOR A POPULATION-MODEL

THE REGULATION OF MALARIA PARASITEMIA - PARAMETER ESTIMATES FOR A POPULATION-MODEL
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DOI:
10.1017/s0031182000063861
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发表时间:
1995-02-01
期刊:
影响因子:
2.4
通讯作者:
KWIATKOWSKI, D
KWIATKOWSKI, D
中科院分区:
医学2区
文献类型:
--
作者:
GRAVENOR, MB;MCLEAN, AR;KWIATKOWSKI, D

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对感染恶性疟原虫的非免疫性个体的经典研究表明,尽管寄生虫具有巨大的生长潜力,但这种感染可能在较长一段时间内以相对稳定的寄生虫密度进行调节。这表明寄生虫种群可能受密度依赖机制的控制,理论上最明显的机制是寄生虫之间对宿主红细胞的竞争。在这里,我们通过对寄生虫和红细胞之间的基本种群相互作用进行建模,以一种允许从临床数据估计所有基本参数的形式来评估这一机制在调节寄生虫血症中的作用。我们的结果表明,竞争不能解释恶性疟原虫的总体调控,但当与免疫机制结合时,它可能发挥比通常认为的更重要的作用。对模型的进一步分析表明,从长期来看,低寄生虫密度下的寄生虫复制可以显著地导致自然感染中观察到的高度贫血,这一结论从简单的临床观察中并不明显。
Classical studies of non-immune individuals infected with Plasmodium falciparum reveal that the infection may be regulated for long periods at a relatively stable parasite density, despite the enormous growth potential of a parasite that continually replicates within host erythrocytes. This suggests that the parasite population may be controlled by density-dependent mechanisms, and in theory the most obvious of these is competition between parasites for host erythrocytes. Here we evaluate the role of this mechanism in the regulation of parasitaemia, by modelling the basic population interaction between parasites and erythrocytes in a form that allows all the essential parameters to be estimated from clinical data. Our results show that competition cannot account for the total regulation of P. falciparum, but when combined with immune mechanisms it may play a more important role than is generally supposed. Further analysis of the model indicates that in the long term, parasite replication at low parasite densities can contribute significantly to the high degree of anaemia observed in natural infection, a conclusion which is not obvious from simple clinical observation.