The within-host cellular dynamics of bloodstage malaria: Theoretical and experimental studies

The within-host cellular dynamics of bloodstage malaria: Theoretical and experimental studies
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DOI:
10.1017/s0031182000066245
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发表时间:
1996-07-01
期刊:
影响因子:
2.4
通讯作者:
Anderson, RM
Anderson, RM
中科院分区:
医学2区
文献类型:
--
作者:
Hetzel, C;Anderson, RM

文献摘要

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研究了单一疟疾菌株血期感染数学模型的特性。通过分析在没有宿主免疫反应的情况下的细胞群动态,我们证明了宿主和寄生虫参数之间的关系,该关系定义了寄生虫成功入侵和持久存在的标准。重要的参数是裂殖子产生和死亡的速率以及红细胞产生、死亡和侵袭的速率。我们提供了旨在评估啮齿动物疟疾系统中红细胞侵袭率的实验数据。该模型生成的寄生虫血症模式与伯氏疟原虫感染中观察到的模式具有良好的定性一致性。在没有免疫力的模型中,寄生虫血症的上升和下降背后的唯一力量是易感红细胞的密度,这表明资源可用性是体内感染初始模式的重要决定因素。当我们将简单的免疫反应纳入模型时,我们发现针对受感染细胞的免疫在抑制寄生虫丰度方面比针对裂殖子的免疫更有效。模拟揭示了类似于 P. c. 的寄生虫丰度的振荡时间模式。 chabaudi 感染,挑战了抗原变异是感染复发模式背后的唯一机制的概念。
The properties of a mathematical model of bloodstage infection with a single strain of malaria were investigated. Analysing the cell population dynamics in the absence of a host immune response we demonstrate a relationship between host and parasite parameters that defines a criterion for the successful invasion and persistence of the parasite. Important parameters are the rates of merozoite production and death and those of erythrocyte production, death and invasion. We present data from experiments designed to evaluate the erythrocyte invasion rate in a rodent malaria system. The model generates patterns of parasitaemia in good qualitative agreement with those seen in Plasmodium berghei infections. The sole force behind the rise and fall in parasitaemia in the model without immunity is the density of susceptible erythrocytes, suggesting that resource availability is an important determinant of the initial pattern of infection in vivo. When we incorporate a simple immune response into the model we find that immunity against the infected cell is much more effective at suppressing parasite abundance than immunity against the merozoite. Simulations reveal oscillating temporal patterns of parasite abundance similar to P. c. chabaudi infection, challenging the concept that antigenic variation is the sole mechanism behind recrudescing patterns of infection.