恶性疟原虫感染的一个干预靶点。
A target for intervention in Plasmodium falciparum infections.
作者信息
McKenzie F E, Bossert W H
机构信息
Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
出版信息
Am J Trop Med Hyg. 1998 Jun;58(6):763-7. doi: 10.4269/ajtmh.1998.58.763.
Abstract
We present a set of simple mathematical models to investigate interactions between malaria parasites and the human immune system and the differentiation of parasites from asexual, pathogenic into sexual, transmissible blood stages. Each model represents a different combination of empirically based hypotheses, and salient behaviors of each fit criteria developed from clinical data. In all models, however, higher gametocyte conversion rates result in lower peak asexual-form densities. Therefore, to the extent that asexual-form densities are associated with disease symptoms, interventions that stimulate gametocytogenesis should produce unexpected clinical benefits.
摘要
我们提出了一组简单的数学模型，以研究疟原虫与人类免疫系统之间的相互作用，以及疟原虫从无性、致病阶段向有性、可传播血液阶段的分化。每个模型代表了基于经验的假设的不同组合，以及根据临床数据制定的每个拟合标准的显著行为。然而，在所有模型中，较高的配子体转化率会导致较低的无性形式密度峰值。因此，就无性形式密度与疾病症状相关的程度而言，刺激配子体生成的干预措施应会产生意想不到的临床益处。
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