Nannyonga B, Mwanga G G, Haario H, Mbalawata I S, Heilio M
Department of Mathematics, Makerere University, P.O. Box 7062, Kampala, Uganda.
Department of Mathematics and Physics, Lappeenranta University of Technology, Box 20, FIN-53851 Lappeenranta, Finland.
Biosystems. 2014 Dec;126:76-84. doi: 10.1016/j.biosystems.2014.09.009. Epub 2014 Sep 26.
Numerous studies have been carried out on within-host Plasmodium falciparum malaria with varying results. Some studies have suggested over estimation of parasite growth within an infected host while others stated that evolution of parasitaemia seems to be quelled by parasite load. Various mathematical models have been designed to understand the dynamics of evolution of within-host malaria. The basic ingredient in most of the models is that the availability of uninfected red blood cells (RBCs) in which the parasite develops is a limiting factor in the propagation of the parasite population. We hypothesize that in severe malaria, due to parasite quest for survival and rapid multiplication, the vicious malaria parasite is sophisticated and can be absorbed in an already infected RBC and speeds up rapture rate. The study reviews the classical models of blood stage malaria and proposes a new model which incorporates double infection. Analysis of the model and parameter identifiability using Markov chain Monte Carlo (MCMC) are presented. MCMC uses distribution of parameters to study the model behavior instead of single points. Results indicate that most infected RBCs rupture quickly due to the disease instead. This may explain anemia in malaria patients and lack of uniformity of oscillations in within-host malaria. Therefore, more needs to be done as far as within-host malaria is concerned, to provide step by step evolution of malaria within a host.
关于宿主体内恶性疟原虫疟疾已经开展了大量研究，结果各异。一些研究表明，感染宿主内寄生虫生长被高估，而其他研究则指出，寄生虫血症的演变似乎受到寄生虫负荷的抑制。已经设计了各种数学模型来理解宿主体内疟疾演变的动态。大多数模型的基本要素是，寄生虫在其中发育的未感染红细胞（RBC）的可用性是寄生虫种群繁殖的限制因素。我们假设，在严重疟疾中，由于寄生虫求生和快速增殖的需求，恶性疟原虫很复杂，能够侵入已经感染的红细胞并加快破裂速度。该研究回顾了血液阶段疟疾的经典模型，并提出了一个包含双重感染的新模型。给出了使用马尔可夫链蒙特卡罗（MCMC）对模型和参数可识别性的分析。MCMC使用参数分布来研究模型行为，而不是单个点。结果表明，大多数受感染的红细胞反而因疾病而迅速破裂。这可能解释了疟疾患者的贫血以及宿主体内疟疾振荡缺乏一致性的现象。因此，就宿主体内疟疾而言，还需要做更多工作，以提供宿主体内疟疾逐步演变的情况。
