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疟疾传播模型中的关键转变始终是由再感染产生的。

Critical transitions in malaria transmission models are consistently generated by superinfection.

机构信息

1 Theoretical and Computational Ecology, Center for Advanced Studies (CEAB-CSIC) , Blanes , Spain.

2 Ecology and Evolutionary Biology, Eno Hall, Princeton University , NJ 08540 , USA.

出版信息

Philos Trans R Soc Lond B Biol Sci. 2019 Jun 24;374(1775):20180275. doi: 10.1098/rstb.2018.0275.

Abstract

The history of modelling vector-borne infections essentially begins with the papers by Ross on malaria. His models assume that the dynamics of malaria can most simply be characterized by two equations that describe the prevalence of malaria in the human and mosquito hosts. This structure has formed the central core of models for malaria and most other vector-borne diseases for the past century, with additions acknowledging important aetiological details. We partially add to this tradition by describing a malaria model that provides for vital dynamics in the vector and the possibility of super-infection in the human host: reinfection of asymptomatic hosts before they have cleared a prior infection. These key features of malaria aetiology create the potential for break points in the prevalence of infected hosts, sudden transitions that seem to characterize malaria's response to control in different locations. We show that this potential for critical transitions is a general and underappreciated feature of any model for vector-borne diseases with incomplete immunity, including the canonical Ross-McDonald model. Ignoring these details of the host's immune response to infection can potentially lead to serious misunderstanding in the interpretation of malaria distribution patterns and the design of control schemes for other vector-borne diseases. This article is part of the theme issue 'Modelling infectious disease outbreaks in humans, animals and plants: approaches and important themes'. This issue is linked with the subsequent theme issue 'Modelling infectious disease outbreaks in humans, animals and plants: epidemic forecasting and control'.

摘要

虫媒传染病建模的历史本质上始于 Ross 关于疟疾的论文。他的模型假设,疟疾的动力学可以通过描述人类和蚊子宿主中疟疾流行的两个方程来最简化地描述。这种结构构成了过去一个世纪中疟疾和大多数其他虫媒传染病模型的核心,并且增加了对重要病因学细节的认识。我们通过描述一个疟疾模型,为蚊子的生命动力学和人类宿主中超级感染的可能性提供了部分补充:在无症状宿主清除先前感染之前,再次感染他们。疟疾病因学的这些关键特征为受感染宿主的流行率产生了突破点的潜力,这种突然的转变似乎是疟疾在不同地点对控制的反应特征。我们表明,这种临界跃迁的可能性是任何具有不完全免疫的虫媒传染病模型的一个普遍但被低估的特征,包括经典的 Ross-McDonald 模型。忽略宿主对感染的免疫反应的这些细节可能会导致对疟疾分布模式的解释和其他虫媒传染病控制方案的设计产生严重误解。本文是主题为“人类、动物和植物传染病暴发建模:方法和重要主题”的一部分。这个问题与后续的主题问题“人类、动物和植物传染病暴发建模:流行预测和控制”有关。

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