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Host–pathogen time series data in wildlife support a transmission function between density and frequency dependence

机译:野生动物中宿主-病原体时间序列数据支持密度和频率依赖性之间的传递函数

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摘要

A key aim in epidemiology is to understand how pathogens spread within their host populations. Central to this is an elucidation of a pathogen's transmission dynamics. Mathematical models have generally assumed that either contact rate between hosts is linearly related to host density (density-dependent) or that contact rate is independent of density (frequency-dependent), but attempts to confirm either these or alternative transmission functions have been rare. Here, we fit infection equations to 6 years of data on cowpox virus infection (a zoonotic pathogen) for 4 natural populations to investigate which of these transmission functions is best supported by the data. We utilize a simple reformulation of the traditional transmission equations that greatly aids the estimation of the relationship between density and host contact rate. Our results provide support for an infection rate that is a saturating function of host density. Moreover, we find strong support for seasonality in both the transmission coefficient and the relationship between host contact rate and host density, probably reflecting seasonal variations in social behavior and/or host susceptibility to infection. We find, too, that the identification of an appropriate loss term is a key component in inferring the transmission mechanism. Our study illustrates how time series data of the host–pathogen dynamics, especially of the number of susceptible individuals, can greatly facilitate the fitting of mechanistic disease models.
机译:流行病学的主要目标是了解病原体如何在其宿主种群中传播。对此的核心是阐明病原体的传播动态。数学模型通常假设主机之间的接触速率与主机密度成线性关系(取决于密度),或者接触速率与密度成线性关系(取决于频率),但是很少尝试确定这些或替代传输函数。在这里,我们将感染方程式与4个自然种群的牛痘病毒感染(一种人畜共患病原体)的6年数据拟合,以调查这些数据中哪种传播功能最能得到支持。我们利用传统传输方程式的简单公式化,极大地有助于估计密度与主体接触率之间的关系。我们的结果为感染率提供了支持,而感染率是宿主密度的饱和函数。此外,我们在传播系数以及寄主接触率与寄主密度之间的关系方面都发现了季节性的强烈支持,这很可能反映了社会行为和/或寄主对感染的易感性的季节性变化。我们还发现,确定适当的损失项是推断传输机制的关键组成部分。我们的研究表明,宿主-病原体动力学的时间序列数据,尤其是易感个体的数量,如何极大地促进机制疾病模型的拟合。

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