首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >Inferring Epidemiological Dynamics with Bayesian Coalescent Inference: The Merits of Deterministic and Stochastic Models
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Inferring Epidemiological Dynamics with Bayesian Coalescent Inference: The Merits of Deterministic and Stochastic Models

机译:贝叶斯联合推断流行病学动态:确定性模型和随机模型的优点

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Estimation of epidemiological and population parameters from molecular sequence data has become central to the understanding of infectious disease dynamics. Various models have been proposed to infer details of the dynamics that describe epidemic progression. These include inference approaches derived from Kingman’s coalescent theory. Here, we use recently described coalescent theory for epidemic dynamics to develop stochastic and deterministic coalescent susceptible–infected–removed (SIR) tree priors. We implement these in a Bayesian phylogenetic inference framework to permit joint estimation of SIR epidemic parameters and the sample genealogy. We assess the performance of the two coalescent models and also juxtapose results obtained with a recently published birth–death-sampling model for epidemic inference. Comparisons are made by analyzing sets of genealogies simulated under precisely known epidemiological parameters. Additionally, we analyze influenza A (H1N1) sequence data sampled in the Canterbury region of New Zealand and HIV-1 sequence data obtained from known United Kingdom infection clusters. We show that both coalescent SIR models are effective at estimating epidemiological parameters from data with large fundamental reproductive number ![Formula][1]/img and large population size ![Formula][2]/img. Furthermore, we find that the stochastic variant generally outperforms its deterministic counterpart in terms of error, bias, and highest posterior density coverage, particularly for smaller ![Formula][3]/img and ![Formula][4]/img. However, each of these inference models is shown to have undesirable properties in certain circumstances, especially for epidemic outbreaks with ![Formula][5]/img close to one or with small effective susceptible populations. [1]: /embed/mml-math-1.gif [2]: /embed/mml-math-2.gif [3]: /embed/mml-math-3.gif [4]: /embed/mml-math-4.gif [5]: /embed/mml-math-5.gif
机译:从分子序列数据估计流行病学和种群参数已成为了解传染病动态的关键。已经提出了各种模型来推断描述流行病进展的动力学细节。其中包括从金曼的合并理论中得出的推论方法。在这里,我们使用流行病动力学的最近描述的聚结理论来发展先验随机和确定性的聚结易感性感染去除树。我们在贝叶斯系统发生推断框架中实施这些操作,以允许对SIR流行病参数和样本族谱进行联合估计。我们评估了这两个合并模型的性能,并且还将与最近发布的流行病推断的出生-死亡采样模型并列的结果并列。通过分析在精确已知的流行病学参数下模拟的家谱集进行比较。此外,我们分析了在新西兰坎特伯雷地区采样的甲型流感(H1N1)序列数据和从英国已知感染群中获得的HIV-1序列数据。我们表明,两个合并的SIR模型都可以有效地从具有较大基本生殖数![公式] [1] 和具有较大人口数量![公式] [2] 的数据估计流行病学参数。此外,我们发现,在误差,偏差和最高后验密度覆盖率方面,随机变量通常优于确定性变量,特别是对于较小的![Formula] [3] 和![Formula] [4] 。但是,在某些情况下,尤其是对于![Formula] [5] 接近一个或有效感染人群较小的流行病暴发,这些推断模型均显示出不良的特性。 [1]:/ embed / mml-math-1.gif [2]:/ embed / mml-math-2.gif [3]:/ embed / mml-math-3.gif [4]:/ embed / mml -math-4.gif [5]:/embed/mml-math-5.gif

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