Popinga Alex, Vaughan Tim, Stadler Tanja, Drummond Alexei J
Department of Computer Science, University of Auckland, Auckland, New Zealand 1010 Allan Wilson Centre for Molecular Ecology and Evolution, Palmerston North, New Zealand 4442.
Department of Computer Science, University of Auckland, Auckland, New Zealand 1010 Allan Wilson Centre for Molecular Ecology and Evolution, Palmerston North, New Zealand 4442 Massey University, Palmerston North, New Zealand 4442.
Genetics. 2015 Feb;199(2):595-607. doi: 10.1534/genetics.114.172791. Epub 2014 Dec 19.
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: see text] and large population size [Formula: see text]. 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: see text] and [Formula: see text]. However, each of these inference models is shown to have undesirable properties in certain circumstances, especially for epidemic outbreaks with [Formula: see text] close to one or with small effective susceptible populations.
从分子序列数据估计流行病学和群体参数已成为理解传染病动态的核心。人们提出了各种模型来推断描述疫情进展的动态细节。这些模型包括源自金曼合并理论的推断方法。在此,我们使用最近描述的疫情动态合并理论来开发随机和确定性的合并易感-感染-移除(SIR)树先验。我们将这些先验应用于贝叶斯系统发育推断框架,以联合估计SIR疫情参数和样本谱系。我们评估了这两种合并模型的性能,并将其结果与最近发表的用于疫情推断的出生-死亡-抽样模型的结果进行了并列比较。通过分析在精确已知的流行病学参数下模拟的谱系集来进行比较。此外,我们分析了在新西兰坎特伯雷地区采集的甲型流感(H1N1)序列数据以及从英国已知感染集群获得的HIV-1序列数据。我们表明,两种合并SIR模型在从具有大基本再生数[公式:见原文]和大群体规模[公式:见原文]的数据中估计流行病学参数方面都是有效的。此外,我们发现,在误差、偏差和最高后验密度覆盖方面,随机变体通常优于其确定性对应物,特别是对于较小的[公式:见原文]和[公式:见原文]。然而,这些推断模型在某些情况下都表现出不良特性,特别是对于基本再生数[公式:见原文]接近1或有效易感群体较小的疫情爆发。