Evolving pathogen phylogenies: a two-level branching approach

对于许多RNA病毒来说，病毒的RNA聚合酶缺乏校对机制导致频繁的突变。较高的病毒变异率、较大的病毒种群规模和较短的复制期产生了丰富的病毒变异性，这是免疫逃逸或耐药性的原因。详细了解维持这种多样性的力量可以帮助对抗病毒感染。由于不同水平的交叉免疫，病原体模式--尤其是系统发育的形状--受到选择压力强度的影响。我们专注于与持久性病毒相关的系统发育的时间结构。我们提出了一个两级(宿主-病原体)分支模型，在不同的缩放机制下，两个水平上都有突变和竞争，其中宿主可以是感染患者，也可以是单个患者内的感染细胞，从而扩展了我们最近在泛发性病毒种群方面的工作。我们将进一步依赖于为测量值(中性)多水平分支动力学和具有突变和竞争的两级多类型分支动力学开发的技术。

For many RNA viruses the lack of a proofreading mechanism in the virus' RNA polymerase results in frequent mutation. The high viral mutation rates, the large virus population size, and the short replication periods produce abundance of viral variability which is responsible for immune escape or drug resistance Understanding in detail the forces which maintain this diversity can assist in the struggle against viral infections. Pathogen patterns - and in particular the shapes of the phylogenies - are affected by the strength of selective pressure due to various levels of cross-immunity. We focus on the temporal structure of phylogenies associated with a persistent virus. We propose a two-level (host-pathogen) branching model with mutation and competition on both levels in different scaling regimes, where hosts can be either the infected patients or the infected cells within a single patient.We thereby extend our recent work on a panmitic virus population. We will further rely on techniques developed for measure-valued (neutral) multilevel branching dynamics and two-level multi-type branching dynamics with mutation and competition.