抗原进化速率与流行率在生态-进化SIR模型中的共同决定
Prevalence and the rate of antigenic evolution are jointly determined in an eco-evolutionary SIR model
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中文总结 AI 辅助
本研究分析生态-进化SIR模型，发现抗原进化速度与流行率相互制约，并扩展至宿主死亡情形，揭示毒力与感染规模的关联。
中文摘要 AI 辅助
甲型流感通过不断改变其宿主群体所识别的抗原而持续存在。其进化速度与感染宿主数量并非相互独立，因为选择新变异的免疫力是由病原体已造成的感染所产生的。我们分析了Andreasen等人提出的一个模型，该模型捕捉了这种生态-进化反馈，并将其扩展到感染可能导致宿主死亡的情形。在该模型中，感染和康复宿主是分布在一维抗原空间上的分布，通过交叉免疫耦合。地方病状态是一个行波脉冲：感染分布保持固定形状，并以恒定速度在抗原空间中前进。在弱抗原突变的极限下，我们渐近地构造了该脉冲，并发现：（i）抗原进化速度随流行率上升而下降；（ii）较少的常驻抗原变异伴随更快或更慢的抗原进化，这取决于病原体在免疫逃逸或宿主寿命方面的差异；（iii）当宿主出生率足够低时，感染宿主总数在中等毒力时达到最大。
英文摘要
Influenza A persists by continually changing the antigens that its host population recognizes. How fast it evolves and how many hosts it infects are not independent, because the immunity that selects new variants is produced by the infections the pathogen has already caused. We analyze a model of Andreasen et.\ al.\ that captures this eco-evolutionary feedback, and we extend it to the case where infection may kill the host. In the model infected and recovered hosts are distributions over a one-dimensional antigenic space coupled by cross-immunity. The endemic state is a traveling pulse: the infected distribution keeps a fixed shape and advances through antigenic space at constant speed. In the limit of weak antigenic mutation we construct the pulse asymptotically and find that: (i) the speed of antigenic evolution decreases as prevalence rises, (ii) less standing antigenic variation accompanies either faster or slower antigenic evolution, depending on whether pathogens differ in immune evasion or host lifespan (iii) the total number of infected hosts is largest at an intermediate virulence when the host birth rate is sufficiently low.
发表机构
- University of New Mexico（新墨西哥大学）
- University of Pennsylvania（宾夕法尼亚大学）
机构由 AI 辅助整理，请以论文原文为准。
