Reactivation of latent infections with migration shapes population-level disease dynamics

Reactivation of latent infections with migration shapes population-level disease dynamics
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DOI:
10.1098/rspb.2020.1829
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发表时间:
2020-09-30
影响因子:
4.7
通讯作者:
Hall, Richard J.
Hall, Richard J.
中科院分区:
生物学1区
文献类型:
--
作者:
Becker, Daniel J.;Ketterson, Ellen D.;Hall, Richard J.

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每年的迁徙在动物类群中很常见,并可能极大地影响传染病的空间和时间模式。尽管在某些情况下,迁徙可以降低感染率,但这些耗资巨大的长途迁徙也可能产生免疫抑制效应,可能以复杂的方式与传播过程相互作用。在这里,我们开发了一个机制模型,用于由与迁移相关的生理变化或能量成本(即‘迁移性复发’)及其对疾病动力学的影响来驱动潜在感染的重新激活。我们确定了迁徙复发可以扩大或降低病原体和宿主特征(如侵染期、毒力、越冬存活、复发时间)和传播物候的感染流行率的条件。我们表明,在迁徙开始或结束时,复发都会显著增加整个年度周期的流行率,并可能对在迁徙人口中保持低传播率和较短感染期的病原体至关重要。相反,在迁徙开始时复发可以通过在代价高昂的迁徙期间扩大对受感染宿主的扑杀来减少高毒力病原体的流行,特别是对于高度可传播的病原体和在迁徙或繁殖季节传播的病原体。我们的研究为了解迁徙宿主复发感染的时空模式提供了机制基础,对于人畜共患监测和了解感染模式将如何响应与环境变化相关的迁移倾向的变化具有重要意义。此外,我们的工作表明,将宿主内的过程纳入病原体传播的种群水平模型,对于协调观察到的跨迁徙物种的迁移-感染关系范围可能至关重要。
Annual migration is common across animal taxa and can dramatically shape the spatial and temporal patterns of infectious disease. Although migration can decrease infection prevalence in some contexts, these energetically costly long-distance movements can also have immunosuppressive effects that may interact with transmission processes in complex ways. Here, we develop a mechanistic model for the reactivation of latent infections driven by physiological changes or energetic costs associated with migration (i.e. 'migratory relapse') and its effects on disease dynamics. We determine conditions under which migratory relapse can amplify or reduce infection prevalence across pathogen and host traits (e.g. infectious periods, virulence, overwinter survival, timing of relapse) and transmission phenologies. We show that relapse at either the start or end of migration can dramatically increase prevalence across the annual cycle and may be crucial for maintaining pathogens with low transmissibility and short infectious periods in migratory populations. Conversely, relapse at the start of migration can reduce the prevalence of highly virulent pathogens by amplifying culling of infected hosts during costly migration, especially for highly transmissible pathogens and those transmitted during migration or the breeding season. Our study provides a mechanistic foundation for understanding the spatio-temporal patterns of relapsing infections in migratory hosts, with implications for zoonotic surveillance and understanding how infection patterns will respond to shifts in migratory propensity associated with environmental change. Further, our work suggests incorporating within-host processes into population-level models of pathogen transmission may be crucial for reconciling the range of migration-infection relationships observed across migratory species.