Within-host disease ecology in the sea fan Gorgonia ventalina:: Modeling the spatial immunodynamics of a coral-pathogen interaction
Within-host disease ecology in the sea fan Gorgonia ventalina:: Modeling the spatial immunodynamics of a coral-pathogen interaction
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DOI：
10.1086/522841
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发表时间：
2007-12-01
影响因子：
2.9
通讯作者：
Harvell, C. Drew
中科院分区：
文献类型：
--
作者：
Ellner, Stephen P.;Jones, Laura E.;Harvell, C. Drew
我们开发了一个空间显式模型的真菌病原体和其珊瑚宿主的免疫反应之间的宿主内的相互作用。该模型是参数化的最近流行的Aspergillus sydowii在海扇柳珊瑚ventalina，但它的结构是适应于许多其他疾病攻击全球珊瑚，真菌感染在其他无脊椎动物和植物，和机会性真菌感染脊椎动物。模型过程包括病原体的生长和传播，通过宿主组织的消耗，未分化的宿主变形细胞的趋化吸引感染，和变形细胞分化为攻击病原体的各种细胞类型。敏感性分析表明，单一局部感染的传播速度主要取决于病原体对宿主组织消耗的潜在速度以及宿主补充未分化变形细胞池并维持长期反应的能力。免疫反应的空间定位在远处病变之间产生了潜在的强间接相互作用，使新的感染迅速增长，而宿主资源集中在较老的较大感染上。这些发现为环境压力源的影响提供了可能的机制解释（例如，例如，在一个实施例中，海洋变暖、营养物富集）对曲霉病流行率和严重程度的影响，以及观察到的疾病影响的高度空间和宿主间变异。
We develop a spatially explicit model for the within-host interactions between a fungal pathogen and the immune response by its coral host. The model is parameterized for the recent epizootic of Aspergillus sydowii in the sea fan Gorgonia ventalina, but its structure is adaptable to many other diseases attacking corals worldwide, fungal infections in other invertebrates and plants, and opportunistic fungal infections in vertebrates. Model processes include pathogen growth and spread through consumption of host tissue, chemotactic attraction of undifferentiated host amoebocytes to infections, and amoebocyte differentiation into various cell types that attack the pathogen. Sensitivity analysis shows that the spread rate of a single localized infection is determined primarily by the pathogen's potential rate of host tissue consumption and by the host's ability to replenish the pool of undifferentiated amoebocytes and sustain a long-term response. The spatial localization of immune responses creates potentially strong indirect interactions between distant lesions, allowing new infections to grow rapidly while host resources are concentrated at older, larger infections. These findings provide possible mechanistic explanations for effects of environmental stressors (e. g., ocean warming, nutrient enrichment) on aspergillosis prevalence and severity and for the observed high spatial and between-host variability in disease impacts.