Gulbudak Hayriye, Cannataro Vincent L, Tuncer Necibe, Martcheva Maia
School of Biological Sciences and School of Mathematics, Georgia Institute of Technology, 310 Ferst Dr, Atlanta, GA, 30332, USA.
Department of Biology, University of Florida, 220 Bartram Hall, PO Box 118525, Gainesville, FL, 32611-8525, USA.
Bull Math Biol. 2017 Feb;79(2):325-355. doi: 10.1007/s11538-016-0239-0. Epub 2016 Dec 28.
Vector-borne disease transmission is a common dissemination mode used by many pathogens to spread in a host population. Similar to directly transmitted diseases, the within-host interaction of a vector-borne pathogen and a host's immune system influences the pathogen's transmission potential between hosts via vectors. Yet there are few theoretical studies on virulence-transmission trade-offs and evolution in vector-borne pathogen-host systems. Here, we consider an immuno-epidemiological model that links the within-host dynamics to between-host circulation of a vector-borne disease. On the immunological scale, the model mimics antibody-pathogen dynamics for arbovirus diseases, such as Rift Valley fever and West Nile virus. The within-host dynamics govern transmission and host mortality and recovery in an age-since-infection structured host-vector-borne pathogen epidemic model. By considering multiple pathogen strains and multiple competing host populations differing in their within-host replication rate and immune response parameters, respectively, we derive evolutionary optimization principles for both pathogen and host. Invasion analysis shows that the [Formula: see text] maximization principle holds for the vector-borne pathogen. For the host, we prove that evolution favors minimizing case fatality ratio (CFR). These results are utilized to compute host and pathogen evolutionary trajectories and to determine how model parameters affect evolution outcomes. We find that increasing the vector inoculum size increases the pathogen [Formula: see text], but can either increase or decrease the pathogen virulence (the host CFR), suggesting that vector inoculum size can contribute to virulence of vector-borne diseases in distinct ways.
媒介传播疾病的传播是许多病原体在宿主群体中传播的常见方式。与直接传播的疾病类似,媒介传播病原体与宿主免疫系统在宿主体内的相互作用会影响病原体通过媒介在宿主之间的传播潜力。然而,关于媒介传播病原体 - 宿主系统中毒力 - 传播权衡与进化的理论研究却很少。在此,我们考虑一个免疫流行病学模型,该模型将宿主体内动态与媒介传播疾病的宿主间传播联系起来。在免疫学尺度上,该模型模拟了虫媒病毒疾病(如裂谷热和西尼罗河病毒)的抗体 - 病原体动态。在一个按感染后时间分层的宿主 - 媒介 - 传播病原体流行模型中,宿主体内动态决定了传播以及宿主的死亡率和恢复情况。通过分别考虑多种病原体菌株和多个在宿主体内复制率和免疫反应参数方面存在差异的竞争宿主群体,我们推导出了病原体和宿主的进化优化原则。入侵分析表明,对于媒介传播病原体,[公式:见原文]最大化原则成立。对于宿主,我们证明进化有利于将病死率(CFR)降至最低。这些结果被用于计算宿主和病原体的进化轨迹,并确定模型参数如何影响进化结果。我们发现,增加媒介接种量会增加病原体的[公式:见原文],但可能会增加或降低病原体的毒力(宿主CFR),这表明媒介接种量可以以不同方式影响媒介传播疾病的毒力。