Vector-Borne Pathogen and Host Evolution in a Structured Immuno-Epidemiological System

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• 作者：Hayriye Gulbudak ; Vincent L. Cannataro ; Necibe Tuncer…
• 关键词：Immuno ; epidemiological modeling ; Rift Valley fever ; West Nile virus ; Vector ; borne pathogen ; Differential equations ; Reproduction number ; Vector inoculum size ; Age ; since ; infection ; Within ; host dynamics ; Coevolutionary attractor ; Trade ; offs
• 刊名：Bulletin of Mathematical Biology
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：79
• 期：2
• 页码：325-355
• 全文大小：
• 刊物类别：Mathematics and Statistics
• 刊物主题：Mathematical and Computational Biology; Life Sciences, general; Cell Biology;
• 出版者：Springer US
• ISSN：1522-9602
• 卷排序：79

文摘

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 \({\mathcal {R}}_0\) 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 \({\mathcal {R}}_0\), 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.