Data from: Covariation between the physiological and behavioral components of pathogen transmission: host heterogeneity determines epidemic outcomes

Although heterogeneity in contact rate, physiology, and behavioral response to infection have all been empirically demonstrated in host–pathogen systems, little is known about how interactions between individual variation in behavior and physiology scale-up to affect pathogen transmission at a population level. The objective of this study is to evaluate how covariation between the behavioral and physiological components of transmission might affect epidemic outcomes in host populations. We tested the consequences of contact rate covarying with susceptibility, infectiousness, and infection status using an individual-based, dynamic network model where individuals initiate and terminate contacts with conspecifics based on their behavioral predispositions and their infection status. Our results suggest that both heterogeneity in physiology and subsequent covariation of physiology with contact rate could powerfully influence epidemic dynamics. Overall, we found that 1) individual variability in susceptibility and infectiousness can reduce the expected maximum prevalence and increase epidemic variability; 2) when contact rate and susceptibility or infectiousness negatively covary, it takes substantially longer for epidemics to spread throughout the population, and rates of epidemic spread remained suppressed even for highly transmissible pathogens; and 3) reductions in contact rate resulting from infection-induced behavioral changes can prevent the pathogen from reaching most of the population. These effects were strongest for theoretical pathogens with lower transmissibility and for populations where the observed variation in contact rate was higher, suggesting that such heterogeneity may be most important for less infectious, more chronic diseases in wildlife. Understanding when and how variability in pathogen transmission should be modelled is a crucial next step for disease ecology.

尽管宿主-病原体（host–pathogen）系统中，接触率、生理特性以及感染诱导的行为响应的异质性均已通过实证得到验证，但目前学界对行为与生理的个体差异间的相互作用如何在种群尺度上放大并影响病原体传播的机制仍不甚明晰。本研究旨在探究传播行为与生理特性的协同变异如何影响宿主种群的流行病传播结局。我们采用基于个体的动态网络模型（individual-based dynamic network model），探究了接触率与易感性、传染力及感染状态的协同变异所产生的效应；该模型中，个体将依据自身行为倾向与感染状态，发起并终止与同种个体的接触互动。研究结果表明，生理特征的异质性及其与接触率的后续协同变异，均可对流行病传播动力学产生显著影响。总体而言，我们的研究发现包括：其一，个体易感性与传染力的差异可降低预期的最大患病率，并提升流行病传播的异质性；其二，当接触率与易感性或传染力呈负协同变异时，流行病在种群内的传播耗时会显著延长，且即便对于高传播性病原体，其传播速率仍会持续受到抑制；其三，感染诱导的行为变化所导致的接触率降低，可阻止病原体扩散至种群内绝大多数个体。上述效应在传播性较低的理论病原体以及接触率变异程度更高的种群中最为显著，这表明此类异质性对于野生动物中低传染性、长病程的疾病而言尤为关键。明确病原体传播变异的建模时机与方式，是疾病生态学领域下一阶段的核心研究方向。