Sato Masato, Dieckmann Ulf, Sasaki Akira
Department of Evolutionary Studies of Biosystems, The Graduate University for Advanced Studies, SOKENDAI, Hayama, Kanagawa 240-0193, Japan.
Bioproduction Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Ibaraki 305-8561, Japan.
Proc Natl Acad Sci U S A. 2024 Dec 24;121(52):e2309272121. doi: 10.1073/pnas.2309272121. Epub 2024 Dec 19.
The epidemiology and evolution of diseases unfold in populations that are rarely homogeneous. Instead, hosts infected by pathogens often form metapopulations, in which local populations connected by the movement of hosts experience different demographic and epidemiological conditions. Here, we develop a general theory of the evolution of pathogens in heterogeneous metapopulations. We reveal the following key insights into the evolution of pathogen virulence and infectiousness: (1) When the mobility (movement rate), productivity (birth rate and carrying capacity), or immunocompetency (immunity-loss rate) differ among local populations, this variance always increases pathogen virulence and infectiousness (2) The increment of pathogen virulence caused by such heterogeneity is approximately proportional to the variance of the corresponding heterogeneous local conditions (3) This increment can be expressed as the covariance between the local selection pressures and the local reproductive values experienced by the pathogen (4) The reason why heterogeneity always increases pathogen virulence is explained by the positive correlation of local selection pressures with reproductive values (5) Combinations of multiple independent heterogeneities further increase virulence and infectiousness, even more so when their covariances are positive. Our key findings robustly hold for different epidemiological frameworks - including SI, SIS, SIR, and SIRS models, with both density- and frequency-dependent transmission as well as with superinfection. They provide insights into the risks of growing pathogen infectiousness in a world in which heterogeneity - caused, e.g., by the concentration of human populations in urban areas - is rising.
疾病的流行病学和进化在很少同质化的人群中展开。相反,被病原体感染的宿主常常形成复合种群,其中通过宿主移动相连的局部种群经历不同的人口统计学和流行病学状况。在此,我们建立了一个关于病原体在异质复合种群中进化的一般理论。我们揭示了关于病原体毒力和传染性进化的以下关键见解:(1)当局部种群之间的迁移率(移动速率)、生产力(出生率和承载能力)或免疫能力(免疫丧失率)不同时,这种差异总是会增加病原体的毒力和传染性;(2)这种异质性导致的病原体毒力增加大致与相应异质局部条件的差异成比例;(3)这种增加可以表示为病原体所经历的局部选择压力与局部繁殖值之间的协方差;(4)异质性总是增加病原体毒力的原因是局部选择压力与繁殖值呈正相关;(5)多个独立异质性的组合会进一步增加毒力和传染性,当它们的协方差为正时更是如此。我们的关键发现对于不同的流行病学框架——包括SI、SIS、SIR和SIRS模型,无论是密度依赖还是频率依赖的传播以及重复感染——都能有力成立。它们为在一个异质性(例如由城市地区人口集中导致)正在增加的世界中病原体传染性增加的风险提供了见解。