新たな病気の出現を予測するための特性を研究(What traits matter when predicting disease emergence in new populations?)

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2025-08-21 ペンシルベニア州立大学 (Penn State)

ペンシルベニア州立大学とミネソタ大学デュルース校の研究チームは、感染症が新たな宿主に伝播した後、感染が自然消滅するか持続するかを予測するための重要な指標を明らかにしました。PLOS Biology誌掲載の研究によれば、初期段階の「感染者の割合(感染有病率)」「ウイルス放出量(viral shedding)」「宿主の感受性」が、病原体が新集団で定着するか否かを見極める鍵となる要素です。特に、「感染有病率」と「ウイルス放出量」がウイルスの持続性を予測する主要因であり、全体のばらつきの半分以上を説明しました。一方で、個体内のウイルス量(感染強度)は持続を予測する上では信頼できる指標ではありませんでした。こうした知見により、数多く発生する「種の壁を越えた感染(spillover)」の中から、リスクが高いものをどのように特定し、効果的な公衆衛生リソース配分につなげるかについて、科学的根拠をもって判断できるようになると研究者らは述べています。

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初期の疫学的特徴は、流出イベント後の集団レベルのウイルスの持続の可能性を説明する Early epidemiological characteristics explain the chance of population-level virus persistence following spillover events

Clara L. Shaw,David A. Kennedy
PLOS Biology  Published: August 21, 2025
DOI:https://doi.org/10.1371/journal.pbio.3003315

新たな病気の出現を予測するための特性を研究(What traits matter when predicting disease emergence in new populations?)

Abstract

Spillover of viruses into novel host species occurs frequently. Often, spillover results in dead-end infections in novel hosts, sometimes, in stuttering transmission chains that die out, and rarely, in large epidemics with sustained transmission. If we could identify early which outcome will occur following a spillover event, we could more appropriately invest in efforts to surveil, respond to, or prevent disease emergence. Our goal was to identify early epidemiological characteristics that correlate with these outcomes, including those predictive of population-level virus persistence in novel hosts. To identify these characteristics, we experimentally induced spillover in the Caenorhabditis nematode-Orsay virus system and measured infection prevalence in exposed populations and virus shedding and infection intensity from infected hosts in replicate populations of eight strains belonging to seven non-native host species. We then passaged 20 adult nematodes from exposed populations to virus-free plates where they reproduced, initiating new populations to which they had the potential to transmit virus. We used quantitative PCR to track virus presence in passaged host populations for 10 passages or until virus was undetectable, indicating its loss. We then used a correlative modeling and a mechanistic modeling approach to understand which epidemiological characteristics were associated with population-level viral persistence. In our correlative models, we found that the number of passages until virus loss was associated with early epidemiological characteristics in the spillover host populations, including infection prevalence in the initially exposed population, the ability of hosts to detectably shed the virus, and the relative susceptibility of the host species, but not infection intensity. When all these characteristics were included simultaneously in a correlative model, only infection prevalence and shedding were significantly associated with virus maintenance, and the model explained over half of the variation in the data. We then developed a mechanistic model that attempts to explain virus passage success by using our epidemiological characteristics data to calculate the probability that at least one worm infectious enough to infect a conspecific is transferred during passage. This mechanistic model explained 38% of the variation in the data on its own. With the goal of understanding how our mechanistic model falls short, we used model selection to test a suite of larger models that included or excluded each epidemiological characteristic and included random effects of strain, experimental line, passage number, and block while the mechanistic prediction was included as an offset. We found that 66% of the variation in our data could be explained by a model that included our mechanistic prediction in addition to infection prevalence, infection intensity, and random effects. Altogether, our study demonstrates that early epidemiological characteristics can play a substantial role in explaining the ultimate outcome of a spillover event.

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