Howerton Emily, Williams Thomas C, Casalegno Jean-Sébastien, Dominguez Samuel, Gunson Rory, Messacar Kevin, Metcalf C Jessica E, Park Sang Woo, Viboud Cécile, Grenfell Bryan T
Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ, USA.
Child Life and Health, University of Edinburgh, Edinburgh, UK.
Nat Commun. 2025 Aug 6;16(1):7261. doi: 10.1038/s41467-025-62358-w.
Respiratory syncytial virus (RSV) and human metapneumovirus (hMPV) are closely related pathogens responsible for a significant burden of acute respiratory infections. Interactions between RSV and hMPV have been hypothesized, but the mechanisms of interaction are largely unknown. Here, we use a mathematical model to quantify the likelihood of interactions from population-level surveillance data and investigate whether interactions could lead to increases in hMPV burden under RSV medical interventions, including active and passive immunization. In Scotland, Korea, and three regions of Canada, annual hMPV outbreaks lag RSV outbreaks by up to 18 weeks; two Canadian regions show patterns consistent with out-of-phase biennial outbreaks. Using a two-pathogen transmission model, we show that a negative effect of RSV infection on hMPV transmissibility can explain these dynamics. We use post-pandemic RSV-hMPV rebound dynamics as an out of sample test for our model, and the model with interactions better predicts this period than a model where the pathogens are assumed to be independent. Finally, our model suggests that hMPV peak timing and magnitude may change under RSV interventions. Our analysis provides a foundation for detecting possible RSV-hMPV interactions at the population level, although such a model oversimplifies important complexities about interaction mechanisms.
呼吸道合胞病毒(RSV)和人偏肺病毒(hMPV)是密切相关的病原体,它们导致了急性呼吸道感染的重大负担。虽然已经推测了RSV和hMPV之间的相互作用,但其相互作用机制在很大程度上仍不清楚。在此,我们使用数学模型从人群水平监测数据中量化相互作用的可能性,并研究在RSV医学干预措施(包括主动和被动免疫)下,相互作用是否会导致hMPV负担增加。在苏格兰、韩国以及加拿大的三个地区,每年的hMPV疫情比RSV疫情滞后长达18周;加拿大的两个地区呈现出与不同步两年一次疫情相符的模式。使用双病原体传播模型,我们表明RSV感染对hMPV传播性的负面影响可以解释这些动态。我们将大流行后RSV - hMPV的反弹动态作为对我们模型的样本外测试,与假设病原体相互独立的模型相比,具有相互作用的模型能更好地预测这一时期。最后,我们的模型表明在RSV干预下,hMPV的峰值时间和幅度可能会发生变化。我们的分析为在人群水平检测可能的RSV - hMPV相互作用提供了基础,尽管这样的模型过度简化了相互作用机制的重要复杂性。