ArticleNature communications2025
Interplay between climate and childhood mixing can explain a sudden shift in RSV seasonality in Japan.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Spatiotemporal Dynamics of Human Metapneumovirus and Potential Impact of Respiratory Syncytial Virus Interventions in the United States.medRxiv : the preprint server for health sciences · 2026Article
- Climate change and infectious diseases.Nature medicine · 2026Review
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9 authors.
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Abstract
Titrating the importance of endogenous and exogenous drivers for host-pathogen systems remains an important research frontier towards predicting future outbreaks. In Japan, respiratory syncytial virus (RSV), a major childhood respiratory pathogen, displayed a sudden, dramatic shift in outbreak seasonality (from winter to fall) in 2016. We use mathematical models to identify processes that could lead to this outcome. In line with previous analyses, we identify a robust quadratic relationship between transmission against mean specific humidity and mean temperature, with maximum transmission occurring at low and high humidity as well as low and high temperature. This drives semiannual patterns of seasonal transmission rates that peak in summer and winter. Under this transmission regime, a subtle increase in population-level susceptibility or transmission can cause a sudden shift in seasonality, where the degree of shift is primarily determined by the interval between the two peaks of seasonal transmission rate. We hypothesize that an increase in children attending childcare facilities may have contributed to the increase in the overall RSV transmission through increased contact rates between susceptible and infected hosts. Our analysis underscores the power of studying infectious disease dynamics to titrate the roles of underlying drivers of dynamical transitions in ecology.
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