ArticlePNAS nexus2025
Adaptive human behavior and delays in information availability autonomously modulate epidemic waves.
Article in PNAS nexus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The paradox of neglecting changes in behavior: How standard epidemic models misestimate both transmissibility and final epidemic size.PLoS computational biology · 2026Article
- Integrated framework to study genomic surveillance of selective sweeps in multivariants dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The impact of human behavioral adaptation stratified by immune status on COVID-19 spread with application to South Korea.PloS one · 2026Article
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Authors and funding
4 authors.
Funding
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Abstract
The recurrence of epidemic waves has been a hallmark of infectious disease outbreaks. Repeated surges in infections pose significant challenges to public health systems, yet the mechanisms that drive these waves remain insufficiently understood. Most prior models attribute epidemic waves to exogenous factors, such as transmission seasonality, viral mutations, or implementation of public health interventions. We show that epidemic waves can emerge autonomously from the feedback loop between infection dynamics and human behavior. Our results are based on a behavioral framework in which individuals continuously adjust their level of risk mitigation subject to their perceived risk of infection, which depends on information availability and disease severity. We show that delayed behavioral responses alone can lead to the emergence of multiple epidemic waves. The magnitude and frequency of these waves depend on the interplay between behavioral factors (delay, severity, and sensitivity of responses) and disease factors (transmission and recovery rates). Notably, if the response is either too prompt or excessively delayed, multiple waves cannot emerge. Our results further align with previous observations that adaptive human behavior can produce nonmonotonic final epidemic sizes, shaped by the trade-offs between various biological and behavioral factors-namely, risk sensitivity, response stringency, and disease generation time. Interestingly, we found that the minimal final epidemic size occurs on regimes that exhibit a few damped oscillations. Altogether, our results emphasize the importance of integrating social and operational factors into infectious disease models, in order to capture the joint evolution of adaptive behavioral responses and epidemic dynamics.
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