Structural causal influence captures the forces of social inequality in models of infectious disease
Mathematical models are central to understanding disease transmission for host-pathogen systems across the biosphere. However, most existing frameworks do not explicitly treat host population heterogeneity as a formal driver of variation in transmission dynamics. This gap is most visible in human disease, where social inequalities are well known to structure infectious disease risk, but applies broadly: ecological, behavioural and demographic structure shapes transmission in non-human host populations as well. Here, we introduce a new metric, structural causal influence, which uses causal analysis to quantify how subpopulations contribute to overall transmission through structural differences in exposure, susceptibility or recovery. Using a multi-population model, we show that even a population whose isolated reproduction number lies below one can be drawn into a sustained epidemic through minimal contact with a more affected group.
Authors
- Lorin Crawford (ORCID: https://orcid.org/0000-0003-0178-8242)
- Sudam Surasinghe
- C. Brandon Ogbunugafor (ORCID: https://orcid.org/0000-0002-1581-8345)
- Swathi Nachiar Manivannan
- Sidney Redner (ORCID: https://orcid.org/0000-0001-5716-2770)
Institutions
- Northeastern University (US)
- Santa Fe Institute (US)
- Yale University (US)
- Yale New Haven Health System (US)
- Microsoft Research (United Kingdom) (GB)
Publication Details
- Journal
- Biology Letters
- Published
- 2026-08-19
- DOI
- https://doi.org/10.1098/rsbl.2025.0655
- Primary Topic
- COVID-19 epidemiological studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00