4.6 Article

Rates of coalescence for common epidemiological models at equilibrium

Journal

JOURNAL OF THE ROYAL SOCIETY INTERFACE
Volume 9, Issue 70, Pages 997-1007

Publisher

ROYAL SOC
DOI: 10.1098/rsif.2011.0495

Keywords

phylodynamics; viral evolution; disease dynamics; epidemiological models; coalescent theory

Funding

  1. RAPIDD of the Science and Technology Directorate, Department of Homeland Security
  2. Fogarty International Centre, National Institutes of Health
  3. NSF
  4. [NSF-EF-08-27416]
  5. Direct For Biological Sciences
  6. Division Of Environmental Biology [0827416] Funding Source: National Science Foundation

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Coalescent theory provides a mathematical framework for quantitatively interpreting gene genealogies. With the increased availability of molecular sequence data, disease ecologists now regularly apply this body of theory to viral phylogenies, most commonly in attempts to reconstruct demographic histories of infected individuals and to estimate parameters such as the basic reproduction number. However, with few exceptions, the mathematical expressions at the core of coalescent theory have not been explicitly linked to the structure of epidemiological models, which are commonly used to mathematically describe the transmission dynamics of a pathogen. Here, we aim to make progress towards establishing this link by presenting a general approach for deriving a model's rate of coalescence under the assumption that the disease dynamics are at their endemic equilibrium. We apply this approach to four common families of epidemiological models: standard susceptible-infected-susceptible/susceptible-infected-recovered/susceptible-infected-recovered-susceptible models, models with individual heterogeneity in infectivity, models with an exposed but not yet infectious class and models with variable distributions of the infectious period. These results improve our understanding of how epidemiological processes shape viral genealogies, as well as how these processes affect levels of viral diversity and rates of genetic drift. Finally, we discuss how a subset of these coalescent rate expressions can be used for phylodynamic inference in non-equilibrium settings. For the ones that are limited to equilibrium conditions, we also discuss why this is the case. These results, therefore, point towards necessary future work while providing intuition on how epidemiological characteristics of the infection process impact gene genealogies.

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