The probability of epidemic burnout in the stochastic SIR model with vital dynamics.

SIR model epidemics extinction stochastic processes

Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
30 Jan 2024
Historique:
medline: 26 1 2024
pubmed: 26 1 2024
entrez: 26 1 2024
Statut: ppublish

Résumé

We present an approach to computing the probability of epidemic "burnout," i.e., the probability that a newly emergent pathogen will go extinct after a major epidemic. Our analysis is based on the standard stochastic formulation of the Susceptible-Infectious-Removed (SIR) epidemic model including host demography (births and deaths) and corresponds to the standard SIR ordinary differential equations (ODEs) in the infinite population limit. Exploiting a boundary layer approximation to the ODEs and a birth-death process approximation to the stochastic dynamics within the boundary layer, we derive convenient, fully analytical approximations for the burnout probability. We demonstrate-by comparing with computationally demanding individual-based stochastic simulations and with semi-analytical approximations derived previously-that our fully analytical approximations are highly accurate for biologically plausible parameters. We show that the probability of burnout always decreases with increased mean infectious period. However, for typical biological parameters, there is a relevant local minimum in the probability of persistence as a function of the basic reproduction number [Formula: see text]. For the shortest infectious periods, persistence is least likely if [Formula: see text]; for longer infectious periods, the minimum point decreases to [Formula: see text]. For typical acute immunizing infections in human populations of realistic size, our analysis of the SIR model shows that burnout is almost certain in a well-mixed population, implying that susceptible recruitment through births is insufficient on its own to explain disease persistence.

Identifiants

pubmed: 38277438
doi: 10.1073/pnas.2313708120
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e2313708120

Subventions

Organisme : Gouvernement du Canada | Natural Sciences and Engineering Research Council of Canada (NSERC)
ID : RGPIN-2021-04068
Organisme : Gouvernement du Canada | Natural Sciences and Engineering Research Council of Canada (NSERC)
ID : RGPIN-2016-06493
Organisme : Gouvernement du Canada | Natural Sciences and Engineering Research Council of Canada (NSERC)
ID : RGPIN-2016-05488

Déclaration de conflit d'intérêts

Competing interests statement:The authors declare no competing interest.

Auteurs

Todd L Parsons (TL)

Laboratoire de Probabilités, Statistique et Modélisation, Sorbonne Université, CNRS UMR 8001, Paris 75005, France.

Benjamin M Bolker (BM)

Department of Biology, McMaster University, Hamilton, Ontario L8S 4K1, Canada.
Department of Mathematics & Statistics, McMaster University, Hamilton, Ontario L8S 4K1, Canada.

Jonathan Dushoff (J)

Department of Biology, McMaster University, Hamilton, Ontario L8S 4K1, Canada.
Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario L8S 4K1, Canada.

David J D Earn (DJD)

Department of Mathematics & Statistics, McMaster University, Hamilton, Ontario L8S 4K1, Canada.
Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario L8S 4K1, Canada.

Classifications MeSH