An exact finite-population stochastic framework for SIR epidemics evolving under Markovian switching between intervention regimes is developed, showing how switching mechanisms affect both the total number of infected individuals and the extinction time, including their dispersion.
Abstract
We develop an exact finite-population stochastic framework for SIR epidemics evolving under Markovian switching between intervention regimes. The epidemic state is augmented by a finite phase component, allowing transmission, recovery, and direct immunity-acquisition rates to depend on the active regime. Phase-transition intensities may depend on the current epidemic state, so that policy escalation can react to the number of infectious individuals. Exploiting the monotonicity of the susceptible compartment, we derive level-wise recursions for the joint Laplace--Stieltjes transform and probability generating function of the extinction time and the number of infections generated before extinction. These recursions yield the infection-count distribution, conditional extinction-time transforms, and mixed moments linking epidemic duration and infection burden, while replacing a large global linear system with small phase-level solves. The framework is illustrated using weekly mpox incidence data from Luxembourg. A baseline one-phase SIR model is calibrated by maximum likelihood under a Poisson observation model. The calibrated baseline is then used for conditional comparisons of fixed control regimes, early versus delayed strict intervention, vaccination-supported control, and state-dependent escalation. The results show how switching mechanisms affect both the total number of infected individuals and the extinction time, including their dispersion. Since the switching mechanisms are specified rather than estimated from the intervention history, the results are conditional model-based comparisons rather than estimates of the historical effects of interventions in Luxembourg.
We introduce a fully stochastic, non-Markovian SIRS-type epidemic model that incorporates varying infectivity, waning immunity and a pulse vaccination strategy that may not confer permanent immunity. The model is constructed at the individual level, where each person is characterized by random infectivity and susceptibility functions, and vaccination campaigns occur at the jump times of a Poisson random measure with arbitrary intensity. We rigorously derive the epidemic dynamics as the large-population limit of an interacting stochastic particle system, leading to a system of nonlinear Volterra-type integral equations governing the average susceptibility and total force of infection. We establish a functional law of large numbers(FLLN) for the empirical processes and provide explicit expressions for the limiting compartmental proportions. The long-term behavior of the system is analyzed: we prove that the infection-free solution is globally asymptotically stable when the basic reproduction number falls below a critical threshold, and that the disease persists when this threshold is exceeded. The threshold is given by the harmonic mean of the maximal susceptibility across individuals and generalizes previous results by incorporating vaccination and memory effects. Our framework provides a probabilistically grounded extension of classical deterministic pulse vaccination models and offers new insights into the control of epidemics through scheduled immunization policies.
This work examines a nonlinear stochastic SIRS epidemic model evolving in a randomly changing environment described by a finite-state Markov chain. The transmission mechanism incorporates regime-dependent nonlinear incidence rates, where the contact interaction between susceptible and infectious individuals is modeled by the term [Formula: see text] . This switching nonlinearity allows the model to capture varying environmental effects and heterogeneous transmission patterns more accurately, thereby providing a more realistic description of epidemic dynamics. To the best of our knowledge, the sufficient criteria governing the persistence and extinction of stochastic SIRS models with transmission rate exponents governed by Markovian switching have not yet been established in the existing literature. The principal contribution of the present study is the derivation of the rigorous sufficient conditions that characterize both the extinction and the long-term persistence of disease dynamics. Specifically, a threshold parameter Λ, expressed in terms of the switching exponents ρξ(t) and ζξ(t), is derived. That is, if Λ > 0, the disease exhibits strong stochastic persistence; conversely, if Λ < 0, the disease-free equilibrium state becomes globally asymptotically stable in probability, leading to eventual disease extinction. In the special case where there is no regime switching and ρξ(t)=ζξ(t)=1, our model recovers the classical threshold found in the literature. To support and validate the theoretical findings, numerical simulations are provided to demonstrate the dynamical behavior of the model under different environmental regimes.
Khalid El Bakkioui, Mourad El Idrissi· Mathematical Biosciences· 0 citations
We develop a stochastic framework for a broad class of heterogeneous SIR epidemic models. In the finite-population construction, each initially susceptible individual is assigned a fixed nonnegative susceptibility, and infection occurs when the accumulated population-level infection pressure exceeds an individual random threshold. Infectious periods are independent and exponentially distributed with a common recovery rate. For any susceptibility distribution with finite mean, we prove a uniform-on-compact law of large numbers for the susceptible, infectious, removed, and cumulative infection-pressure processes. In the limit, an individual with susceptibility lambda remains susceptible under cumulative pressure x with probability exp(-x lambda). It follows that the susceptible fraction is given by the Laplace transform of the initial susceptibility distribution, while the incidence rate is governed by the mean susceptibility among those who remain susceptible. The resulting limits recover several familiar heterogeneous SIR systems, including the classical power-law model, and also yield other closed nonlinear incidence forms. The framework therefore provides a unified probabilistic foundation for deterministic epidemic models with persistent individual heterogeneity.
O. Izyumtseva, Wasiur R. KhudaBukhsh, M. Gomes et al.· 0 citations
Early epidemic control often relies on case-finding operations. To assess their theoretical efficacy, we develop an infection-age structured early growth transmission model that incorporates symptom-based diagnosis, mass screening, and both forward and backward contact tracing. By deriving integral equations for the forward and backward tracing rates and coupling them with a Lotka-Euler-type equation for the early growth rate, we obtain a closed deterministic system. This system enables the computation of early growth rates and reproduction numbers under different case-finding scenarios. Using parameter values calibrated from the 2021 Yangzhou outbreak, the theoretical scenario comparisons show that diagnosis alone provides limited control of early epidemic growth, whereas the integrated case-finding scenario substantially suppresses transmission. The results further show that reducing the effective reproduction number below one requires stronger mass screening and contact tracing when infected individuals generate more secondary infections on average. Together, these findings indicate that the theoretical efficacy of case-finding operations depends jointly on intervention intensity and the effective transmission structure.
Xiaoqian Wang, Zhen Jin, Gui-Rong Liu et al.· Journal of Theoretical Biolo...· 0 citations
Host individuals with vaccinations for infectious diseases often transition among different states of susceptibility and infectivity. Thus, we derive a class of epidemic models in which susceptible and infected individuals have a discrete set of susceptibility and infectivity states, respectively. Our model is based on double-dose vaccination and accounts for all possible state transitions between states. A comprehensive mathematical analysis of the proposed model is conducted, including assessing the control reproduction number and the global dynamical behaviors of the solutions. Using an improved affine-invariant ensemble Markov Chain Monte Carlo method, we also fit the model with measles case data in the United States. The results indicate that despite high vaccination coverage and efficacy rates, sporadic or small-scale measles outbreaks still occur. This suggests that reliance solely on vaccination policies is insufficient to fully interrupt its transmission chain. Consequently, enhancing the diagnosis rate of measles cases is another crucial measure for controlling measles transmission and outbreaks, building upon existing vaccination efforts.
Wenxuan Li, Chiyu Zhang, Xu Chen et al.· International Journal of Bio...· 0 citations
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