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Register a new userStochastic amplification in an epidemic model with seasonal forcing
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We study the stochastic susceptible-infected-recovered (SIR) model with time-dependent forcing using analytic techniques which allow us to disentangle the interaction of stochasticity and external forcing. The model is formulated as a continuous time Markov process, which is decomposed into a deterministic dynamics together with stochastic corrections, by using an expansion in inverse system size. The forcing induces a limit cycle in the deterministic dynamics, and a complete analysis of the fluctuations about this time-dependent solution is given. This analysis is applied when the limit cycle is annual, and after a period-doubling when it is biennial. The comprehensive nature of our approach allows us to give a coherent picture of the dynamics which unifies past work, but which also provides a systematic method for predicting the periods of oscillations seen in whooping cough and measles epidemics.
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Between pandemics, the influenza virus exhibits periods of incremental evolution via a process known as antigenic drift. This process gives rise to a sequence of strains of the pathogen that are continuously replaced by newer strains, preventing a build up of immunity in the host population. In this paper, a parsimonious epidemic model is defined that attempts to capture the dynamics of evolving strains within a host population. The `evolving strains epidemic model has many properties that lie in-between the Susceptible-Infected-Susceptible and the Susceptible-Infected-Removed epidemic models, due to the fact that individuals can only be infected by each strain once, but remain susceptible to reinfection by newly emerged strains. Coupling results are used to identify key properties, such as the time to extinction. A range of reproduction numbers are explored to characterize the model, including a novel quasi-stationary reproduction number that can be used to describe the re-emergence of the pathogen into a population with `average levels of strain immunity, analogous to the beginning of the winter peak in influenza. Finally the quasi-stationary distribution of the evolving strains model is explored via simulation.
Pairwise models are used widely to model epidemic spread on networks. These include the modelling of susceptible-infected-removed (SIR) epidemics on regular networks and extensions to SIS dynamics and contact tracing on more exotic networks exhibiting degree heterogeneity, directed and/or weighted links and clustering. However, extra features of the disease dynamics or of the network lead to an increase in system size and analytical tractability becomes problematic. Various `closures can be used to keep the system tractable. Focusing on SIR epidemics on regular but clustered networks, we show that even for the most complex closure we can determine the epidemic threshold as an asymptotic expansion in terms of the clustering coefficient.We do this by exploiting the presence of a system of fast variables, specified by the correlation structure of the epidemic, whose steady state determines the epidemic threshold. While we do not find the steady state analytically, we create an elegant asymptotic expansion of it. We validate this new threshold by comparing it to the numerical solution of the full system and find excellent agreement over a wide range of values of the clustering coefficient, transmission rate and average degree of the network. The technique carries over to pairwise models with other closures [1] and we note that the epidemic threshold will be model dependent. This emphasises the importance of model choice when dealing with realistic outbreaks.
The spread of an epidemic process is considered in the context of a spatial SIR stochastic model that includes a parameter $0le ple 1$ that assigns weights $p$ and $1- p$ to global and local infective contacts respectively. The model was previously studied by other authors in different contexts. In this work we characterized the behavior of the system around the threshold for epidemic spreading. We first used a deterministic approximation of the stochastic model and checked the existence of a threshold value of $p$ for exponential epidemic spread. An analytical expression, which defines a function of the quotient $alpha$ between the transmission and recovery rates, is obtained to approximate this threshold. We then performed different analyses based on intensive stochastic simulations and found that this expression is also a good estimate for a similar threshold value of $p$ obtained in the stochastic model. The dynamics of the average number of infected individuals and the average size of outbreaks show a behavior across the threshold that is well described by the deterministic approximation. The distributions of the outbreak sizes at the threshold present common features for all the cases considered corresponding to different values of $alpha>1$. These features are otherwise already known to hold for the standard stochastic SIR model at its threshold, $alpha=1$: (i) the probability of having an outbreak of size $n$ goes asymptotically as $n^{-3/2}$ for an infinite system, (ii) the maximal size of an outbreak scales as $N^{2/3}$ for a finite system of size $N$.
A pandemic caused by a new coronavirus (COVID-19) has spread worldwide, inducing an epidemic still active in Argentina. In this chapter, we present a case study using an SEIR (Susceptible-Exposed-Infected-Recovered) diffusion model of fractional order in time to analyze the evolution of the epidemic in Buenos Aires and neighboring areas (Region Metropolitana de Buenos Aires, (RMBA)) comprising about 15 million inhabitants. In the SEIR model, individuals are divided into four classes, namely, susceptible (S), exposed (E), infected (I) and recovered (R). The SEIR model of fractional order allows for the incorporation of memory, with hereditary properties of the system, being a generalization of the classic SEIR first-order system, where such effects are ignored. Furthermore, the fractional model provides one additional parameter to obtain a better fit of the data. The parameters of the model are calibrated by using as data the number of casualties officially reported. Since infinite solutions honour the data, we show a set of cases with different values of the lockdown parameters, fatality rate, and incubation and infectious periods. The different reproduction ratios R0 and infection fatality rates (IFR) so obtained indicate the results may differ from recent reported values, constituting possible alternative solutions. A comparison with results obtained with the classic SEIR model is also included. The analysis allows us to study how isolation and social distancing measures affect the time evolution of the epidemic.
We consider an SIR-type (Susceptible $to$ Infected $to$ Recovered) stochastic epidemic process with multiple modes of transmission on a contact network. The network is given by a random graph following a multilayer configuration model where edges in different layers correspond to potentially infectious contacts of different types. We assume that the graph structure evolves in response to the epidemic via activation or deactivation of edges. We derive a large graph limit theorem that gives a system of ordinary differential equations (ODEs) describing the evolution of quantities of interest, such as the proportions of infected and susceptible vertices, as the number of nodes tends to infinity. Analysis of the limiting system elucidates how the coupling of edge activation and deactivation to infection status affects disease dynamics, as illustrated by a two-layer network example with edge types corresponding to community and healthcare contacts. Our theorem extends some earlier results deriving the deterministic limit of stochastic SIR processes on static, single-layer configuration model graphs. We also describe precisely the conditions for equivalence between our limiting ODEs and the systems obtained via pair approximation, which are widely used in the epidemiological and ecological literature to approximate disease dynamics on networks. Potential applications include modeling Ebola dynamics in West Africa, which was the motivation for this study.
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