We consider the effect of a nonvanishing fraction of initially infected nodes (seeds) on the SIR epidemic model on random networks. This is relevant when, for example, the number of arriving infected individuals is large, but also to the modeling of a large number of infected individuals, but also to more general situations such as the spread of ideas in the presence of publicity campaigns. This model is frequently studied by mapping to a bond percolation problem, in which edges in the network are occupied with the probability, $p$, of eventual infection along an edge connecting an infected individual to a susceptible neighbor. This approach allows one to calculate the total final size of the infection and epidemic threshold in the limit of a vanishingly small seed fraction. We show, however, that when the initial infection occupies a nonvanishing fraction $f$ of the network, this method yields ambiguous results, as the correspondence between edge occupation and contagion transmission no longer holds. We propose instead to measure the giant component of recovered individuals within the original contact network. This has an unambiguous interpretation and correctly captures the dependence of the epidemic size on $f$. We give exact equations for the size of the epidemic and the epidemic threshold in the infinite size limit. We observe a second order phase transition as in the original formulation, however with an epidemic threshold which decreases with increasing $f$. When the seed fraction $f$ tends to zero we recover the standard results.
The SIR infection theory initiated by Kermack-Mckendrick in 1927 discusses the infection in an isolated population with uniform properties such as the uniform population distribution. In the infection, there exist two aspects: (1) The quantitative aspect and (2) the temporal aspect. Since the SIR theory is a mean-field theory, it can't match both aspects simultaneously. If the quantitative aspect is matched, the temporal aspect can't be matched, versa. The infection starts from a cluster, and it spreads to different places increasing the size of the infection. In general, even in the case of t…
We study the problem of identifying a single infection source in a network under the susceptible-infected-recovered-infected (SIRI) model. We describe the infection model via a state-space model, and utilizing a state propagation approach, we derive an algorithm known as the heterogeneous infection spreading source (HISS) estimator, to infer the infection source. The HISS estimator uses the observations of node states at a particular time, where the elapsed time from the start of the infection is unknown. It is able to incorporate side information (if any) of the observed states of a subset of…
Transmission rates in epidemic outbreaks may vary over time depending on the societal response. Non-pharmacological mitigation strategies such as social distancing and the adoption of protective equipment aim precisely at reducing transmission rates by reducing infectious contacts. To investigate the effects of mitigation strategies on the evolution of epidemics, nonlinear transmission rates that are influenced by the levels of infections, deaths or recoveries have been included in many variants of the classical SIR model. This class of models is particularly relevant to the COVID-19 epidemic,…
We study the phase transition from the persistence phase to the extinction phase for the SIRS (susceptible/ infected/ refractory/ susceptible) model of diseases spreading on the networks. We derive an analytical expression of the probability for the descendants nodes to re-infect their ancestors nodes. We find that, in the case of the recovery time $τ_R$ is larger than the infection time $τ_I$, the infection will flow directionally from the ancestors to the descendants however, the descendants will not able to reinfect their ancestors during their infection time. This behavior leads us to dedu…
Epidemics like Covid-19 and Ebola have impacted people's lives significantly. The impact of mobility of people across the countries or states in the spread of epidemics has been significant. The spread of disease due to factors local to the population under consideration is termed the endogenous spread. The spread due to external factors like migration, mobility, etc. is called the exogenous spread. In this paper, we introduce the Exo-SIR model, an extension of the popular SIR model and a few variants of the model. The novelty in our model is that it captures both the exogenous and endogenous …
Analysis of non pharmaceutical interventions with SIR epidemic models: decreasing the infection peak vs. minimizing the epidemic size
Instituto Balseiro, Universidad Nacional de Cuyo（巴塞尔罗研究所，门多萨国立大学）；Comisión Nacional de Energía Atómica（国家原子能委员会）；Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET)（国家科学研究委员会）；Centro Atómico Bariloche (CNEA)（巴里洛切原子中心）
Finding the infection sources in a network when we only know the network topology and infected nodes, but not the rates of infection, is a challenging combinatorial problem, and it is even more difficult in practice where the underlying infection spreading model is usually unknown a priori. In this paper, we are interested in finding a source estimator that is applicable to various spreading models, including the Susceptible-Infected (SI), Susceptible-Infected-Recovered (SIR), Susceptible-Infected-Recovered-Infected (SIRI), and Susceptible-Infected-Susceptible (SIS) models. We show that under …
In this paper, we introduce a general framework for co-infection as cooperative SIR dynamics. We first solve analytically CGCG model [1] and then the generalized model in symmetric scenarios. We calculate transition points, order parameter, i.e. total number of infected hosts. Also we show analytically there is a saddle-node bifurcation for two cooperative SIR dynamics and the transition is hybrid. Moreover, we investigate where symmetric solution is stable for initial fluctuations. Then we study asymmetric cases of parameters. The more asymmetry, for the primary and secondary infection rates …
In this article, we discuss an age-structured SIR model in which disease not only spread through direct person to person contacts for e.g. infection due to surface contamination but it can also spread through indirect contacts. It is evident that age also plays a crucial role in SARS virus infection including COVID-19 infection. We formulate our model as an abstract semilinear Cauchy problem in an appropriate Banach space to show the existence of solution and also show the existence of steady states. It is assumed in this work that the population is in a demographic stationary state and show t…
We introduce an epidemic spreading model on a network using concepts from percolation theory. The model is motivated by discussing the standard SIR model, with extensions to describe effects of lockdowns within a population. The underlying ideas and behavior of the lattice model, implemented using the same lockdown scheme as for the SIR scheme, are discussed in detail and illustrated with extensive simulations. A comparison between both models is presented for the case of COVID-19 data from the USA. Both fits to the empirical data are very good, but some differences emerge between the two appr…
In this article, we model and study the spread of COVID-19 in Germany, Japan, India and highly impacted states in India, i.e., in Delhi, Maharashtra, West Bengal, Kerala and Karnataka. We consider recorded data published in Worldometers and COVID-19 India websites from April 2020 to July 2021, including periods of interest where these countries and states were hit severely by the pandemic. Our methodology is based on the classic susceptible-infected-removed (SIR) model and can track the evolution of infections in communities, where we (a) allow for the susceptible and infected populations to b…
We propose a novel SIR epidemic model which is driven by the transmission of infection packets in networks. Specifically, infected nodes generate and deliver infection packets causing the spread of the epidemic, while recovered nodes block the delivery of infection packets, and this inhibits the epidemic spreading. The efficient routing protocol governed by a control parameter $α$ is used in the packet transmission. We obtain the maximum instantaneous population of infected nodes, the maximum population of ever infected nodes, as well as the corresponding optimal $α$ through simulation. We fin…
Mathematical models of infectious diseases exhibit robust dynamics such as stable endemic or a disease-free equilibrium, or convergence of the solutions to periodic epidemic waves. The present work shows that the accuracy of such dynamics can be significantly improved by incorporating both local and global dynamics of the infection in disease models. To demonstrate improved accuracies, we extended a standard Susceptible-Infected-Recovered (SIR) model by incorporating global dynamics of the COVID-19 pandemic. The extended SIR model assumes three possibilities for the susceptible individuals tra…
Cator and Van Mieghem [Cator E, Van Mieghem P., Phys. Rev. E 89, 052802 (2014)] stated that the correlation of infection at the same time between any pair of nodes in a network is non-negative for the Markovian SIS and SIR epidemic models. The arguments used to obtain this result rely strongly on the graphical construction of the stochastic process, as well as the FKG inequality. In this note we show that although the approach used by the authors applies to the SIS model, it cannot be used for the SIR model as stated in their work. In particular, we observe that monotonicity in the process is …
Policy-makers require data-driven tools to assess the spread of COVID-19 and inform the public of their risk of infection on an ongoing basis. We propose a rigorous hybrid model-and-data-driven approach to risk scoring based on a time-varying SIR epidemic model that ultimately yields a simplified color-coded risk level for each community. The risk score $Γ_t$ that we propose is proportional to the probability of someone currently healthy getting infected in the next 24 hours. We show how this risk score can be estimated using another useful metric of infection spread, $R_t$, the time-varying a…
We introduce a new method to efficiently approximate the number of infections resulting from a given initially-infected node in a network of susceptible individuals. Our approach is based on counting the number of possible infection walks of various lengths to each other node in the network. We analytically study the properties of our method, in particular demonstrating different forms for SIS and SIR disease spreading (e.g. under the SIR model our method counts self-avoiding walks). In comparison to existing methods to infer the spreading efficiency of different nodes in the network (based on…
The non-population conserving SIR (SIR-NC) model to describe the spread of infections in a community is proposed and studied. Unlike the standard SIR model, SIR-NC does not assume population conservation. Although similar in form to the standard SIR, SIR-NC admits a closed form solution while allowing us to model mortality, and also provides different, and arguably a more realistic, interpretation of the model parameters. Numerical comparisons of this SIR-NC model with the standard, population conserving, SIR model are provided. Extensions to include imported infections, interacting communitie…
We study epidemic processes with immunization on very large 1-dimensional lattices, where at least some of the infections are non-local, with rates decaying as power laws p(x) ~ x^{-sigma-1} for large distances x. When starting with a single infected site, the cluster of infected sites stays always bounded if $σ>1$ (and dies with probability 1, of its size is allowed to fluctuate down to zero), but the process can lead to an infinite epidemic for sigma <1. For sigma <0 the behavior is essentially of mean field type, but for 0 < sigma <= 1 the behavior is non-trivial, both for the critical and …
We study the phase transition from the persistence phase to the extinction phase for the SIRS (susceptible/ infected/ refractory/ susceptible) model of diseases spreading on small world network. We show the effects of all the parameters associated with this model on small world network and we create the full phase space. The results we obtained are consistent with those obtained in Ref.[7] in terms of the existence of a phase transition from a fluctuating endemic state to self-sustained oscillations in the size of the infected subpopulation at a finite value of the disorder of the network. And…
The concept of the effective infection opportunity population (EIOP) was incorporated into the SIQR model, and it was assumed that this EIOP would change with the spread of infection, and this was named as the effective SIQR model. When calculated with this model, the uninfected population S decreases with the passage of time. However, when the EIOP N increases because of any reason, the infection threshold becomes larger than 1. Even after the first wave seems to have subsided, the infection begins to spread again. Firstly, we find the curve of EIOP change so that the calculation result by th…
This paper studies the problem of detecting the information source in a network in which the spread of information follows the popular Susceptible-Infected-Recovered (SIR) model. We assume all nodes in the network are in the susceptible state initially except the information source which is in the infected state. Susceptible nodes may then be infected by infected nodes, and infected nodes may recover and will not be infected again after recovery. Given a snapshot of the network, from which we know all infected nodes but cannot distinguish susceptible nodes and recovered nodes, the problem is t…
Studies on how to model the interplay between diseases and behavioral responses (so-called coupled disease-behavior interaction) have attracted increasing attention. Owing to the lack of obvious clinical evidence of diseases, or the incomplete information related to the disease, the risks of infection cannot be perceived and may lead to inappropriate behavioral responses. Therefore, how to quantitatively analyze the impacts of asymptomatic infection on the interplay between diseases and behavioral responses is of particular importance. In this Letter, under the complex network framework, we st…
The classic SIR model of epidemic dynamics is solved completely by quadratures, including a time integral transform expanded in a series of incomplete gamma functions. The model is also generalized to arbitrary time-dependent infection rates and solved explicitly when the control parameter depends on the accumulated infections at time $t$. Numerical results are presented by way of comparison. Autonomous and non-autonomous generalizations of SIR for interacting regions are also considered, including non-separability for two or more interacting regions. A reduction of simple SIR models to one va…
Infectious diseases spread through human networks. Susceptible-Infected-Removed (SIR) model is one of the epidemic models to describe infection dynamics on a complex network connecting individuals. In the metapopulation SIR model, each node represents a population (group) which has many individuals. In this paper, we propose a modified metapopulation SIR model in which a latent period is taken into account. We call it SIIR model. We divide the infection period into two stages: an infected stage, which is the same as the previous model, and a seriously ill stage, in which individuals are infect…
The Susceptible-Infected-Recovered (SIR) model has successfully mimicked the propagation of such airborne diseases as influenza A (H1N1). Although the SIR model has recently been studied in a multilayer networks configuration, in almost all the research the isolation of infected individuals is disregarded. Hence we focus our study in an epidemic model in a two-layer network, and we use an isolation parameter to measure the effect of isolating infected individuals from both layers during an isolation period. We call this process the Susceptible-Infected-Isolated-Recovered ($SI_IR$) model. The i…
We propose two SIR models which incorporate sociological behavior of groups of individuals. It is these differences in behaviors which impose different infection rates on the individual susceptible populations, rather than biological differences. We compute the basic reproduction number for each model, as well as analyze the sensitivity of $R_0$ to changes in sociological parameter values.
The spread of an infectious disease depends on intrinsic properties of the disease as well as the connectivity and actions of the population. This study investigates the dynamics of an SIR type model which accounts for human tendency to avoid infection while also maintaining preexisting, interpersonal relationships. Specifically, we use a network model in which individuals probabilistically deactivate connections to infected individuals and later reconnect to the same individuals upon recovery. To analyze this network model, a mean field approximation consisting of a system of fourteen ordinar…
The Susceptible-Infectious-Recovered (SIR) model is the canonical model of epidemics of infections that make people immune upon recovery. Many of the open questions in computational epidemiology concern the underlying contact structure's impact on models like the SIR model. Temporal networks constitute a theoretical framework capable of encoding structures both in the networks of who could infect whom and when these contacts happen. In this article, we discuss the detailed assumptions behind such simulations -- how to make them comparable with analytically tractable formulations of the SIR mod…
This paper introduces a theoretical framework for the analysis and control of the stochastic susceptible-infected-removed (SIR) spreading process over a network of heterogeneous agents. In our analysis, we analyze the exact networked Markov process describing the SIR model, without resorting to mean-field approximations, and introduce a convex optimization framework to find an efficient allocation of resources to contain the expected number of accumulated infections over time. Numerical simulations are presented to illustrate the effectiveness of the obtained results.
This paper utilizes a stochastic Susceptible-Infected-recovered (SIR) model with a non-linear incidence rate to perform a detailed mathematical study of optimal lock-down intensity and vaccination rate under the COVID-19 pandemic environment. We use a Feynman-type path integral control approach to determine a Fokker-Plank type equation of this system. Since we assume the availability of information on the COVID-19 pandemic is complete and perfect, we can show a unique fixed point. A non-linear incidence rate is used because, it can be raised from saturation effects that if the proportion of in…
Spatially explicit models have been widely used in today's mathematical ecology and epidemiology to study persistence and extinction of populations as well as their spatial patterns. Here we extend the earlier work--static dispersal between neighbouring individuals to mobility of individuals as well as multi-patches environment. As is commonly found, the basic reproductive ratio is maximized for the evolutionary stable strategy (ESS) on diseases' persistence in mean-field theory. This has important implications, as it implies that for a wide range of parameters that infection rate will tend ma…
We study the effect of external infection sources on phase transitions in epidemic processes. In particular, we consider an epidemic spreading on a network via the SIS/SIR dynamics, which in addition is aided by external agents - sources unconstrained by the graph, but possessing a limited infection rate or virulence. Such a model captures many existing models of externally aided epidemics, and finds use in many settings - epidemiology, marketing and advertising, network robustness, etc. We provide a detailed characterization of the impact of external agents on epidemic thresholds. In particul…
The epidemic curve and the final extent of the COVID-19 pandemic are usually predicted from the rate of early exponential raising using the SIR model. These predictions implicitly assume a full social mixing, which is not plausible generally. Here I am showing a counterexample to the these predictions, based on random propagation of an epidemic in Barabási--Albert scale-free network models. The start of the epidemic suggests $R_0=2.6$, but unlike $Ω\approx 70\%{}$ predicted by the SIR model, they reach a final extent of only $Ω\approx 4\%{}$ without external mitigation and $Ω\approx 0.5$--$1.5…
In the Susceptible-Infectious-Recovered (SIR) model of disease spreading, the time to extinction of the epidemics happens at an intermediate value of the per-contact transmission probability. Too contagious infections burn out fast in the population. Infections that are not contagious enough die out before they spread to a large fraction of people. We characterize how the maximal extinction time in SIR simulations on networks depend on the network structure. For example we find that the average distances in isolated components, weighted by the component size, is a good predictor of the maximal…
We numerically study the dynamics of the SIR disease model on small-world networks by using a large-deviation approach. This allows us to obtain the probability density function of the total fraction of infected nodes and of the maximum fraction of simultaneously infected nodes down to very small probability densities like $10^{-2500}$. We analyze the structure of the disease dynamics and observed three regimes in all probability density functions, which correspond to quick mild, quick extremely severe and sustained severe dynamical evolutions, respectively. Furthermore, the mathematical rate …
We study dynamics of a variant of the SIR the model, where we assume that individuals respond differently to dynamics of the epidemic. Their heterogeneous response is modeled by the Preisach hysteresis operator. The degree of heterogeneity of the response is measured by the variance $σ^2$ of the corresponding distribution (the Preisach density function). The proposed model has a continuum of endemic equilibrium states characterized by different proportions of susceptible, infected and recovered populations. We consider how the limit point of the epidemic trajectory and the infection peak along…
In this work we study a modified Susceptible-Infected-Susceptible (SIS) model in which the infection rate $λ$ decays exponentially with the number of reinfections $n$, saturating after $n=l$. We find a critical decaying rate $ε_{c}(l)$ above which a finite fraction of the population becomes permanently infected. From the mean-field solution and computer simulations on hypercubic lattices we find evidences that the upper critical dimension is 6 like in the SIR model, which can be mapped in ordinary percolation.
Cities have long served as nucleating centers for human development and advancement. Cities have facilitated the spread of both human creativity and human disease, and at the same time, efforts to minimize the spread of disease have influenced the design of cities. The purpose of this paper is to explore the dynamics of epidemics on networks in order to help design a multi-network city of the future aimed at minimizing the spread of epidemics. In order to do this, we start with the SIR model (susceptible, infected, removed) on a network in which nodes represent cities or regions and edges are …
In contrast to the common assumption in epidemic models that the rate of infection between individuals is constant, in reality, an individual's viral load determines their infectiousness. We compare the average and individual reproductive numbers and epidemic dynamics for a model incorporating time-dependent infectiousness and a standard SIR model for both fully-mixed and category-mixed populations. We find that the reproductive number only depends on the total infectious exposure and the largest eigenvalue of the mixing matrix and that these two effects are independent of each other. When we …
We investigate phase transitions associated with three control methods for epidemics on small world networks. Motivated by the behavior of SARS-CoV-2, we construct a theoretical SIR model of a virus that exhibits presymptomatic, asymptomatic, and symptomatic stages in two possible pathways. Using agent-based simulations on small world networks, we observe phase transitions for epidemic spread related to: 1) Global social distancing with a fixed probability of adherence. 2) Individually initiated social isolation when a threshold number of contacts are infected. 3) Viral shedding rate. The prim…
We examine how the behaviour of high degree vertices in a network affects whether an infection spreads through communities or jumps between them. We study two stochastic susceptible-infected-recovered (SIR) processes and represent our network with a spatial preferential attachment (SPA) network. In one of the two epidemic scenarios we adjust the contagiousness of high degree vertices so that they are less contagious. We show that, for this scenario, the infection travels through communities rather than jumps between them. We conjecture that this is not the case in the other scenario, when cont…
The epidemic spreading on arbitrary complex networks is studied in SIR (Susceptible Infected Recovered) compartment model. We propose our implementation of a Naive SIR algorithm for epidemic simulation spreading on networks that uses data structures efficiently to reduce running time. The Naive SIR algorithm models full epidemic dynamics and can be easily upgraded to parallel version. We also propose novel algorithm for epidemic simulation spreading on networks called the FastSIR algorithm that has better average case running time than the Naive SIR algorithm. The FastSIR algorithm uses novel …
Case isolation, that is, detection and isolation of infected individuals in order to prevent spread, is a strategy to curb infectious disease epidemics. Here, we study the efficiency of a case isolation strategy subject to time delays in terms of its ability to stabilize the epidemic spread in heterogeneous contact networks. For an SIR epidemic model, we characterize the stability boundary analytically and show how it depends on the time delay between infection and isolation as well as the heterogeneity of the inter-individual contact network, quantified by the variance in contact rates. We sh…
Motivated by the ongoing pandemic COVID-19, we propose a closed-loop framework that combines inference from testing data, learning the parameters of the dynamics and optimal resource allocation for controlling the spread of the susceptible-infected-recovered (SIR) epidemic on networks. Our framework incorporates several key factors present in testing data, such as the fact that high risk individuals are more likely to undergo testing. We then present two tractable optimization problems to evaluate the trade-off between controlling the growth-rate of the epidemic and the cost of non-pharmaceuti…
An ultrametric model of epidemic spread of infections based on the classical SIR model is proposed. Ultrametrics on a set of individuals based on theire hierarchical clustering relativly to the average time of infectious contact is introduced. The general equations of the ultrametric SIR model are written down and their particular implementation using $p$-adic parameterization is presented. A numerical analysis of the $p$-adic SIR model and a comparison of its behavior with the classical SIR model are performed. The concept of hierarchical isolation and the scenario of its management in order …
Waiting times between two consecutive infection and recovery events in spreading processes are often assumed to be exponentially distributed, which results in Markovian (i.e., memoryless) continuous spreading dynamics. However, this is not taking into account memory (correlation) effects and discrete interactions that have been identified as relevant in social, transportation, and disease dynamics. We introduce a framework to model continuous, discrete, and hybrid forms of (non-)Markovian susceptible-infected-recovered (SIR) stochastic processes on networks. The hybrid SIR processes that we st…
We study the SIR epidemiological model, with a variable contagion rate, applied to the evolution of COVID19 in Cuba. It is highlighted that an increase in the predictive character depends on understanding the dynamics for the temporal evolution of the rate of contagion $β^*$. A semi-empirical model for this dynamics is formulated, where reaching $β^*\approx0$ due to isolation is achieved after the mean duration of the disease $τ=1/γ$, in which the number of infected in the confined families has decreased. It is considered that $β^*(t)$ should have an abrupt decrease on the day of initiation of…
Empirical studies suggest that contact patterns follow heterogeneous inter-event times, meaning that intervals of high activity are followed by periods of inactivity. Combined with birth and death of individuals, these temporal constraints affect the spread of infections in a non-trivial way and are dependent on the particular contact dynamics. We propose a stochastic model to generate temporal networks where vertices make instantaneous contacts following heterogeneous inter-event times, and leave and enter the system at fixed rates. We study how these temporal properties affect the prevalence…
We consider a very general stochastic model for an SIR epidemic on a network which allows an individual's infectious period, and the time it takes to contact each of its neighbours after becoming infected, to be correlated. We write down the message passing system of equations for this model and prove, for the first time, that it has a unique feasible solution. We also generalise an earlier result by proving that this solution provides a rigorous upper bound for the expected epidemic size (cumulative number of infection events) at any fixed time $t>0$. We specialise these results to a homogene…
Epidemic models are increasingly used in real-world networks to understand diffusion phenomena (such as the spread of diseases, emotions, innovations, failures) or the transport of information (such as news, memes in social on-line networks). A new analysis of the prevalence, the expected number of infected nodes in a network, is presented and physically interpreted. The analysis method is based on spectral decomposition and leads to a universal, analytic curve, that can bound the time-varying prevalence in any finite time interval. Moreover, that universal curve also applies to various types …
