The interplay of biological, social, structural and random factors makes disease forecasting extraordinarily complex. The course of an epidemic exhibits average growth dynamics determined by features of the pathogen and the population, yet also features significant variability reflecting the stochastic nature of disease spread. In this work, we reframe a stochastic branching process analysis in terms of probability generating functions and compare it to continuous time epidemic simulations on networks. In doing so, we predict the diversity of emerging epidemic courses on both homogeneous and heterogeneous networks. We show how the challenge of inferring the early course of an epidemic falls on the randomness of disease spread more so than on the heterogeneity of contact patterns. We provide an analysis which helps quantify, in real time, the probability that an epidemic goes supercritical or conversely, dies stochastically. These probabilities are often assumed to be one and zero, respectively, if the basic reproduction number, or R0, is greater than 1, ignoring the heterogeneity and randomness inherent to disease spread. This framework can give more insight into early epidemic spread by weighting standard deterministic models with likelihood to inform pandemic preparedness with probabilistic forecasts.
In this paper, we investigate the epidemic spreading for SIR model in weighted scale-free networks with nonlinear infectivity, where the transmission rate in our analytical model is weighted. Concretely, we introduce the infectivity exponent $α$ and the weight exponent $β$ into the analytical SIR model, then examine the combination effects of $α$ and $β$ on the epidemic threshold and phase transition. We show that one can adjust the values of $α$ and $β$ to rebuild the epidemic threshold to a finite value, and it is observed that the steady epidemic prevalence $R$ grows in an exponential form …
We propose a targeted intervention protocol where recovery is restricted to individuals that have the least number of infected neighbours. Our recovery strategy is highly efficient on any kind of network, since epidemic outbreaks are minimal when compared to the baseline scenario of spontaneous recovery. In the case of spatially embedded networks, we find that an epidemic stays strongly spatially confined with a characteristic length scale undergoing a random walk. We demonstrate numerically and analytically that this dynamics leads to an epidemic spot with a flat surface structure and a radiu…
We study Susceptible-Exposed-Asymptomatic-Infectious-Recovered (SEAIR) epidemic spreading model of COVID-19. It captures two important characteristics of the infectiousness of COVID-19: delayed start and its appearance before onset of symptoms, or even with total absence of them. The model is theoretically analyzed in continuous-time compartmental version and discrete-time version on random regular graphs and complex networks. We show analytically that there are relationships between the epidemic thresholds and the equations for the susceptible populations at the endemic equilibrium in all thr…
Drug resistance and strong contacts actually play crucial roles in epidemic spread in complex systems. Nevertheless, neither theoretical model or methodology is proposed to address this. We thus consider an edge-based epidemic spread model considering the two key ingredients, in which the contacts are grouped into two classes: strong contacts and normal ones. Next, we present a unified edge-based compartmental approach to the spread dynamics on Erdös-Rényi (ER) networks and validate its results by extensive numerical simulations. In case that epidemic is totally drug-resistant, we both numeric…
In this paper, we study the interplay between individual behaviors and epidemic spreading in a dynamical network. We distribute agents on a square-shaped region with periodic boundary conditions. Every agent is regarded as a node of the network and a wireless link is established between two agents if their geographical distance is less than a certain radius. At each time, every agent assesses the epidemic situation and make decisions on whether it should stay in or leave its current place. An agent will leave its current place with a speed if the number of infected neighbors reaches or exceeds…
Just like the degrees of human and animal interaction networks, the distribution of the times between interactions is known to often be right-skewed and fat-tailed. Both these distributions affect epidemic dynamics strongly, but, as we show in this Letter, for very different reasons. Whereas the high degrees of the tail are critical for facilitating epidemics, it is the small interevent times that control the dynamics of epidemics. We investigate this effect both analytically and numerically for different versions of the Susceptible-Infected-Recovered model on different types of networks.
Understanding and predicting outbreaks of contagious diseases are crucial to the development of society and public health, especially for underdeveloped countries. However, challenging problems are encountered because of complex epidemic spreading dynamics influenced by spatial structure and human dynamics (including both human mobility and human interaction intensity). We propose a systematical model to depict nationwide epidemic spreading in Côte d'Ivoire, which integrates multiple factors, such as human mobility, human interaction intensity, and demographic features. We provide insights to …
A configuration model for epidemic spread, based on a scale-free network, is introduced. We obtain the analytical solutions describing both unstable and stable dynamics of the epidemic spreading, and demonstrate how these regimes can interchange during the epidemic. We apply the model to the COVID-19 case and demonstrate the predictive features of our model.
We study a susceptible-vaccinated--infected--recovered (SVIR) epidemic-spreading model with diversity of infection rate of the individuals. By means of analytical arguments as well as extensive computer simulations, we demonstrate that the heterogeneity in infection rate can either impede or accelerate the epidemic spreading, which depends on the amount of vaccinated individuals introduced in the population as well as the contact pattern among the individuals. Remarkably, as long as the individuals with different capability of acquiring the disease interact with unequal frequency, there always…
On the base of logic discrete equations system mathematical modeling of COVID-19 epidemic spread was carried out in the world and in the countries with the largest number of infected people such as the USA, Brasil, Russia and India in the first half of 2020. It was shown that for the countries with strong restrictive measures the spread of COVID-19 fit on a single wave with small capacity as for a number of countries with violation of restrictive measures the spread of the epidemic fit on a waves superposition. For countries with large population mixing, the spread of the epidemic today also f…
In the present work the spread of epidemic is studied over complex networks which are characterized by power law degree distribution of links and heterogeneous rate of disease transmission. The random allocation of epidemic transmission rates to the nodes results in the heterogeneity, which in turn causes the segregation of nodes in terms of various sub populations. The aim of the study is to gain microscopic insight into the effect of interactions among various sub populations in the spreading processes of disease over such networks. The discrete time Markov chain method based upon the suscep…
We review and introduce a generalized reaction-diffusion approach to epidemic spreading in a metapopulation modeled as a complex network. The metapopulation consists of susceptible and infected individuals that are grouped in subpopulations symbolising cities and villages that are coupled by human travel in a transportation network. By analytic methods and numerical simulations we calculate the fraction of infected people in the metaopoluation in the long time limit, as well as the relevant parameters characterising the epidemic threshold that separates an epidemic from a non-epidemic phase. W…
In this paper, the authors develop a method of detecting correlations between epidemic patterns in different regions that are due to human movement and introduce a null model in which the travel-induced correlations are cancelled. They apply this method to the well-documented cases of seasonal influenza outbreaks in the United States and France. In the United States (using data for 1972-2002), the authors observed strong short-range correlations between several states and their immediate neighbors, as well as robust long-range spreading patterns resulting from large domestic air-traffic flows.…
We develop a generalized group-based epidemic model (GgroupEM) framework for any compartmental epidemic model (for example; susceptible-infected-susceptible, susceptible-infected-recovered, susceptible-exposed-infected-recovered). Here, a group consists of a collection of individual nodes. This model can be used to understand the important dynamic characteristics of a stochastic epidemic spreading over very large complex networks, being informative about the state of groups. Aggregating nodes by groups, the state space becomes smaller than the individual-based approach at the cost of aggregati…
We propose a theoretical framework for the study of epidemics in structured metapopulations, with heterogeneous agents, subjected to recurrent mobility patterns. We propose to represent the heterogeneity in the composition of the metapopulations as layers in a multiplex network, where nodes would correspond to geographical areas and layers account for the mobility patterns of agents of the same class. We analyze both the classical Susceptible-Infected-Susceptible and the Susceptible-Infected-Removed epidemic models within this framework, and compare macroscopic and microscopic indicators of th…
Epidemic spread in a population is traditionally modeled via compartmentalized models which represent the free evolution of disease in absence of any intervention policies. In addition, these models assume full observability of disease cases and do not account for under-reporting. We present a mathematical model, namely PolSIRD, which accounts for the under-reporting by introducing an observation mechanism. It also captures the effects of intervention policies on the disease spread parameters by leveraging intervention policy data along with the reported disease cases. Furthermore, we allow ou…
Resource support between individuals is of particular importance in controlling or mitigating epidemic spreading, especially during pandemics. Whereas there remains the question of how we can protect ourselves from being infected while helping others by donating resources in fighting against the epidemic. To answer the question, we propose a novel resource allocation model by considering the awareness of self-protection of individuals. In the model, a tuning parameter is introduced to quantify the reaction strength of individuals when they are aware of the disease. And then, a coupled model of…
In December 2019, COVID-19 were detected in Wuhan City, Hubei Province of China. SARS-CoV-2 rapidly spread to the whole Chinese mainland with the people during the Chinese Spring Festival Travel Rush. As of 19 February 2020, 74576 confirmed cases of COVID-19 had been reported in Chinese Mainland. What kind of cities have more confirmed cases, and is there any relationship between GDP and confirmed cases? In this study, we explored the relationship between the confirmed cases of COVID-19 and GDP at the prefectural-level, found a positive correlation between them. This finding warns high GDP are…
In this work, we address a multicoupled dynamics on complex networks with tunable structural segregation. Specifically, we work on a networked epidemic spreading under a vaccination campaign with agents in favor and against the vaccine. Our results show that such coupled dynamics exhibits a myriad of phenomena such as nonequilibrium transitions accompanied by bistability. Besides we observe the emergence of an intermediate optimal segregation level where the community structure enhances negative opinions over vaccination but counterintuitively hinders - rather than favoring - the global diseas…
For preventing the spread of epidemics such as the coronavirus disease COVID-19, social distancing and the isolation of infected persons are crucial. However, existing reaction-diffusion equations for epidemic spreading are incapable of describing these effects. We present an extended model for disease spread based on combining an SIR model with a dynamical density functional theory where social distancing and isolation of infected persons are explicitly taken into account. The model shows interesting nonequilibrium phase separation associated with a reduction of the number of infections, and …
In the study of disease spreading on empirical complex networks in SIR model, initially infected nodes can be ranked according to some measure of their epidemic impact. The highest ranked nodes, also referred to as "superspreaders", are associated to dominant epidemic risks and therefore deserve special attention. In simulations on studied empirical complex networks, it is shown that the ranking depends on the dynamical regime of the disease spreading. A possible mechanism leading to this dependence is illustrated in an analytically tractable example. In systems where the allocation of resourc…
The compartmental models used to study epidemic spreading often assume the same susceptibility for all individuals, and are therefore, agnostic about the effects that differences in susceptibility can have on epidemic spreading. Here we show that--for the SIS model--differential susceptibility can make networks more vulnerable to the spread of diseases when the correlation between a node's degree and susceptibility are positive, and less vulnerable when this correlation is negative. Moreover, we show that networks become more likely to contain a pocket of infection when individuals are more li…
When an epidemic spreads in a population, individuals may adaptively change the structure of their social contact network to reduce risk of infection. Here we study the spread of an epidemic on an adaptive network with community structure. We model the effect of two communities with different average degrees. The disease model is susceptible-infected-susceptible (SIS), and adaptation is rewiring of links between susceptibles and infectives. The bifurcation structure is obtained, and a mean field model is developed that accurately predicts the steady state behavior of the system. We show that a…
Deterministic models are developed for the spatial spread of epidemic diseases in geographical settings. The models are focused on outbreaks that arise from a small number of infected hosts imported into sub-regions of the geographical settings. The goal is to understand how spatial heterogeneity influences the transmission dynamics of the susceptible and infected populations. The models consist of systems of partial differential equations with diffusion terms describing the spatial spread of the underlying microbial infectious agents. The model is compared with real data from seasonal influen…
Passenger contact in public transit (PT) networks can be a key mediate in the spreading of infectious diseases. This paper proposes a time-varying weighted PT encounter network to model the spreading of infectious diseases through the PT systems. Social activity contacts at both local and global levels are also considered. We select the epidemiological characteristics of coronavirus disease 2019 (COVID-19) as a case study along with smart card data from Singapore to illustrate the model at the metropolitan level. A scalable and lightweight theoretical framework is derived to capture the time-v…
Time-varying network topologies can deeply influence dynamical processes mediated by them. Memory effects in the pattern of interactions among individuals are also known to affect how diffusive and spreading phenomena take place. In this paper we analyze the combined effect of these two ingredients on epidemic dynamics on networks. We study the susceptible-infected-susceptible (SIS) and the susceptible-infected-removed (SIR) models on the recently introduced activity-driven networks with memory. By means of an activity-based mean-field approach we derive, in the long time limit, analytical pre…
The spread of infectious epidemics is often accelerated by super-spreader events. Understanding their effect is important, particularly in the context of standard epidemiological models, which require estimates for parameters such as $R_0$. In this letter, we show that the effective value of $R_0$ in super-spreader situations is significantly large, of the order of hundreds, suggesting a delta-function-like behavior during the event. Use of a well-mixed room model supports these findings. They elucidate infection kinetic modeling in enclosed environments, which differ from the standard SIR mod…
University of Oxford（牛津大学）；Massachusetts Institute of Technology (MIT)（麻省理工学院）；TU Delft（代尔夫特理工大学）；German Aerospace Center (DLR)（德国航空航天中心）；Proxima Robotics srl（普罗xima机器人有限公司）
When an epidemic spreads into a population, it is often unpractical or impossible to have a continuous monitoring of all subjects involved. As an alternative, algorithmic solutions can be used to infer the state of the whole population from a limited amount of measures. We analyze the capability of deep neural networks to solve this challenging task. Our proposed architecture is based on Graph Convolutional Neural Networks. As such it can reason on the effect of the underlying social network structure, which is recognized as the main component in the spreading of an epidemic. We test the propo…
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 …
Knowing which individuals can be more efficient in spreading a pathogen throughout a determinate environment is a fundamental question in disease control. Indeed, over the last years the spread of epidemic diseases and its relationship with the topology of the involved system have been a recurrent topic in complex network theory, taking into account both network models and real-world data. In this paper we explore possible correlations between the heterogeneous spread of an epidemic disease governed by the susceptible-infected-recovered (SIR) model, and several attributes of the originating ve…
Initially emerged in the Chinese city Wuhan and subsequently spread almost worldwide causing a pandemic, the SARS-CoV-2 virus follows reasonably well the SIR (Susceptible-Infectious-Recovered) epidemic model on contact networks in the Chinese case. In this paper, we investigate the prediction accuracy of the SIR model on networks also for Italy. Specifically, the Italian regions are a metapopulation represented by network nodes and the network links are the interactions between those regions. Then, we modify the network-based SIR model in order to take into account the different lockdown measu…
Epidemic spreading of infectious diseases is ubiquitous and has often considerable impact on public health and economic wealth. The large variability in spatio-temporal patterns of epidemics prohibits simple interventions and demands for a detailed analysis of each epidemic with respect to its infectious agent and the corresponding routes of transmission. To facilitate this analysis, a mathematical framework is introduced which links epidemic patterns to the topology and dynamics of the underlying transmission network. The evolution both in disease prevalence and transmission network topology …
We propose a dynamical model for describing the spread of epidemics. This model is an extension of the SIQR (susceptible-infected-quarantined-recovered) and SIRP (susceptible-infected-recovered-pathogen) models used earlier to describe various scenarios of epidemic spreading. As compared to the basic SIR model, our model takes into account two possible routes of contagion transmission: direct from the infected compartment to the susceptible compartment and indirect via some intermediate medium or fomites. Transmission rates are estimated in terms of average distances between the individuals in…
Effects of predators of juvenile mice on the spread of the Hantavirus are analyzed in the context of a recently proposed model. Two critical values of the predation probability are identified. When the smaller of them is exceeded, the hantavirus infection vanishes without extinguishing the mice population. When the larger is exceeded, the entire mice population vanishes. These results suggest the possibility of control of the spread of the epidemic by introducing predators in areas of mice colonies in a suitable way so that such control does not kill all the mice but lowers the epidemic spread…
We analyze the dynamics of a population of independent random walkers on a graph and develop a simple model of epidemic spreading. We assume that each walker visits independently the nodes of a finite ergodic graph in a discrete-time markovian walk governed by his specific transition matrix. With this assumption, we first derive an upper bound for the reproduction numbers. Then we assume that a walker is in one of the states: susceptible, infectious, or recovered. An infectious walker remains infectious during a certain characteristic time. If an infectious walker meets a susceptible one on th…
We study the effect of the connectivity pattern of complex networks on the propagation dynamics of epidemics. The growth time scale of outbreaks is inversely proportional to the network degree fluctuations, signaling that epidemics spread almost instantaneously in networks with scale-free degree distributions. This feature is associated with an epidemic propagation that follows a precise hierarchical dynamics. Once the highly connected hubs are reached, the infection pervades the network in a progressive cascade across smaller degree classes. The present results are relevant for the developmen…
We consider the spread of infectious disease through contact networks of Configuration Model type. We assume that the disease spreads through contacts and infected individuals recover into an immune state. We discuss a number of existing mathematical models used to investigate this system, and show relations between the underlying assumptions of the models. In the process we offer simplifications of some of the existing models. The distinctions between the underlying assumptions are subtle, and in many if not most cases this subtlety is irrelevant. Indeed, under appropriate conditions the mode…
We present an epidemiological compartment model, SAIR(S), that explicitly captures the dynamics of asymptomatic infected individuals in an epidemic spread process. We first present a group model and then discuss networked versions. We provide an investigation of equilibria and stability properties for these models, and present simulation results illustrating the effects of asymptomatic-infected individuals on the spread of the disease. We also discuss local isolation effects on the epidemic dynamics in terms of the networked models. Finally, we provide initial parameter estimation results base…
A simple, but ``classical``, stochastic model for epidemic spread in a finite, but large, population is studied. The progress of the epidemic can be divided into three different phases that requires different tools to analyse. Initially the process is approximated by a branching process. It is discussed for how long time this approximation is valid. When a non-negligible proportion of the population is already infected the process can be studied using differential equations. In a final phase the spread will fade out. The results are used to investigate what happens if two strains of infectious…
The Susceptible-Infected-Recovered (SIR) model is studied in multilayer networks with arbitrary number of links across the layers. By following the mapping to bond percolation we give the analytical expression for the epidemic threshold and the fraction of the infected individuals in arbitrary number of layers. These results provide an exact prediction of the epidemic threshold for infinite locally tree-like multilayer networks, and an lower bound of the epidemic threshold for more general multilayer networks. The case of a multilayer network formed by two interconnected networks is specifical…
A key characteristic of the spread of infectious diseases is their ability to use efficient transmission paths within contact graphs. This enables the pathogen to maximise infection rates and spread within a target population. In this work, we devise techniques to localise infections and decrease infection rates based on a principled analysis of disease transmission paths within human-contact networks (proximity graphs). Experimental results of disease spreading shows that that at low visibility rates contact tracing slows disease spreading. However to stop disease spreading, contact tracing r…
Advances in mathematical epidemiology have led to a better understanding of the risks posed by epidemic spreading and informed strategies to contain disease spread. However, a challenge that has been overlooked is that, as a disease becomes more prevalent, it can limit the availability of the capital needed to effectively treat those who have fallen ill. Here we use a simple mathematical model to gain insight into the dynamics of an epidemic when the recovery of sick individuals depends on the availability of healing resources that are generated by the healthy population. We find that epidemic…
We study the statistical properties of the SIR epidemics in heterogeneous networks, when an epidemic is defined as only those SIR propagations that reach or exceed a minimum size s_c. Using percolation theory to calculate the average fractional size <M_SIR> of an epidemic, we find that the strength of the spanning link percolation cluster $P_{\infty}$ is an upper bound to <M_SIR>. For small values of s_c, $P_{\infty}$ is no longer a good approximation, and the average fractional size has to be computed directly. The value of s_c for which $P_{\infty}$ is a good approximation is found to depend…
Although traditional models of epidemic spreading focus on the number of infected, susceptible and recovered individuals, a lot of attention has been devoted to integrate epidemic models with population genetics. Here we develop an individual-based model for epidemic spreading on networks in which viruses are explicitly represented by finite chains of nucleotides that can mutate inside the host. Under the hypothesis of neutral evolution we compute analytically the average pairwise genetic distance between all infecting viruses over time. We also derive a mean-field version of this equation tha…
We consider the edge-based compartmental models for epidemic spread developed in Part I. We show conditions under which simpler models may be substituted for more detailed models, and in so doing we define a hierarchy of epidemic models. In particular we provide conditions under which it is appropriate to use the standard mass action SIR model, and we show what happens when these conditions fail. Using our hierarchy, we provide a procedure leading to the choice of the appropriate model for a given population. Our result about the convergence of models to the Mass Action model gives clear, rigo…
Pathogens can spread epidemically through populations. Beneficial contagions, such as viruses that enhance host survival or technological innovations that improve quality of life, also have the potential to spread epidemically. How do the dynamics of beneficial biological and social epidemics differ from those of detrimental epidemics? We investigate this question using three theoretical approaches. First, in the context of population genetics, we show that a horizontally-transmissible element that increases fitness, such as viral DNA, spreads superexponentially through a population, more quic…
We consider a model for an epidemic in a population that occupies geographically distinct locations. The disease is spread within subpopulations by contacts between infective and susceptible individuals, and is spread between subpopulations by the migration of infected individuals. We show how susceptible individuals can act collectively to limit the spread of disease during the initial phase of an epidemic, by specifying the distribution that minimises the growth rate of the epidemic when the infectives are migrating so as to maximise the growth rate. We also give an explicit strategy that mi…
We develop an analytical method to calculate encounter times of two random walkers in one dimension when each individual is segregated in its own spatial domain and shares with its neighbor only a fraction of the available space, finding very good agreement with numerically-exact calculations. We model a population of susceptible and infected territorial individuals with this spatial arrangement, and which may transmit an epidemic when they meet. We apply the results on encounter times to determine analytically the macroscopic propagation speed of the epidemic as a function of the microscopic …
