Time evolution of epidemic disease on finite and infinite networks
Pierre-André Noël, Bahman Davoudi, Robert C. Brunham, Louis J. Dubé, Babak Pourbohloul
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17 pages, 7 figures. This version (v4) has been accepted by Physical Review E on December 9, 2008. The first version (v1) of this paper supersedes arXiv:0710.3420 . Version v2, v3 and v4 consist of the first (discrete time) part of v1. It contains a new section IV for comparison with different models. The continuous time part of v1 will appear as a separate contribution
Mathematical models of infectious diseases, which are in principle analytically tractable, use two general approaches. The first approach, generally known as compartmental modeling, addresses the time evolution of disease propagation at the expense of simplifying the pattern of transmission. The second approach uses network theory to incorporate detailed information pertaining to the underlying contact structure among individuals while disregarding the progression of time during outbreaks. So far, the only alternative that enables the integration of both aspects of disease propagation simultaneously while preserving the variety of outcomes has been to abandon the analytical approach and rely on computer simulations. We offer a new analytical framework, which incorporates both the complexity of contact network structure and the time progression of disease spread. Furthermore, we demonstrate that this framework is equally effective on finite- and "infinite"-size networks. This formalism can be equally applied to similar percolation phenomena on networks in other areas of science and technology.
The propagation of model epidemics on a small-world network under the action of immunization is studied. Although the connectivity in this kind of networks is rather uniform, a vaccination strategy focused on the best connected individuals yields a considerable improvement of disease control. The model exhibits a transition from disease localization to propagation as the disorder of the underlying network grows. As a consequence, for fixed disorder, a threshold immunization level exists above which the disease remains localized.
To model the evolution of diseases with extended latency periods and the presence of asymptomatic patients like COVID-19, we define a simple discrete time stochastic SIR-type epidemic model. We include both latent periods as well as the presence of quarantine areas, to capture the evolutionary dynamics of such diseases.
This paper presents a disease-severity-structured epidemic model with treatment necessary only to severe infective individuals to discuss the effect of the treatment capacity on the disease transmission. It is shown that a backward bifurcation occurs in the basic reproduction number R0, where a stable endemic equilibrium co-exists with a stable disease-free equilibrium when R0 <1, if the capacity is relatively small. This epidemiological implication is that, when there is not enough capacity for treatment, the requirement R0 <1 is not sufficient for effective disease control and disease outbre…
We study the classic Susceptible-Infected-Recovered (SIR) model for the spread of an infectious disease. In this stochastic process, there are two competing mechanism: infection and recovery. Susceptible individuals may contract the disease from infected individuals, while infected ones recover from the disease at a constant rate and are never infected again. Our focus is the behavior at the epidemic threshold where the rates of the infection and recovery processes balance. In the infinite population limit, we establish analytically scaling rules for the time-dependent distribution functions t…
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…
In contrast to the conventional wisdom that scale-free networks are prone to epidemic propagation, in the paper we present that disease spreading is inhibited in fractal scale-free networks. We first propose a novel network model and show that it simultaneously has the following rich topological properties: scale-free degree distribution, tunable clustering coefficient, "large-world" behavior, and fractal scaling. Existing network models do not display these characteristics. Then, we investigate the susceptible-infected-removed (SIR) model of the propagation of diseases in our fractal scale-fr…
For an eco-epidemic model with disease in the prey and periodic coefficients it is conjectured in [Xingge Niu, Tailei Zhang, Zhidong Teng, The asymptotic behavior of a nonautonomous eco-epidemic model with disease in the prey, Applied Mathematical Modelling 35, 457-470 (2011)] that, when the infected prey is permanent, there is a positive periodic orbit that is globally asymptotically stable in the interior of $(\R^+)^3$. In this paper we prove the existence part of the conjecture.
We study metapopulation models for the spread of epidemics in which different subpopulations (cities) are connected by fluxes of individuals (travelers). This framework allows to describe the spread of a disease on a large scale and we focus here on the computation of the arrival time of a disease as a function of the properties of the seed of the epidemics and of the characteristics of the network connecting the various subpopulations. Using analytical and numerical arguments, we introduce an easily computable quantity which approximates this average arrival time. We show on the example of a …
Common respiratory viruses cause seasonal epidemics in sequential patterns. The underlying mechanisms for this pattern have been debated for some time. For influenza, contenders include temperature, humidity, and vitamin D levels. While such seasonal drivers may be sufficient to explain midwinter peaking it is unclear if other respiratory viruses peaking in spring, summer, or fall have individual environmental drivers. Here we present a dynamic model of interacting diseases, in an effort to explain observed seasonal patterns without requiring multiple seasonal drivers. Our model extends the cl…
In this research, we study the propagation patterns of epidemic diseases such as the COVID-19 coronavirus, from a mathematical modeling perspective. The study is based on an extensions of the well-known susceptible-infected-recovered (SIR) family of compartmental models. It is shown how social measures such as distancing, regional lockdowns, quarantine and global public health vigilance, influence the model parameters, which can eventually change the mortality rates and active contaminated cases over time, in the real world. As with all mathematical models, the predictive ability of the model …
Background: While many infectious disease epidemics are initially characterized by an exponential growth in time, we show that district-level Ebola virus disease (EVD) outbreaks in West Africa follow slower polynomial-based growth kinetics over several generations of the disease. Methods: We analyzed epidemic growth patterns at three different spatial scales (regional, national, and subnational) of the Ebola virus disease epidemic in Guinea, Sierra Leone and Liberia by compiling publicly available weekly time series of reported EVD case numbers from the patient database available from the Worl…
We study vaccine control for disease spread on an adaptive network modeling disease avoidance behavior. Control is implemented by adding Poisson distributed vaccination of susceptibles. We show that vaccine control is much more effective in adaptive networks than in static networks due to an interaction between the adaptive network rewiring and the vaccine application. Disease extinction rates using vaccination are computed, and orders of magnitude less vaccine application is needed to drive the disease to extinction in an adaptive network than in a static one.
We present a differential equations model in which contagious disease transmission is affected by contagious fear of the disease and contagious fear of the control, in this case vaccine. The three contagions are coupled. The two fears evolve and interact in ways that shape distancing behavior, vaccine uptake, and their relaxation. These behavioral dynamics in turn can amplify or suppress disease transmission, which feeds back to affect behavior. The model reveals several coupled contagion mechanisms for multiple epidemic waves. Methodologically, the paper advances infectious disease modeling b…
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…
Mathematical disease modelling has long operated under the assumption that any one infectious disease is caused by one transmissible pathogen spreading among a population. This paradigm has been useful in simplifying the biological reality of epidemics and has allowed the modelling community to focus on the complexity of other factors such as population structure and interventions. However, there is an increasing amount of evidence that the strain diversity of pathogens, and their interplay with the host immune system, can play a large role in shaping the dynamics of epidemics. Here, we introd…
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…
In the study of infectious diseases on networks, researchers calculate epidemic thresholds to help forecast whether a disease will eventually infect a large fraction of a population. Because network structure typically changes in time, which fundamentally influences the dynamics of spreading processes on them and in turn affects epidemic thresholds for disease propagation, it is important to examine epidemic thresholds in temporal networks. Most existing studies of epidemic thresholds in temporal networks have focused on models in discrete time, but most real-world networked systems evolve con…
The discovery of SARS-CoV-2, the responsible virus for the Covid-19 epidemic, has sparked a global health concern with many countries affected. Developing models that can interpret the epidemic and give common trend parameters are useful for prediction purposes by other countries that are at an earlier phase of the epidemic; it is also useful for future planning against viral respiratory diseases. One model is developed to interpret the fast-growth phase of the epidemic and another model for an interpretation of the entire data set. Both models agree reasonably with the data. It is shown by th…
In most models of the spread of disease over contact networks it is assumed that the probabilities per unit time of disease transmission and recovery from disease are constant, implying exponential distributions of the time intervals for transmission and recovery. Time intervals for real diseases, however, have distributions that in most cases are far from exponential, which leads to disagreements, both qualitative and quantitative, with the models. In this paper, we study a generalized version of the SIR (susceptible-infected-recovered) model of epidemic disease that allows for arbitrary dist…
Mathematical models of epidemic dynamics offer significant insight into predicting and controlling infectious diseases. The dynamics of a disease model generally follow a susceptible, infected, and recovered (SIR) model, with some standard modifications. In this paper, we extend the work of Munz et.al (2009) on the application of disease dynamics to the so-called "zombie apocalypse", and then apply the identical methods to influenza dynamics. Unlike Munz et.al (2009), we include data taken from specific depictions of zombies in popular culture films and apply Markov Chain Monte Carlo (MCMC) me…
Many pathogens spread primarily via direct contact between infected and susceptible hosts. Thus, the patterns of contacts or contact network of a population fundamentally shapes the course of epidemics. While there is a robust and growing theory for the dynamics of single epidemics in networks, we know little about the impacts of network structure on long term epidemic or endemic transmission. For seasonal diseases like influenza, pathogens repeatedly return to populations with complex and changing patterns of susceptibility and immunity acquired through prior infection. Here, we develop two m…
We use a stochastic Markovian dynamics approach to describe the spreading of vector-transmitted diseases, like dengue, and the threshold of the disease. The coexistence space is composed by two structures representing the human and mosquito populations. The human population follows a susceptible-infected-recovered (SIR) type dynamics and the mosquito population follows a susceptible-infected-susceptible (SIS) type dynamics. The human infection is caused by infected mosquitoes and vice-versa so that the SIS and SIR dynamics are interconnected. We develop a truncation scheme to solve the evoluti…
Sheep pox is a highly transmissible disease which can cause serious loss of livestock and can therefore have major economic impact. We present data from sheep pox epidemics which occurred between 1994 and 1998. The data include weekly records of infected farms as well as a number of covariates. We implement Bayesian stochastic regression models which, in addition to various explanatory variables like seasonal and environmental/meteorological factors, also contain serial correlation structure based on variants of the Ornstein-Uhlenbeck process. We take a predictive view in model selection by ut…
Recent evidences show that individuals who recovered from COVID-19 can be reinfected. However, this phenomenon has rarely been studied using mathematical models. In this paper, we propose a SEIRE epidemic model to describe the spread of the epidemic with reinfection. We obtain the important thresholds $R_0$ (the basic reproduction number) and Rc (a threshold less than one). Our investigations show that when $R_0 > 1$, the system has an endemic equilibrium, which is globally asymptotically stable. When $R_c < R_0 < 1$, the epidemic system exhibits bistable dynamics. That is, the system has back…
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…
Insect-borne plant diseases recur commonly in wild plants and in agricultural crops, and are responsible for severe losses in terms of produce yield and monetary return. Mathematical models of insect-borne plant diseases are therefore an essential tool to help predicting the progression of an epidemic disease and aid in decision making when control strategies are to be implemented in the field. While retaining a generalized applicability of the proposed model to plant epidemics vectored by insects, we specifically investigated the epidemics of Flavescence dorée phytoplasma (FD) in grapevine pl…
An SEIRS epidemic with disease fatalities is introduced in a growing population (modelled as a super-critical linear birth and death process). The study of the initial phase of the epidemic is stochastic, while the analysis of the major outbreaks is deterministic. Depending on the values of the parameters, the following scenarios are possible. i) The disease dies out quickly, only infecting few; ii) the epidemic takes off, the \textit{number} of infected individuals grows exponentially, but the \textit{fraction} of infected individuals remains negligible; iii) the epidemic takes off, the \text…
We study the propagation of an SIR (susceptible-infectious-recovered) disease over an agent population which, at any instant, is fully divided into couples of agents. Couples are occasionally allowed to exchange their members. This process of couple recombination can compensate the instantaneous disconnection of the interaction pattern and thus allow for the propagation of the infection. We study the incidence of the disease as a function of its infectivity and of the recombination rate of couples, thus characterizing the interplay between the epidemic dynamics and the evolution of the populat…
In this paper, we introduce a modified epidemic model on regular and scale-free networks respectively. We consider the birth rate $δ$, cure rate $γ$, infection rate $λ$, $α$ from the infectious disease, and death rate $β$ from other factors. Through mean-field analysis, we find that on regular network there is an epidemic threshold $λ_{c}$ dependent on the parameters $δ$, $γ$, $α$, and $β$; while for power law degree distribution network epidemic threshold is absent in the thermodynamic limit. The result is the same as that of the standard SIS model. This reminds us the structure of the networ…
We present a compartmental SEIAR model of epidemic spread as a generalization of the SEIR model. We believe that the asymptomatic infectious cohort is an omitted part of the understanding of the epidemic dynamics of disease COVID-19. We introduce and derive the basic reproduction number as the weighted arithmetic mean of the basic reproduction numbers of the symptomatic and asymptomatic cohorts. Since the asymptomatic subjects people are not detected, they can spread the disease much longer, and this increases the COVID-19 $R_0$ up to around 9. We show that European epidemic outbreaks in vario…
A model of an Ebola epidemic is developed with infected individuals structured according to disease age. The transmission of the infection is tracked by disease age through an initial incubation (exposed) phase, followed by an infectious phase with variable transmission infectiousness. The removal of infected individuals is dependent on disease age, with three types of removal rates: (1) removal due to hospitalization (isolation), (2) removal due to mortality separate from hospitalization, and (3) removal due to recovery separate from hospitalization. The model is applied to the Ebola epidemic…
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…
The global SARS-CoV-2 pandemic suggests a novel type of disease spread dynamics. WHO states that there is currently no evidence that people who have recovered from COVID-19 and have antibodies are immune from a second infection [WHO]. Conventional mathematical models consider cases for which a recovered individual either becomes susceptible again or develops an immunity. Here, we study the case where infected agents recover and only develop immunity if they are continuously infected for some time. Otherwise, they become susceptible again. We show that field theory bounds the peak of the infect…
We consider an age-structured epidemic model with two basic public health interventions: (i) identifying and isolating symptomatic cases, and (ii) tracing and quarantine of the contacts of identified infectives. The dynamics of the infected population are modeled by a nonlinear infection-age-dependent partial differential equation, which is coupled with an ordinary differential equation that describes the dynamics of the susceptible population. Theoretical results about global existence and uniqueness of positive solutions are proved. We also present two practical applications of our model: (1…
The commonly observed negative correlation between the number of species in an ecological community and disease risk, typically referred to as "the dilution effect", has received a substantial amount of attention over the past decade. Attempts to test this relationship experimentally have revealed that, in addition to the mean disease risk decreasing with species number, so too does the variance of disease risk. This is referred to as the "variance reduction effect", and has received relatively little attention in the disease-diversity literature. Here, we set out to clarify and quantify some …
Effective intervention strategies for epidemics rely on the identification of their origin and on the robustness of the predictions made by network disease models. We introduce a Bayesian uncertainty quantification framework to infer model parameters for a disease spreading on a network of communities from limited, noisy observations; the state-of-the-art computational framework compensates for the model complexity by exploiting massively parallel computing architectures. Using noisy, synthetic data, we show the potential of the approach to perform robust model fitting and additionally demonst…
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 h…
Vector-transmitted diseases such as dengue fever and chikungunya have been spreading rapidly in many parts of the world. The Zika virus has been known since 1947 and invaded South America in 2013. It can be transmitted not only by (mosquito) vectors but also directly through sexual contact. Zika has developed into a serious global health problem because, while most cases are asymptomatic or very light, babies born to Zika - infected mothers may develop microcephaly and other very serious birth defects. We formulate and analyze two epidemic models for vector-transmitted diseases, one appropriat…
Motivated by the increasing number of COVID-19 cases that have been observed in many countries after the vaccination and relaxation of non-pharmaceutical interventions, we propose a mathematical model on time-varying networks for the spread of recurrent epidemic diseases in a partially vaccinated population. The model encapsulates several realistic features, such as the different effectiveness of the vaccine against transmission and development of severe symptoms, testing practices, the possible implementation of non-pharmaceutical interventions to reduce the transmission, isolation of detecte…
Predicting the spread of vector-borne diseases in response to incursions requires knowledge of both host and vector demographics in advance of an outbreak. Whereas host population data is typically available, for novel disease introductions there is a high chance of the pathogen utilising a vector for which data is unavailable. This presents a barrier to estimating the parameters of dynamical models representing host-vector-pathogen interaction, and hence limits their ability to provide quantitative risk forecasts. The Theileria orientalis (Ikeda) outbreak in New Zealand cattle demonstrates th…
Various theoretical models have been proposed to understand the basic nature of epidemics. Recent studies focus on the effects of mobility to epidemic process. However, uncorrelated random walk is typically assumed as the type of movement. In our daily life, the movement of people sometimes tends to be limited to a certain direction, which can be described by biased random walk. Here, we developed an agent-based model of susceptible-infected-recovered (SIR) epidemic process in a 2D continuous space where agents tend to move in a certain direction in addition to random movement. Moreover, we ma…
The interpretation of sampling data plays a crucial role in policy response to the spread of a disease during an epidemic, such as the COVID-19 epidemic of 2020. However, this is a non-trivial endeavor due to the complexity of real world conditions and limits to the availability of diagnostic tests, which necessitate a bias in testing favoring symptomatic individuals. A thorough understanding of sampling confidence and bias is necessary in order make accurate conclusions. In this manuscript, we provide a stochastic model of sampling for assessing confidence in disease metrics such as trend det…
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 outbreak of enterohemorrhagic Escherichia coli (EHEC) in May 2011 warns the potential threats of the world vegetables trade network (VTN) in spreading fatal infectious diseases. The heterogeneous weight distribution and multi-scale activity of intermediary networks affects the diffusion, proliferation and extinction of epidemics. Here, we constructed a dual-weighted VTN with 118 major countries and territories from FAO 2008 statistic data about global vegetation production and trade, and develop a reaction-diffusion model to simulate the epidemic behaviors in through VTN. We found an emerg…
Emerging marine infectious diseases pose a substantial threat to marine ecosystems and the conservation of their biodiversity. Compartmental models of epidemic transmission in marine sessile organisms, available only recently, are based on non-spatial descriptions in which space is homogenised and parasite mobility is not explicitly accounted for. However, in realistic scenarios epidemic transmission is conditioned by the spatial distribution of hosts and the parasites mobility patterns, calling for a explicit description of space. In this work we develop a spatially-explicit individual-based …
We investigate the effects of heterogeneous and clustered contact patterns on the timescale and final size of infectious disease epidemics. The abundance of transitive relationships (the number of 3 cliques) in a network and the variance of the degree distribution are shown to have large effects on the number ultimately infected and how quickly the epidemic propagates. The network model is based on a simple generalization of the configuration model, and epidemic dynamics are modeled with a low dimensional system of ordinary differential equations. Because of the simplicity of this model, we ar…
One of the major issues in the theoretical modeling of epidemic spreading is the development of methods to control the transmission of an infectious agent. Human behavior plays a fundamental role in the spreading dynamics and can be used to stop a disease from spreading or to reduce its burden, as individuals aware of the presence of a disease can take measures to reduce their exposure to contagion. In this paper, we propose a mathematical model for the spread of diseases with awareness in complex networks. Unlike previous models, the information is propagated following a generalized Maki-Thom…
The spread of certain diseases can be promoted, in some cases substantially, by prior infection with another disease. One example is that of HIV, whose immunosuppressant effects significantly increase the chances of infection with other pathogens. Such coinfection processes, when combined with nontrivial structure in the contact networks over which diseases spread, can lead to complex patterns of epidemiological behavior. Here we consider a mathematical model of two diseases spreading through a single population, where infection with one disease is dependent on prior infection with the other. …
In this paper we consider a simple two-patch model in which a population affected by a disease can freely move. We assume that the capacity of the interconnected paths is limited, and thereby influencing the migration rates. Possible habitat disruptions due to human activities or natural events are accounted for. The demographic assumptions prevent the ecosystem to be wiped out, and the disease remains endemic in both populated patches at a stable equilibrium, but possibly also with an oscillatory behavior in the case of unidirectional migrations. Interestingly, if infected cannot migrate, it …
Connecting the different scales of epidemic dynamics, from individuals to communities to nations, remains one of the main challenges of disease modeling. Here, we revisit one of the largest public health efforts deployed against a localized epidemic: the 2014-2016 Ebola Virus Disease (EVD) epidemic in Sierra Leone. We leverage the data collected by the surveillance and contact tracing protocols of the Sierra Leone Ministry of Health and Sanitation, the US Centers for Disease Control and Prevention, and other responding partners to validate a network epidemiology framework connecting the popula…
Understanding the impact of collective social phenomena in epidemic dynamics is a crucial task to effectively contain the disease spread. In this work we build a mathematical description for assessing the interplay between opinion polarization and the evolution of a disease. The proposed kinetic approach describes the evolution of aggregate quantities characterizing the agents belonging to epidemiologically relevant states, and will show that the spread of the disease is closely related to consensus dynamics distribution in which opinion polarization may emerge. In the present modelling framew…
Most infectious diseases including more than half of known human pathogens are not restricted to just one host, yet much of the mathematical modeling of infections has been limited to a single species. We investigate consequences of a single epidemic propagating in multiple species and compare and contrast it with the endemic steady state of the disease. We use the two-species Susceptible-Infected-Recovered (SIR) model to calculate the severity of post-epidemic collapses in populations of two host species as a function of their initial population sizes, the times individuals remain infectious,…
This paper studies the dynamics of a network-based SIRS epidemic model with vaccination and a nonmonotone incidence rate. This type of nonlinear incidence can be used to describe the psychological or inhibitory effect from the behavioral change of the susceptible individuals when the number of infective individuals on heterogeneous networks is getting larger. Using the analytical method, epidemic threshold $R_0$ is obtained. When $R_0$ is less than one, we prove the disease-free equilibrium is globally asymptotically stable and the disease dies out, while $R_0$ is greater than one, there exist…
