Subscribe to the gold package and get unlimited access to Shamra Academy
Register a new userModeling the propagation of riots, collective behaviors, and epidemics
84
0
0.0
(
0
)
Authors
Henri Berestycki
Ask ChatGPT about the research
No Arabic abstract
This paper is concerned with a family of Reaction-Diffusion systems that we introduced in [15], and that generalizes the SIR type models from epidemiology. Such systems are now also used to describe collective behaviors.In this paper, we propose a modeling approach for these apparently diverse phenomena through the example of the dynamics of social unrest. The model involves two quantities: the level of social unrest, or more generally activity, u, and a field of social tension v, which play asymmetric roles. We think of u as the actually observed or explicit quantity while v is an ambiant, sometimes implicit, field of susceptibility that modulates the dynamics of u. In this article, we explore this class of model and prove several theoretical results based on the framework developed in [15], of which the present work is a companion paper. We particularly emphasize here two subclasses of systems: tension inhibiting and tension enhancing. These are characterized by respectively a negative or a positivefeedback of the unrest on social tension. We establish several properties for these classes and also study some extensions. In particular, we describe the behavior of the system following an initial surge of activity. We show that the model can give rise to many diverse qualitative dynamics. We also provide a variety of numerical simulations to illustrate our results and to reveal further properties and open questions.
rate research
Read More
It has been recently discovered that the measles virus can wipe out the adaptive immune system, destroying B lymphocytes and reducing the diversity of non-specific B cells of the infected host. In particular, this implies that previously acquired immunization from vaccination or direct exposition to other pathogens could be erased in a phenomenon named immune amnesia, whose effects can become particularly worrisome given the actual rise of anti-vaccination movements. Here we present the first attempt to incorporate immune amnesia into standard models of epidemic spreading. In particular, we analyze diverse variants of a model that describes the spreading of two concurrent pathogens causing measles and another generic disease: the SIR-IA model. Analytical and computational studies confirm that immune amnesia can indeed have important consequences for epidemic spreading, significantly altering the vaccination coverage required to reach herd-immunity for concurring infectious diseases. More specifically, we uncover the existence of novel propagating and endemic phases which are induced by immune amnesia, that appear both in fully-connected and more structured networks, such as random networks and power-law degree-distributed ones. In particular, the transitions from a quiescent state into these novel phases can become rather abrupt in some cases that we specifically analyze. Furthermore, we discuss the meaning and consequences of our results and their relation with, e.g., immunization strategies, together with the possibility that explosive types of transitions may emerge, making immune-amnesia effects particularly dramatic. This work opens the door to further developments and analyses of immune amnesia effects, contributing, more generally, to the theory of interacting epidemics on complex networks.
In this paper we present ACEMod, an agent-based modelling framework for studying influenza epidemics in Australia. The simulator is designed to analyse the spatiotemporal spread of contagion and influenza spatial synchrony across the nation. The individual-based epidemiological model accounts for mobility (worker and student commuting) patterns and human interactions derived from the 2006 Australian census and other national data sources. The high-precision simulation comprises 19.8 million stochastically generated software agents and traces the dynamics of influenza viral infection and transmission at several scales. Using this approach, we are able to synthesise epidemics in Australia with varying outbreak locations and severity. For each scenario, we investigate the spatiotemporal profiles of these epidemics, both qualitatively and quantitatively, via incidence curves, prevalence choropleths, and epidemic synchrony. This analysis exemplifies the nature of influenza pandemics within Australia and facilitates future planning of effective intervention, mitigation and crisis management strategies.
To forecast the time dynamics of an epidemic, we propose a discrete stochastic model that unifies and generalizes previous approaches to the subject. Viewing a given population of individuals or groups of individuals with given health state attributes as living in and moving between the nodes of a graph, we use Monte-Carlo Markov Chain techniques to simulate the movements and health state changes of the individuals according to given probabilities of stay that have been preassigned to each of the nodes. We utilize this model to either capture and predict the future geographic evolution of an epidemic in time, or the evolution of an epidemic inside a heterogeneous population which is divided into homogeneous sub-populations, or, more generally, its evolution in a combination or superposition of the previous two contexts. We also prove that when the size of the population increases and a natural hypothesis is satisfied, the stochastic process associated to our model converges to a deterministic process. Indeed, when the length of the time step used in the discrete model converges to zero, in the limit this deterministic process is driven by a differential equation yielding the evolution of the expectation value of the number of infected as a function of time. In the second part of the paper, we apply our model to study the evolution of the Covid-19 epidemic. We deduce a decomposition of the function yielding the number of infectious individuals into wavelets, which allows to trace in time the expectation value for the number of infections inside each sub-population. Within this framework, we also discuss possible causes for the occurrence of multiple epidemiological waves.
The recent COVID-19 pandemic has led to an increasing interest in the modeling and analysis of infectious diseases. The pandemic has made a significant impact on the way we behave and interact in our daily life. The past year has witnessed a strong interplay between human behaviors and epidemic spreading. In this paper, we propose an evolutionary game-theoretic framework to study the coupled evolutions of herd behaviors and epidemics. Our framework extends the classical degree-based mean-field epidemic model over complex networks by coupling it with the evolutionary game dynamics. The statistically equivalent individuals in a population choose their social activity intensities based on the fitness or the payoffs that depend on the state of the epidemics. Meanwhile, the spreading of the infectious disease over the complex network is reciprocally influenced by the players social activities. We analyze the coupled dynamics by studying the stationary properties of the epidemic for a given herd behavior and the structural properties of the game for a given epidemic process. The decisions of the herd turn out to be strategic substitutes. We formulate an equivalent finite-player game and an equivalent network to represent the interactions among the finite populations. We develop structure-preserving approximation techniques to study time-dependent properties of the joint evolution of the behavioral and epidemic dynamics. The resemblance between the simulated coupled dynamics and the real COVID-19 statistics in the numerical experiments indicates the predictive power of our framework.
Human mobility is a key component of large-scale spatial-transmission models of infectious diseases. Correctly modeling and quantifying human mobility is critical for improving epidemic control policies, but may be hindered by incomplete data in some regions of the world. Here we explore the opportunity of using proxy data or models for individual mobility to describe commuting movements and predict the diffusion of infectious disease. We consider three European countries and the corresponding commuting networks at different resolution scales obtained from official census surveys, from proxy data for human mobility extracted from mobile phone call records, and from the radiation model calibrated with census data. Metapopulation models defined on the three countries and integrating the different mobility layers are compared in terms of epidemic observables. We show that commuting networks from mobile phone data well capture the empirical commuting patterns, accounting for more than 87% of the total fluxes. The distributions of commuting fluxes per link from both sources of data - mobile phones and census - are similar and highly correlated, however a systematic overestimation of commuting traffic in the mobile phone data is observed. This leads to epidemics that spread faster than on census commuting networks, however preserving the order of infection of newly infected locations. Match in the epidemic invasion pattern is sensitive to initial conditions: the radiation model shows higher accuracy with respect to mobile phone data when the seed is central in the network, while the mobile phone proxy performs better for epidemics seeded in peripheral locations. Results suggest that different proxies can be used to approximate commuting patterns across different resolution scales in spatial epidemic simulations, in light of the desired accuracy in the epidemic outcome under study.
Log in to be able to interact and post comments
comments
Fetching comments
Sign in to be able to follow your search criteria
