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Register a new userA viral load-based model for epidemic spread on spatial networks
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In this paper, we propose a Boltzmann-type kinetic model of the spreading of an infectious disease on a network. The latter describes the connections among countries, cities or districts depending on the spatial scale of interest. The disease transmission is represented in terms of the viral load of the individuals and is mediated by social contacts among them, taking into account their displacements across the nodes of the network. We formally derive the hydrodynamic equations for the density and the mean viral load of the individuals on the network and we analyse the large-time trends of these quantities with special emphasis on the cases of blow-up or eradication of the infection. By means of numerical tests, we also investigate the impact of confinement measures, such as quarantine or localised lockdown, on the diffusion of the disease on the network.
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Mathematical models are formal and simplified representations of the knowledge related to a phenomenon. In classical epidemic models, a neglected aspect is the heterogeneity of disease transmission and progression linked to the viral load of each infectious individual. Here, we attempt to investigate the interplay between the evolution of individuals viral load and the epidemic dynamics from a theoretical point of view. In the framework of multi-agent systems, we propose a particle stochastic model describing the infection transmission through interactions among agents and the individual physiological course of the disease. Agents have a double microscopic state: a discrete label, that denotes the epidemiological compartment to which they belong and switches in consequence of a Markovian process, and a microscopic trait, representing a normalized measure of their viral load, that changes in consequence of binary interactions or interactions with a background. Specifically, we consider Susceptible--Infected--Removed--like dynamics where infectious individuals may be isolated from the general population and the isolation rate may depend on the viral load sensitivity and frequency of tests. We derive kinetic evolution equations for the distribution functions of the viral load of the individuals in each compartment, whence, via suitable upscaling procedures, we obtain a macroscopic model for the densities and viral load momentum. We perform then a qualitative analysis of the ensuing macroscopic model, and we present numerical tests in the case of both constant and viral load-dependent isolation control. Also, the matching between the aggregate trends obtained from the macroscopic descriptions and the original particle dynamics simulated by a Monte Carlo approach is investigated.
Understanding network flows such as commuter traffic in large transportation networks is an ongoing challenge due to the complex nature of the transportation infrastructure and of human mobility. Here we show a first-principles based method for traffic prediction using a cost based generalization of the radiation model for human mobility, coupled with a cost-minimizing algorithm for efficient distribution of the mobility fluxes through the network. Using US census and highway traffic data we show that traffic can efficiently and accurately be computed from a range-limited, network betweenness type calculation. The model based on travel time costs captures the lognormal distribution of the traffic and attains a high Pearson correlation coefficient (0.75) when compared to real traffic. Due to its principled nature, this method can inform many applications related to human mobility driven flows in spatial networks, ranging from transportation, through urban planning to mitigation of the effects of catastrophic events.
We consider the emergent behavior of viral spread when agents in a large population interact with each other over a contact network. When the number of agents is large and the contact network is a complete graph, it is well known that the population behavior -- that is, the fraction of susceptible, infected and recovered agents -- converges to the solution of an ordinary differential equation (ODE) known as the classical SIR model as the population size approaches infinity. In contrast, we study interactions over contact networks with generic topologies and derive conditions under which the population behavior concentrates around either the classic SIR model or other deterministic models. Specifically, we show that when most vertex degrees in the contact network are sufficiently large, the population behavior concentrates around an ODE known as the network SIR model. We then study the short and intermediate-term evolution of the network SIR model and show that if the contact network has an expander-type property or the initial set of infections is well-mixed in the population, the network SIR model reduces to the classical SIR model. To complement these results, we illustrate through simulations that the two models can yield drastically different predictions, hence use of the classical SIR model can be misleading in certain cases.
One of the popular dynamics on complex networks is the epidemic spreading. An epidemic model describes how infections spread throughout a network. Among the compartmental models used to describe epidemics, the Susceptible-Infected-Susceptible (SIS) model has been widely used. In the SIS model, each node can be susceptible, become infected with a given infection rate, and become again susceptible with a given curing rate. In this paper, we add a new compartment to the classic SIS model to account for human response to epidemic spread. Each individual can be infected, susceptible, or alert. Susceptible individuals can become alert with an alerting rate if infected individuals exist in their neighborhood. An individual in the alert state is less probable to become infected than an individual in the susceptible state; due to a newly adopted cautious behavior. The problem is formulated as a continuous-time Markov process on a general static graph and then modeled into a set of ordinary differential equations using mean field approximation method and the corresponding Kolmogorov forward equations. The model is then studied using results from algebraic graph theory and center manifold theorem. We analytically show that our model exhibits two distinct thresholds in the dynamics of epidemic spread. Below the first threshold, infection dies out exponentially. Beyond the second threshold, infection persists in the steady state. Between the two thresholds, the infection spreads at the first stage but then dies out asymptotically as the result of increased alertness in the network. Finally, simulations are provided to support our findings. Our results suggest that alertness can be considered as a strategy of controlling the epidemics which propose multiple potential areas of applications, from infectious diseases mitigations to malware impact reduction.
Real epidemic spreading networks often composed of several kinds of networks interconnected with each other, and the interrelated networks have the different topologies and epidemic dynamics. Moreover, most human diseases are derived from animals, and the zoonotic infections always spread on interconnected networks. In this paper, we consider the epidemic spreading on one-way circular-coupled network consist of three interconnected subnetworks. Here, two one-way three-layer circular interactive networks are established by introducing the heterogeneous mean-field approach method, then we get the basic reproduction numbers and prove the global stability of the disease-free equilibrium and endemic equilibrium of the models. Through mathematical analysis and numerical simulations, it is found that the basic reproduction numbers $R_0$ of the two models are dependent on the infection rates, infection periods, average degrees and degree ratios. In the first model, the network structures of the inner contact patterns have a bigger impact on $R_0$ than that of the cross contact patterns. Under the same contact pattern, the internal infection rates have greater influence on $R_0$ than the cross-infection rates. In the second model, the disease prevails in a heterogeneous network has a greater impact on $R_0$ than the disease from a homogeneous network, and the infections among the three subnetworks all play a important role in the propagation process. Numerical examples verify and expand these theoretical results very well.
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