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We introduce an epidemic model with varying infectivity and general exposed and infectious periods, where the infectivity of each individual is a random function of the elapsed time since infection, those function being i.i.d. for the various individuals in the population. This approach models infection-age dependent infectivity, and extends the classical SIR and SEIR models. We focus on the infectivity process (total force of infection at each time), and prove a functional law of large number (FLLN). In the deterministic limit of this LLN, the infectivity process and the susceptible process are determined by a two-dimensional deterministic integral equation. From its solutions, we then derive the exposed, infectious and recovered processes, again using integral equations. For the early phase, we study the stochastic model directly by using an approximate (non--Markovian) branching process, and show that the epidemic grows at an exponential rate on the event of non-extinction, which matches the rate of growth derived from the deterministic linearized equations. We also use these equations to derive the basic reproduction number $R_0$ during the early stage of an epidemic, in terms of the average individual infectivity function and the exponential rate of growth of the epidemic.
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We extend the measure-valued fluid model, which tracks residuals of patience and service times, to allow for time-varying arrivals. The fluid model can be characterized by a one-dimensional convolution equation involving both the patience and service time distributions. We also make an interesting connection to the measure-valued fluid model tracking the elapsed waiting and service times. Our analysis shows that the two fluid models are actually characterized by the same one-dimensional convolution equation.
We study non-Markovian stochastic epidemic models (SIS, SIR, SIRS, and SEIR), in which the infectious (and latent/exposing, immune) periods have a general distribution. We provide a representation of the evolution dynamics using the time epochs of infection (and latency/exposure, immunity). Taking the limit as the size of the population tends to infinity, we prove both a functional law of large number (FLLN) and a functional central limit theorem (FCLT) for the processes of interest in these models. In the FLLN, the limits are a unique solution to a system of deterministic Volterra integral equations, while in the FCLT, the limit processes are multidimensional Gaussian solutions of linear Volterra stochastic integral equations. In the proof of the FCLT, we provide an important Poisson random measures representation of the diffusion-scaled processes converging to Gaussian components driving the limit process.
In this paper, we propose two novel immunization strategies, i.e., combined immunization and duplex immunization, for SIS model in directed scale-free networks, and obtain the epidemic thresholds for them with linear and nonlinear infectivities. With the suggested two new strategies, the epidemic thresholds after immunization are greatly increased. For duplex immunization, we demonstrate that its performance is the best among all usual immunization schemes with respect to degree distribution. And for combined immunization scheme, we show that it is more effective than active immunization. Besides, we give a comprehensive theoretical analysis on applying targeted immunization to directed networks. For targeted immunization strategy, we prove that immunizing nodes with large out-degrees are more effective than immunizing nodes with large in-degrees, and nodes with both large out-degrees and large in-degrees are more worthy to be immunized than nodes with only large out-degrees or large in-degrees. Finally, some numerical analysis are performed to verify and complement our theoretical results. This work is the first to divide the whole population into different types and embed appropriate immunization scheme according to the characteristics of the population, and it will benefit the study of immunization and control of infectious diseases on complex networks.
We introduce the effect of site contamination in a model for spatial epidemic spread and show that the presence of site contamination may have a strict effect on the model in the sense that it can make an otherwise subcritical process supercritical. Each site on $mathbb{Z}^d$ is independently assigned a random number of particles and these then perform random walks restricted to bounded regions around their home locations. At time 0, the origin is infected along with all its particles. The infection then spread in that an infected particle that jumps to a new site causes the site along with all particles located there to be infected. Also, a healthy particle that jumps to a site where infection is presents, either in that the site is infected or in the presence of infected particles, becomes infected. Particles and sites recover at rate $lambda$ and $gamma$, respectively, and then become susceptible to the infection again. We show that, for each given value of $lambda$, there is a positive probability that the infection survives indefinitely if $gamma$ is sufficiently small, and that, for each given value of $gamma$, the infection dies out almost surely if $lambda$ is large enough. Several open problems and modifications of the model are discussed, and some natural conjectures are supported by simulations.
Social interactions are stratified in multiple contexts and are subject to complex temporal dynamics. The systematic study of these two features of social systems has started only very recently mainly thanks to the development of multiplex and time-varying networks. However, these two advancements have progressed almost in parallel with very little overlap. Thus, the interplay between multiplexity and the temporal nature of connectivity patterns is poorly understood. Here, we aim to tackle this limitation by introducing a time-varying model of multiplex networks. We are interested in characterizing how these two properties affect contagion processes. To this end, we study SIS epidemic models unfolding at comparable time-scale respect to the evolution of the multiplex network. We study both analytically and numerically the epidemic threshold as a function of the overlap between, and the features of, each layer. We found that, the overlap between layers significantly reduces the epidemic threshold especially when the temporal activation patterns of overlapping nodes are positively correlated. Furthermore, when the average connectivity across layers is very different, the contagion dynamics are driven by the features of the more densely connected layer. Here, the epidemic threshold is equivalent to that of a single layered graph and the impact of the disease, in the layer driving the contagion, is independent of the overlap. However, this is not the case in the other layers where the spreading dynamics are sharply influenced by it. The results presented provide another step towards the characterization of the properties of real networks and their effects on contagion phenomena
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