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Albeit epidemic models have evolved into powerful predictive tools for the spread of diseases and opinions, most assume memoryless agents and independent transmission channels. We develop an infection mechanism that is endowed with memory of past exposures and simultaneously incorporates the joint effect of multiple infectious sources. Analytic equations and simulations of the susceptible-infected-susceptible model in unstructured substrates reveal the emergence of an additional phase that separates the usual healthy and endemic ones. This intermediate phase shows fundamentally distinct characteristics, and the system exhibits either excitability or an exotic variant of bistability. Moreover, the transition to endemicity presents hybrid aspects. These features are the product of an intricate balance between two memory modes and indicate that non-Markovian effects significantly alter the properties of spreading processes.
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We investigate the effect of degree correlation on a susceptible-infected-susceptible (SIS) model with a nonlinear cooperative effect (synergy) in infectious transmissions. In a mean-field treatment of the synergistic SIS model on a bimodal network with tunable degree correlation, we identify a discontinuous transition that is independent of the degree correlation strength unless the synergy is absent or extremely weak. Regardless of synergy (absent or present), a positive and negative degree correlation in the model reduces and raises the epidemic threshold, respectively. For networks with a strongly positive degree correlation, the mean-field treatment predicts the emergence of two discontinuous jumps in the steady-state infected density. To test the mean-field treatment, we provide approximate master equations of the present model, which accurately describe the synergistic SIS dynamics. We quantitatively confirm all qualitative predictions of the mean-field treatment in numerical evaluations of the approximate master equations.
By incorporating delayed epidemic information and self-restricted travel behavior into the SIS model, we have investigated the coupled effects of timely and accurate epidemic information and peoples sensitivity to the epidemic information on contagion. In the population with only local random movement, whether the epidemic information is delayed or not has no effect on the spread of the epidemic. Peoples high sensitivity to the epidemic information leads to their risk aversion behavior and the spread of the epidemic is suppressed. In the population with only global person-to-person movement, timely and accurate epidemic information helps an individual cut off the connections with the infected in time and the epidemic is brought under control in no time. A delay in the epidemic information leads to an individuals misjudgment of who has been infected and who has not, which in turn leads to rapid progress and a higher peak of the epidemic. In the population with coexistence of local and global movement, timely and accurate epidemic information and peoples high sensitivity to the epidemic information play an important role in curbing the epidemic. A theoretical analysis indicates that peoples misjudgment caused by the delayed epidemic information leads to a higher encounter probability between the susceptible and the infected and peoples self-restricted travel behavior helps reduce such an encounter probability. A functional relation between the ratio of infected individuals and the susceptible-infected encounter probability has been found.
Power-law behaviors are common in many disciplines, especially in network science. Real-world networks, like disease spreading among people, are more likely to be interconnected communities, and show richer power-law behaviors than isolated networks. In this paper, we look at the system of two communities which are connected by bridge links between a fraction $r$ of bridge nodes, and study the effect of bridge nodes to the final state of the Susceptible-Infected-Recovered model, by mapping it to link percolation. By keeping a fixed average connectivity, but allowing different transmissibilities along internal and bridge links, we theoretically derive different power-law asymptotic behaviors of the total fraction of the recovered $R$ in the final state as $r$ goes to zero, for different combinations of internal and bridge link transmissibilities. We also find crossover points where $R$ follows different power-law behaviors with $r$ on both sides when the internal transmissibility is below but close to its critical value, for different bridge link transmissibilities. All of these power-law behaviors can be explained through different mechanisms of how finite clusters in each community are connected into the giant component of the whole system, and enable us to pick effective epidemic strategies and to better predict their impacts.
In the past few decades, the frequency of pandemics has been increased due to the growth of urbanization and mobility among countries. Since a disease spreading in one country could become a pandemic with a potential worldwide humanitarian and economic impact, it is important to develop models to estimate the probability of a worldwide pandemic. In this paper, we propose a model of disease spreading in a structural modular complex network (having communities) and study how the number of bridge nodes $n$ that connect communities affects disease spread. We find that our model can be described at a global scale as an infectious transmission process between communities with global infectious and recovery time distributions that depend on the internal structure of each community and $n$. We find that near the critical point as $n$ increases, the disease reaches most of the communities, but each community has only a small fraction of recovered nodes. In addition, we obtain that in the limit $n to infty$, the probability of a pandemic increases abruptly at the critical point. This scenario could make the decision on whether to launch a pandemic alert or not more difficult. Finally, we show that link percolation theory can be used at a global scale to estimate the probability of a pandemic since the global transmissibility between communities has a weak dependence on the global recovery time.
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 aggregation error, which is strongly bounded by the isoperimetric inequality. We also develop a mean-field approximation of this framework to further reduce the state-space size. Finally, we extend the GgroupEM to multilayer networks. Since the group-based framework is computationally less expensive and faster than an individual-based framework, then this framework is useful when the simulation time is important.
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