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Epidemic spreading phenomena are ubiquitous in nature and society. Examples include the spreading of diseases, information, and computer viruses. Epidemics can spread by local spreading, where infected nodes can only infect a limited set of direct target nodes and global spreading, where an infected node can infect every other node. In reality, many epidemics spread using a hybrid mixture of both types of spreading. In this study we develop a theoretical framework for studying hybrid epidemics, and examine the optimum balance between spreading mechanisms in terms of achieving the maximum outbreak size. We show the existence of critically hybrid epidemics where neither spreading mechanism alone can cause a noticeable spread but a combination of the two spreading mechanisms would produce an enormous outbreak. Our results provide new strategies for maximising beneficial epidemics and estimating the worst outcome of damaging hybrid epidemics.
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Time-varying network topologies can deeply influence dynamical processes mediated by them. Memory effects in the pattern of interactions among individuals are also known to affect how diffusive and spreading phenomena take place. In this paper we analyze the combined effect of these two ingredients on epidemic dynamics on networks. We study the susceptible-infected-susceptible (SIS) and the susceptible-infected-removed (SIR) models on the recently introduced activity-driven networks with memory. By means of an activity-based mean-field approach we derive, in the long time limit, analytical predictions for the epidemic threshold as a function of the parameters describing the distribution of activities and the strength of the memory effects. Our results show that memory reduces the threshold, which is the same for SIS and SIR dynamics, therefore favouring epidemic spreading. The theoretical approach perfectly agrees with numerical simulations in the long time asymptotic regime. Strong aging effects are present in the preasymptotic regime and the epidemic threshold is deeply affected by the starting time of the epidemics. We discuss in detail the origin of the model-dependent preasymptotic corrections, whose understanding could potentially allow for epidemic control on correlated temporal networks.
We study a multi-type SIR epidemic process among a heterogeneous population that interacts through a network. When we base social contact on a random graph with given vertex degrees, we give limit theorems on the fraction of infected individuals. For a given social distancing individual strategies, we establish the epidemic reproduction number $R_0$ which can be used to identify network vulnerability and inform vaccination policies. In the second part of the paper we study the equilibrium of the social distancing game, in which individuals choose their social distancing level according to an anticipated global infection rate, which then must equal the actual infection rate following their choices. We give conditions for the existence and uniqueness of equilibrium. For the case of random regular graphs, we show that voluntary social distancing will always be socially sub-optimal.
Recent empirical research has shown that links between groups reinforce individuals within groups to adopt cooperative behaviour. Moreover, links between networks may induce cascading failures, competitive percolation, or contribute to efficient transportation. Here we show that there in fact exists an intermediate fraction of links between groups that is optimal for the evolution of cooperation in the prisoners dilemma game. We consider individual groups with regular, random, and scale-free topology, and study their different combinations to reveal that an intermediate interdependence optimally facilitates the spreading of cooperative behaviour between groups. Excessive between-group links simply unify the two groups and make them act as one, while too rare between-group links preclude a useful information flow between the two groups. Interestingly, we find that between-group links are more likely to connect two cooperators than in-group links, thus supporting the conclusion that they are of paramount importance.
The detection and management of diseases become quite complicated when pathogens contain asymptomatic phenotypes amongst their ranks, as evident during the recent COVID-19 pandemic. Spreading of diseases has been studied extensively under the paradigm of Susceptible - Infected - Recovered - Deceased (SIRD) dynamics. Various game-theoretic approaches have also addressed disease spread, many of which consider S, I, R, and D as strategies rather than as states. Remarkably, most studies from the above approaches do not account for the distinction between the symptomatic or asymptomatic aspect of the disease. It is well-known that precautionary measures like washing hands, wearing masks and social distancing significantly mitigate the spread of many contagious diseases. Herein, we consider the adoption of such precautions as strategies and treat S, I, R, and D as states. We also attempt to capture the differences in epidemic spreading arising from symptomatic and asymptomatic diseases on various network topologies. Through extensive computer simulations, we examine that the cost of maintaining precautionary measures as well as the extent of mass testing in a population affects the final fraction of socially responsible individuals. We observe that the lack of mass testing could potentially lead to a pandemic in case of asymptomatic diseases. Network topology also seems to play an important role. We further observe that the final fraction of proactive individuals depends on the initial fraction of both infected as well as proactive individuals. Additionally, edge density can significantly influence the overall outcome. Our findings are in broad agreement with the lessons learnt from the ongoing COVID-19 pandemic.
Spreading processes have been largely studied in the literature, both analytically and by means of large-scale numerical simulations. These processes mainly include the propagation of diseases, rumors and information on top of a given population. In the last two decades, with the advent of modern network science, we have witnessed significant advances in this field of research. Here we review the main theoretical and numerical methods developed for the study of spreading processes on complex networked systems. Specifically, we formally define epidemic processes on single and multilayer networks and discuss in detail the main methods used to perform numerical simulations. Throughout the review, we classify spreading processes (disease and rumor models) into two classes according to the nature of time: (i) continuous-time and (ii) cellular automata approach, where the second one can be further divided into synchronous and asynchronous updating schemes. Our revision includes the heterogeneous mean-field, the quenched-mean field, and the pair quenched mean field approaches, as well as their respective simulation techniques, emphasizing similarities and differences among the different techniques. The content presented here offers a whole suite of methods to study epidemic-like processes in complex networks, both for researchers without previous experience in the subject and for experts.
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