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Register a new userMass testing and proactiveness affect epidemic spreading
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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.
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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.
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.
The impact that information diffusion has on epidemic spreading has recently attracted much attention. As a disease begins to spread in the population, information about the disease is transmitted to others, which in turn has an effect on the spread of disease. In this paper, using empirical results of the propagation of H7N9 and information about the disease, we clearly show that the spreading dynamics of the two-types of processes influence each other. We build a mathematical model in which both types of spreading dynamics are described using the SIS process in order to illustrate the influence of information diffusion on epidemic spreading. Both the simulation results and the pairwise analysis reveal that information diffusion can increase the threshold of an epidemic outbreak, decrease the final fraction of infected individuals and significantly decrease the rate at which the epidemic propagates. Additionally, we find that the multi-outbreak phenomena of epidemic spreading, along with the impact of information diffusion, is consistent with the empirical results. These findings highlight the requirement to maintain social awareness of diseases even when the epidemics seem to be under control in order to prevent a subsequent outbreak. These results may shed light on the in-depth understanding of the interplay between the dynamics of epidemic spreading and information diffusion.
In spite of the extensive previous efforts on traffic dynamics and epidemic spreading in complex networks, the problem of traffic-driven epidemic spreading on {em correlated} networks has not been addressed. Interestingly, we find that the epidemic threshold, a fundamental quantity underlying the spreading dynamics, exhibits a non-monotonic behavior in that it can be minimized for some critical value of the assortativity coefficient, a parameter characterizing the network correlation. To understand this phenomenon, we use the degree-based mean-field theory to calculate the traffic-driven epidemic threshold for correlated networks. The theory predicts that the threshold is inversely proportional to the packet-generation rate and the largest eigenvalue of the betweenness matrix. We obtain consistency between theory and numerics. Our results may provide insights into the important problem of controlling/harnessing real-world epidemic spreading dynamics driven by traffic flows.
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