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Background: Controlling global epidemics in the real world and accelerating information propagation in the artificial world are of great significance, which have activated an upsurge in the studies on networked spreading dynamics. Lots of efforts have been made to understand the impacts of macroscopic statistics (e.g., degree distribution and average distance) and mesoscopic structures (e.g., communities and rich clubs) on spreading processes while the microscopic elements are less concerned. In particular, roles of ties are not yet clear to the academic community. Methodology/Principle Findings: Every edges is stamped by its strength that is defined solely based on the local topology. According to a weighted susceptible-infected-susceptible model, the steady-state infected density and spreading speed are respectively optimized by adjusting the relationship between edges strength and spreading ability. Experiments on six real networks show that the infected density is increased when strong ties are favored in the spreading, while the speed is enhanced when weak ties are favored. Significance of these findings is further demonstrated by comparing with a null model. Conclusions/Significance: Experimental results indicate that strong and weak ties play distinguishable roles in spreading dynamics: the former enlarge the infected density while the latter fasten the process. The proposed method provides a quantitative way to reveal the qualitatively different roles of ties, which could find applications in analyzing many networked dynamical processes with multiple performance indices, such as synchronizability and converging time in synchronization and throughput and delivering time in transportation.
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Understanding spreading dynamics will benefit society as a whole in better preventing and controlling diseases, as well as facilitating the socially responsible information while depressing destructive rumors. In network-based spreading dynamics, edges with different weights may play far different roles: a friend from afar usually brings novel stories, and an intimate relationship is highly risky for a flu epidemic. In this article, we propose a weighted susceptible-infected-susceptible model on complex networks, where the weight of an edge is defined by the topological proximity of the two associated nodes. Each infected individual is allowed to select limited number of neighbors to contact, and a tunable parameter is introduced to control the preference to contact through high-weight or low-weight edges. Experimental results on six real networks show that the epidemic prevalence can be largely promoted when strong ties are favored in the spreading process. By comparing with two statistical null models respectively with randomized topology and randomly redistributed weights, we show that the distribution pattern of weights, rather than the topology, mainly contributes to the experimental observations. Further analysis suggests that the weight-weight correlation strongly affects the results: high-weight edges are more significant in keeping high epidemic prevalence when the weight-weight correlation is present.
Algorithms for search of communities in networks usually consist discrete variations of links. Here we discuss a flow method, driven by a set of differential equations. Two examples are demonstrated in detail. First is a partition of a signed graph into two parts, where the proposed equations are interpreted in terms of removal of a cognitive dissonance by agents placed in the network nodes. There, the signs and values of links refer to positive or negative interpersonal relationships of different strength. Second is an application of a method akin to the previous one, dedicated to communities identification, to the Sierpinski triangle of finite size. During the time evolution, the related graphs are weighted; yet at the end the discrete character of links is restored. In the case of the Sierpinski triangle, the method is supplemented by adding a small noise to the initial connectivity matrix. By breaking the symmetry of the network, this allows to a successful handling of overlapping nodes.
Comparing with single networks, the multiplex networks bring two main effects on the spreading process among individuals. First, the pathogen or information can be transmitted to more individuals through different layers at one time, which enlarges the spreading scope. Second, through different layers, an individual can also transmit the pathogen or information to the same individuals more than once at one time, which makes the spreading more effective. To understand the different roles of the spreading scope and effectiveness, we propose an epidemic model on multiplex networks with link overlapping, where the spreading effectiveness of each interaction as well as the variety of channels (spreading scope) can be controlled by the number of overlapping links. We find that for Poisson degree distribution, increasing the epidemic scope (the first effect) is more efficient than enhancing epidemic probability (the second effect) to facilitate the spreading process. However, for power-law degree distribution, the effects of the two factors on the spreading dynamics become complicated. Enhancing epidemic probability makes pathogen or rumor easier to outbreak in a finite system. But after that increasing epidemic scopes is still more effective for a wide spreading. Theoretical results along with reasonable explanation for these phenomena are all given in this paper, which indicates that the epidemic scope could play an important role in the spreading dynamics.
The study of the weak-ties phenomenon has a long and well documented history, research into the application of this social phenomenon has recently attracted increasing attention. However, further exploration of the reasons behind the weak-ties phenomenon is still challenging. Fortunately, data-driven network science provides a novel way with substantial explanatory power to analyze the causal mechanism behind social phenomenon. Inspired by this perspective, we propose an approach to further explore the driving factors behind the temporal weak-ties phenomenon. We find that the obvious intuition underlying the weak-ties phenomenon is incorrect, and often large numbers of unknown mutual friends associated with these weak ties is one of the key reason for the emergence of the weak-ties phenomenon. In particular, for example scientific collaborators with weak ties prefer to be involved in direct collaboration rather than share ideas with mutual colleagues -- there is a natural tendency to collapse short strong chains of connection.
Most real networks are characterized by connectivity patterns that evolve in time following complex, non-Markovian, dynamics. Here we investigate the impact of this ubiquitous feature by studying the Susceptible-Infected-Recovered (SIR) and Susceptible-Infected-Susceptible (SIS) epidemic models on activity driven networks with and without memory (i.e., Markovian and non-Markovian). We show that while memory inhibits the spreading process in SIR models, where the epidemic threshold is moved to larger values, it plays the opposite effect in the case of the SIS, where the threshold is lowered. The heterogeneity in tie strengths, and the frequent repetition of connections that it entails, allows in fact less virulent SIS-like diseases to survive in tightly connected local clusters that serve as reservoir for the virus. We validate this picture by evaluating the threshold of both processes in a real temporal network. Our findings confirm the important role played by non-Markovian network dynamics on dynamical processes
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