No Arabic abstract
Empirical temporal networks display strong heterogeneities in their dynamics, which profoundly affect processes taking place on these networks, such as rumor and epidemic spreading. Despite the recent wealth of data on temporal networks, little work has been devoted to the understanding of how such heterogeneities can emerge from microscopic mechanisms at the level of nodes and links. Here we show that long-term memory effects are present in the creation and disappearance of links in empirical networks. We thus consider a simple generative modeling framework for temporal networks able to incorporate these memory mechanisms. This allows us to study separately the role of each of these mechanisms in the emergence of heterogeneous network dynamics. In particular, we show analytically and numerically how heterogeneous distributions of contact durations, of inter-contact durations and of numbers of contacts per link emerge. We also study the individual effect of heterogeneities on dynamical processes, such as the paradigmatic Susceptible-Infected epidemic spreading model. Our results confirm in particular the crucial role of the distributions of inter-contact durations and of the numbers of contacts per link.
Most previous studies of epidemic dynamics on complex networks suppose that the disease will eventually stabilize at either a disease-free state or an endemic one. In reality, however, some epidemics always exhibit sporadic and recurrent behaviour in one region because of the invasion from an endemic population elsewhere. In this paper we address this issue and study a susceptible-infected-susceptible epidemiological model on a network consisting of two communities, where the disease is endemic in one community but alternates between outbreaks and extinctions in the other. We provide a detailed characterization of the temporal dynamics of epidemic patterns in the latter community. In particular, we investigate the time duration of both outbreak and extinction, and the time interval between two consecutive inter-community infections, as well as their frequency distributions. Based on the mean-field theory, we theoretically analyze these three timescales and their dependence on the average node degree of each community, the transmission parameters, and the number of intercommunity links, which are in good agreement with simulations, except when the probability of overlaps between successive outbreaks is too large. These findings aid us in better understanding the bursty nature of disease spreading in a local community, and thereby suggesting effective time-dependent control strategies.
Individual heterogeneity is a key characteristic of many real-world systems, from organisms to humans. However its role in determining the systems collective dynamics is typically not well understood. Here we study how individual heterogeneity impacts the system network dynamics by comparing linking mechanisms that favor similar or dissimilar individuals. We find that this heterogeneity-based evolution can drive explosive network behavior and dictates how a polarized population moves toward consensus. Our model shows good agreement with data from both biological and social science domains. We conclude that individual heterogeneity likely plays a key role in the collective development of real-world networks and communities, and cannot be ignored.
Vaccination is an important measure available for preventing or reducing the spread of infectious diseases. In this paper, an epidemic model including susceptible, infected, and imperfectly vaccinated compartments is studied on Watts-Strogatz small-world, Barabasi-Albert scale-free, and random scale-free networks. The epidemic threshold and prevalence are analyzed. For small-world networks, the effective vaccination intervention is suggested and its influence on the threshold and prevalence is analyzed. For scale-free networks, the threshold is found to be strongly dependent both on the effective vaccination rate and on the connectivity distribution. Moreover, so long as vaccination is effective, it can linearly decrease the epidemic prevalence in small-world networks, whereas for scale-free networks it acts exponentially. These results can help in adopting pragmatic treatment upon diseases in structured populations.
Understanding network flows such as commuter traffic in large transportation networks is an ongoing challenge due to the complex nature of the transportation infrastructure and of human mobility. Here we show a first-principles based method for traffic prediction using a cost based generalization of the radiation model for human mobility, coupled with a cost-minimizing algorithm for efficient distribution of the mobility fluxes through the network. Using US census and highway traffic data we show that traffic can efficiently and accurately be computed from a range-limited, network betweenness type calculation. The model based on travel time costs captures the lognormal distribution of the traffic and attains a high Pearson correlation coefficient (0.75) when compared to real traffic. Due to its principled nature, this method can inform many applications related to human mobility driven flows in spatial networks, ranging from transportation, through urban planning to mitigation of the effects of catastrophic events.
Proximity networks are time-varying graphs representing the closeness among humans moving in a physical space. Their properties have been extensively studied in the past decade as they critically affect the behavior of spreading phenomena and the performance of routing algorithms. Yet, the mechanisms responsible for their observed characteristics remain elusive. Here, we show that many of the observed properties of proximity networks emerge naturally and simultaneously in a simple latent space network model, called dynamic-$mathbb{S}^{1}$. The dynamic-$mathbb{S}^{1}$ does not model node mobility directly, but captures the connectivity in each snapshot---each snapshot in the model is a realization of the $mathbb{S}^{1}$ model of traditional complex networks, which is isomorphic to hyperbolic geometric graphs. By forgoing the motion component the model facilitates mathematical analysis, allowing us to prove the contact, inter-contact and weight distributions. We show that these distributions are power laws in the thermodynamic limit with exponents lying within the ranges observed in real systems. Interestingly, we find that network temperature plays a central role in network dynamics, dictating the exponents of these distributions, the time-aggregated agent degrees, and the formation of unique and recurrent components. Further, we show that paradigmatic epidemic and rumor spreading processes perform similarly in real and modeled networks. The dynamic-$mathbb{S}^{1}$ or extensions of it may apply to other types of time-varying networks and constitute the basis of maximum likelihood estimation methods that infer the node coordinates and their evolution in the latent spaces of real systems.