The dynamic of social networks is driven by the interplay between diverse mechanisms that still challenge our theoretical and modelling efforts. Amongst them, two are known to play a central role in shaping the networks evolution, namely the heterogeneous propensity of individuals to i) be socially active and ii) establish a new social relationships with their alters. Here, we empirically characterise these two mechanisms in seven real networks describing temporal human interactions in three different settings: scientific collaborations, Twitter mentions, and mobile phone calls. We find that the individuals’ social activity and their strategy in choosing ties where to allocate their social interactions can be quantitatively described and encoded in a simple stochastic network modelling framework. The Master Equation of the model can be solved in the asymptotic limit. The analytical solutions provide an explicit description of both the system dynamic and the dynamical scaling laws characterising crucial aspects about the evolution of the networks. The analytical predictions match with accuracy the empirical observations, thus validating the theoretical approach. Our results provide a rigorous dynamical system framework that can be extended to include other processes shaping social dynamics and to generate data driven predictions for the asymptotic behaviour of social networks.

We investigate the effects of modular and temporal connectivity patterns on epidemic spreading. To this end, we introduce and analytically characterise a model of time-varying networks with tunable modularity. Within this framework, we study the epidemic size of Susceptible-Infected-Recovered, SIR, models and the epidemic threshold of Susceptible-Infected-Susceptible, SIS, models. Interestingly, we find that while the presence of tightly connected clusters inhibits SIR processes, it speeds up SIS phenomena. In this case, we observe that modular structures induce a reduction of the threshold with respect to time-varying networks without communities. We confirm the theoretical results by means of extensive numerical simulations both on synthetic graphs as well as on a real modular and temporal network.

The recent developments in the field of social networks shifted the focus from static to dynamical representations, calling for new methods for their analysis and modelling. Observations in real social systems identified two main mechanisms that play a primary role in networks’ evolution and influence ongoing spreading processes: the strategies individuals adopt when selecting between new or old social ties, and the bursty nature of the social activity setting the pace of these choices. We introduce a time-varying network model accounting both for ties selection and burstiness and we analytically study its phase diagram. The interplay of the two effects is non trivial and, interestingly, the effects of burstiness might be suppressed in regimes where individuals exhibit a strong preference towards previously activated ties. The results are tested against numerical simulations and compared with two empirical datasets with very good agreement. Consequently, the framework provides a principled method to classify the temporal features of real networks, and thus yields new insights to elucidate the effects of social dynamics on spreading processes.

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 present an extensive analysis of transport properties in superdiffusive twodimensional quenched random media, obtained by packing disks with radii distributed according to a Lévy law. We consider transport and scaling properties in samples packed with two different procedures, at fixed filling fraction and at self-similar packing, and we clarify the role of the two procedures in the superdiffusive effects. Using the behavior of the filling fraction in finite size systems as the main geometrical parameter, we define an effective Lévy exponent that correctly estimates the finite size effects. The effective Lévy exponent rules the dynamical scaling of the main transport properties and identifies the region where superdiffusive effects can be detected.