Vincent Marceau

Abstract:
Many complex systems have been shown to share universal properties of organization, such as scale independence, modularity, and self-similarity. We borrow tools from statistical physics in order to study structural preferential attachment (SPA), a recently proposed growth principle for the emergence of the aforementioned properties. We study the corresponding stochastic process in terms of its time evolution, its asymptotic behavior, and the scaling properties of its statistical steady state. Moreover, approximations are introduced to facilitate the modeling of real systems, mainly complex networks, using SPA. Finally, we investigate a particular behavior observed in the stochastic process, the peloton dynamics, and show how it predicts some features of real growing systems using prose samples as an example.

Abstract:
By generating the specifics of a network structure only when needed (on-the-fly), we derive a simple stochastic process that exactly models the time evolution of susceptible-infectious dynamics on finite-size networks. The small number of dynamical variables of this birth-death Markov process greatly simplifies analytical calculations. We show how a dual analytical description, treating large scale epidemics with a Gaussian approximation and small outbreaks with a branching process, provides an accurate approximation of the distribution even for rather small networks. The approach also offers important computational advantages and generalizes to a vast class of systems.

Abstract:
We introduce a mechanism which models the emergence of the universal properties of complex networks, such as scale independence, modularity and self-similarity, and unifies them under a scale-free organization beyond the link. This brings a new perspective on network organization where communities, instead of links, are the fundamental building blocks of complex systems. We show how our simple model can reproduce social and information networks by predicting their community structure and more importantly, how their nodes or communities are interconnected, often in a self-similar manner.

Abstract:
Epidemics seldom occur as isolated phenomena. Typically, two or more viral agents spread within the same host population and may interact dynamically with each other. We present a general model where two viral agents interact via an immunity mechanism as they propagate simultaneously on two networks connecting the same set of nodes. By exploiting a correspondence between the propagation dynamics and a dynamical process performing progressive network generation, we develop an analytical approach that accurately captures the dynamical interaction between epidemics on overlay networks. The formalism allows for overlay networks with arbitrary joint degree distribution and overlap. To illustrate the versatility of our approach, we consider a hypothetical delayed intervention scenario in which an immunizing agent is disseminated in a host population to hinder the propagation of an undesirable agent (e.g., the spread of preventive information in the context of an emerging infectious disease).

Abstract:
Analytical description of propagation phenomena on random networks has flourished in recent years, yet more complex systems have mainly been studied through numerical means. In this paper, a mean-field description is used to coherently couple the dynamics of the network elements (such as nodes, vertices, individuals, etc.) on the one hand and their recurrent topological patterns (such as subgraphs, groups, etc.) on the other hand. In a susceptible-infectious-susceptible (SIS) model of epidemic spread on social networks with community structure, this approach yields a set of ordinary differential equations for the time evolution of the system, as well as analytical solutions for the epidemic threshold and equilibria. The results obtained are in good agreement with numerical simulations and reproduce the behavior of random networks in the appropriate limits which highlights the influence of topology on the processes. Finally, it is demonstrated that our model predicts higher epidemic thresholds for clustered structures than for equivalent random topologies in the case of networks with zero degree correlation.br>

Abstract:
Adaptive networks have been recently introduced in the context of disease propagation on complex networks. They account for the mutual interaction between the network topology and the states of the nodes. Until now, existing models have been analyzed using low complexity analytical formalisms, revealing nevertheless some novel dynamical features. However, current methods have failed to reproduce with accuracy the simultaneous time evolution of the disease and the underlying network topology. In the framework of the adaptive susceptible-infectious-susceptible (SIS) model of Gross et al.[Phys. Rev. Lett. 96, 208701 (2006)], we introduce an improved compartmental formalism able to handle this coevolutionary task successfully. With this approach, we analyze the interplay and outcomes of both dynamical elements, process and structure, on adaptive networks featuring different degree distributions at the initial stage.