Modeling the dynamical interaction between epidemics on overlay networks

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. Exploiting a correspondence between the propagation dynamics and a dynamical process performing progressive network generation, we develop an analytic 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).Comment: Accepted for publication in Phys. Rev. E. 15 pages, 7 figure

Time-Polynomial Lieb-Robinson bounds for finite-range spin-network models

The Lieb-Robinson bound sets a theoretical upper limit on the speed at which information can propagate in non-relativistic quantum spin networks. In its original version, it results in an exponentially exploding function of the evolution time, which is partially mitigated by an exponentially decreasing term that instead depends upon the distance covered by the signal (the ratio between the two exponents effectively defining an upper bound on the propagation speed). In the present paper, by properly accounting for the free parameters of the model, we show how to turn this construction into a stronger inequality where the upper limit only scales polynomially with respect to the evolution time. Our analysis applies to any chosen topology of the network, as long as the range of the associated interaction is explicitly finite. For the special case of linear spin networks we present also an alternative derivation based on a perturbative expansion approach which improves the previous inequality. In the same context we also establish a lower bound to the speed of the information spread which yields a non trivial result at least in the limit of small propagation times.Comment: 10 pages, 5 figure

Structural Properties of the Caenorhabditis elegans Neuronal Network

Despite recent interest in reconstructing neuronal networks, complete wiring diagrams on the level of individual synapses remain scarce and the insights into function they can provide remain unclear. Even for Caenorhabditis elegans, whose neuronal network is relatively small and stereotypical from animal to animal, published wiring diagrams are neither accurate nor complete and self-consistent. Using materials from White et al. and new electron micrographs we assemble whole, self-consistent gap junction and chemical synapse networks of hermaphrodite C. elegans. We propose a method to visualize the wiring diagram, which reflects network signal flow. We calculate statistical and topological properties of the network, such as degree distributions, synaptic multiplicities, and small-world properties, that help in understanding network signal propagation. We identify neurons that may play central roles in information processing and network motifs that could serve as functional modules of the network. We explore propagation of neuronal activity in response to sensory or artificial stimulation using linear systems theory and find several activity patterns that could serve as substrates of previously described behaviors. Finally, we analyze the interaction between the gap junction and the chemical synapse networks. Since several statistical properties of the C. elegans network, such as multiplicity and motif distributions are similar to those found in mammalian neocortex, they likely point to general principles of neuronal networks. The wiring diagram reported here can help in understanding the mechanistic basis of behavior by generating predictions about future experiments involving genetic perturbations, laser ablations, or monitoring propagation of neuronal activity in response to stimulation

Information Flow in Interaction Networks

Interaction networks, consisting of agents linked by their interactions, are ubiquitous across many disciplines of modern science. Many methods of analysis of interaction networks have been proposed, mainly concentrating on node degree distribution or aiming to discover clusters of agents that are very strongly connected between themselves. These methods are principally based on graph-theory or machine learning. We present a mathematically simple formalism for modelling context-specific information propagation in interaction networks based on random walks. The context is provided by selection of sources and destinations of information and by use of potential functions that direct the flow towards the destinations. We also use the concept of dissipation to model the aging of information as it diffuses from its source. Using examples from yeast protein-protein interaction networks and some of the histone acetyltransferases involved in control of transcription, we demonstrate the utility of the concepts and the mathematical constructs introduced in this paper.Comment: 30 pages, 5 figures. This paper was published in 2007 in Journal of Computational Biology. The version posted here does not include post peer-review change

Dynamical and bursty interactions in social networks

We present a modeling framework for dynamical and bursty contact networks made of agents in social interaction. We consider agents' behavior at short time scales, in which the contact network is formed by disconnected cliques of different sizes. At each time a random agent can make a transition from being isolated to being part of a group, or vice-versa. Different distributions of contact times and inter-contact times between individuals are obtained by considering transition probabilities with memory effects, i.e. the transition probabilities for each agent depend both on its state (isolated or interacting) and on the time elapsed since the last change of state. The model lends itself to analytical and numerical investigations. The modeling framework can be easily extended, and paves the way for systematic investigations of dynamical processes occurring on rapidly evolving dynamical networks, such as the propagation of an information, or spreading of diseases

Disease and information spreading at different speeds in multiplex networks

Nowadays, one of the challenges we face when carrying out modeling of epidemic spreading is to develop methods to control disease transmission. In this article we study how the spreading of knowledge of a disease affects the propagation of that disease in a population of interacting individuals. For that, we analyze the interaction between two different processes on multiplex networks: the propagation of an epidemic using the susceptible-infected-susceptible dynamics and the dissemination of information about the disease—and its prevention methods—using the unaware-aware-unaware dynamics, so that informed individuals are less likely to be infected. Unlike previous related models where disease and information spread at the same time scale, we introduce here a parameter that controls the relative speed between the propagation of the two processes. We study the behavior of this model using a mean-field approach that gives results in good agreement with Monte Carlo simulations on homogeneous complex networks. We find that increasing the rate of information dissemination reduces the disease prevalence, as one may expect. However, increasing the speed of the information process as compared to that of the epidemic process has the counterintuitive effect of increasing the disease prevalence. This result opens an interesting discussion about the effects of information spreading on disease propagation

Identification of redundant and synergetic circuits in triplets of electrophysiological data

Neural systems are comprised of interacting units, and relevant information regarding their function or malfunction can be inferred by analyzing the statistical dependencies between the activity of each unit. Whilst correlations and mutual information are commonly used to characterize these dependencies, our objective here is to extend interactions to triplets of variables to better detect and characterize dynamic information transfer. Our approach relies on the measure of interaction information (II). The sign of II provides information as to the extent to which the interaction of variables in triplets is redundant (R) or synergetic (S). Here, based on this approach, we calculated the R and S status for triplets of electrophysiological data recorded from drug-resistant patients with mesial temporal lobe epilepsy in order to study the spatial organization and dynamics of R and S close to the epileptogenic zone (the area responsible for seizure propagation). In terms of spatial organization, our results show that R matched the epileptogenic zone while S was distributed more in the surrounding area. In relation to dynamics, R made the largest contribution to high frequency bands (14-100Hz), whilst S was expressed more strongly at lower frequencies (1-7Hz). Thus, applying interaction information to such clinical data reveals new aspects of epileptogenic structure in terms of the nature (redundancy vs. synergy) and dynamics (fast vs. slow rhythms) of the interactions. We expect this methodology, robust and simple, can reveal new aspects beyond pair-interactions in networks of interacting units in other setups with multi-recording data sets (and thus, not necessarily in epilepsy, the pathology we have approached here).Comment: 31 pages, 6 figures, 3 supplementary figures. To appear in the Journal of Neural Engineering in its current for