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To improve the accuracy of network-based SIS models we introduce and study a multilayer representation of a time-dependent network. In particular, we assume that individuals have their long-term (permanent) contacts that are always present, identifying in this way the first network layer. A second network layer also exists, where the same set of nodes can be connected by occasional links, created with a given probability. While links of the first layer are permanent, a link of the second layer is only activated with some probability and under the condition that the two nodes, connected by this link, are simultaneously participating to the temporary link. We develop a model for the SIS epidemic on this time-dependent network, analyze equilibrium and stability of the corresponding mean-field equations, and shed some light on the role of the temporal layer on the spreading process.
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Networks are a convenient way to represent complex systems of interacting entities. Many networks contain communities of nodes that are more densely connected to each other than to nodes in the rest of the network. In this paper, we investigate the detection of communities in temporal networks represented as multilayer networks. As a focal example, we study time-dependent financial-asset correlation networks. We first argue that the use of the modularity quality function---which is defined by comparing edge weights in an observed network to expected edge weights in a null network---is application-dependent. We differentiate between null networks and null models in our discussion of modularity maximization, and we highlight that the same null network can correspond to different null models. We then investigate a multilayer modularity-maximization problem to identify communities in temporal networks. Our multilayer analysis only depends on the form of the maximization problem and not on the specific quality function that one chooses. We introduce a diagnostic to measure emph{persistence} of community structure in a multilayer network partition. We prove several results that describe how the multilayer maximization problem measures a trade-off between static community structure within layers and larger values of persistence across layers. We also discuss some computational issues that the popular Louvain heuristic faces with temporal multilayer networks and suggest ways to mitigate them.
Defining an optimal protection strategy against viruses, spam propagation or any other kind of contamination process is an important feature for designing new networks and architectures. In this work, we consider decentralized optimal protection strategies when a virus is propagating over a network through a SIS epidemic process. We assume that each node in the network can fully protect itself from infection at a constant cost, or the node can use recovery software, once it is infected. We model our system using a game theoretic framework and find pure, mixed equilibria, and the Price of Anarchy (PoA) in several network topologies. Further, we propose both a decentralized algorithm and an iterative procedure to compute a pure equilibrium in the general case of a multiple communities network. Finally, we evaluate the algorithms and give numerical illustrations of all our results.
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
In this work, we use the spectral properties of graphons to study stability and sensitivity to noise of deterministic SIS epidemics over large networks. We consider the presence of additive noise in a linearized SIS model and we derive a noise index to quantify the deviation from the disease-free state due to noise. For finite networks, we show that the index depends on the adjacency eigenvalues of its graph. We then assume that the graph is a random sample from a piecewise Lipschitz graphon with finite rank and, using the eigenvalues of the associated graphon operator, we find an approximation of the index that is tight when the network size goes to infinity. A numerical example is included to illustrate the results.
Stochastic epidemic models on networks are inherently high-dimensional and the resulting exact models are intractable numerically even for modest network sizes. Mean-field models provide an alternative but can only capture average quantities, thus offering little or no information about variability in the outcome of the exact process. In this paper we conjecture and numerically prove that it is possible to construct PDE-limits of the exact stochastic SIS epidemics on regular and ErdH{o}s-Renyi networks. To do this we first approximate the exact stochastic process at population level by a Birth-and-Death process (BD) (with a state space of $O(N)$ rather than $O(2^N)$) whose coefficients are determined numerically from Gillespie simulations of the exact epidemic on explicit networks. We numerically demonstrate that the coefficients of the resulting BD process are density-dependent, a crucial condition for the existence of a PDE limit. Extensive numerical tests for Regular and ErdH{o}s-Renyi networks show excellent agreement between the outcome of simulations and the numerical solution of the Fokker-Planck equations. Apart from a significant reduction in dimensionality, the PDE also provides the means to derive the epidemic outbreak threshold linking network and disease dynamics parameters, albeit in an implicit way. Perhaps more importantly, it enables the formulation and numerical evaluation of likelihoods for epidemic and network inference as illustrated in a worked out example.
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