Epidemic Spreading with External Agents

We study epidemic spreading processes in large networks, when the spread is assisted by a small number of external agents: infection sources with bounded spreading power, but whose movement is unrestricted vis-\`a-vis the underlying network topology. For networks which are `spatially constrained', we show that the spread of infection can be significantly speeded up even by a few such external agents infecting randomly. Moreover, for general networks, we derive upper-bounds on the order of the spreading time achieved by certain simple (random/greedy) external-spreading policies. Conversely, for certain common classes of networks such as line graphs, grids and random geometric graphs, we also derive lower bounds on the order of the spreading time over all (potentially network-state aware and adversarial) external-spreading policies; these adversarial lower bounds match (up to logarithmic factors) the spreading time achieved by an external agent with a random spreading policy. This demonstrates that random, state-oblivious infection-spreading by an external agent is in fact order-wise optimal for spreading in such spatially constrained networks

Epidemic Thresholds with External Agents

We study the effect of external infection sources on phase transitions in epidemic processes. In particular, we consider an epidemic spreading on a network via the SIS/SIR dynamics, which in addition is aided by external agents - sources unconstrained by the graph, but possessing a limited infection rate or virulence. Such a model captures many existing models of externally aided epidemics, and finds use in many settings - epidemiology, marketing and advertising, network robustness, etc. We provide a detailed characterization of the impact of external agents on epidemic thresholds. In particular, for the SIS model, we show that any external infection strategy with constant virulence either fails to significantly affect the lifetime of an epidemic, or at best, sustains the epidemic for a lifetime which is polynomial in the number of nodes. On the other hand, a random external-infection strategy, with rate increasing linearly in the number of infected nodes, succeeds under some conditions to sustain an exponential epidemic lifetime. We obtain similar sharp thresholds for the SIR model, and discuss the relevance of our results in a variety of settings.Comment: 12 pages, 2 figures (to appear in INFOCOM 2014

From Public Outrage to the Burst of Public Violence: An Epidemic-Like Model

This study extends classical models of spreading epidemics to describe the phenomenon of contagious public outrage, which eventually leads to the spread of violence following a disclosure of some unpopular political decisions and/or activity. Accordingly, a mathematical model is proposed to simulate from the start, the internal dynamics by which an external event is turned into internal violence within a population. Five kinds of agents are considered: "Upset" (U), "Violent" (V), "Sensitive" (S), "Immune" (I), and "Relaxed" (R), leading to a set of ordinary differential equations, which in turn yield the dynamics of spreading of each type of agents among the population. The process is stopped with the deactivation of the associated issue. Conditions coinciding with a twofold spreading of public violence are singled out. The results shed a new light to understand terror activity and provides some hint on how to curb the spreading of violence within population globally sensitive to specific world issues. Recent world violent events are discussed.Comment: 22 pages, 9 figure

Effect of Coupling on the Epidemic Threshold in Interconnected Complex Networks: A Spectral Analysis

In epidemic modeling, the term infection strength indicates the ratio of infection rate and cure rate. If the infection strength is higher than a certain threshold -- which we define as the epidemic threshold - then the epidemic spreads through the population and persists in the long run. For a single generic graph representing the contact network of the population under consideration, the epidemic threshold turns out to be equal to the inverse of the spectral radius of the contact graph. However, in a real world scenario it is not possible to isolate a population completely: there is always some interconnection with another network, which partially overlaps with the contact network. Results for epidemic threshold in interconnected networks are limited to homogeneous mixing populations and degree distribution arguments. In this paper, we adopt a spectral approach. We show how the epidemic threshold in a given network changes as a result of being coupled with another network with fixed infection strength. In our model, the contact network and the interconnections are generic. Using bifurcation theory and algebraic graph theory, we rigorously derive the epidemic threshold in interconnected networks. These results have implications for the broad field of epidemic modeling and control. Our analytical results are supported by numerical simulations.Comment: 7 page