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

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

Distinguishing Infections on Different Graph Topologies

The history of infections and epidemics holds famous examples where understanding, containing and ultimately treating an outbreak began with understanding its mode of spread. Influenza, HIV and most computer viruses, spread person to person, device to device, through contact networks; Cholera, Cancer, and seasonal allergies, on the other hand, do not. In this paper we study two fundamental questions of detection: first, given a snapshot view of a (perhaps vanishingly small) fraction of those infected, under what conditions is an epidemic spreading via contact (e.g., Influenza), distinguishable from a "random illness" operating independently of any contact network (e.g., seasonal allergies); second, if we do have an epidemic, under what conditions is it possible to determine which network of interactions is the main cause of the spread -- the causative network -- without any knowledge of the epidemic, other than the identity of a minuscule subsample of infected nodes? The core, therefore, of this paper, is to obtain an understanding of the diagnostic power of network information. We derive sufficient conditions networks must satisfy for these problems to be identifiable, and produce efficient, highly scalable algorithms that solve these problems. We show that the identifiability condition we give is fairly mild, and in particular, is satisfied by two common graph topologies: the grid, and the Erdos-Renyi graphs