Identifying spatial invasion of pandemics on metapopulation networks via anatomizing arrival history

Spatial spread of infectious diseases among populations via the mobility of humans is highly stochastic and heterogeneous. Accurate forecast/mining of the spread process is often hard to be achieved by using statistical or mechanical models. Here we propose a new reverse problem, which aims to identify the stochastically spatial spread process itself from observable information regarding the arrival history of infectious cases in each subpopulation. We solved the problem by developing an efficient optimization algorithm based on dynamical programming, which comprises three procedures: i, anatomizing the whole spread process among all subpopulations into disjoint componential patches; ii, inferring the most probable invasion pathways underlying each patch via maximum likelihood estimation; iii, recovering the whole process by assembling the invasion pathways in each patch iteratively, without burdens in parameter calibrations and computer simulations. Based on the entropy theory, we introduced an identifiability measure to assess the difficulty level that an invasion pathway can be identified. Results on both artificial and empirical metapopulation networks show the robust performance in identifying actual invasion pathways driving pandemic spread.Comment: 14pages, 8 figures; Accepted by IEEE Transactions on Cybernetic

Hybrid Epidemics - A Case Study on Computer Worm Conficker

Conficker is a computer worm that erupted on the Internet in 2008. It is unique in combining three different spreading strategies: local probing, neighbourhood probing, and global probing. We propose a mathematical model that combines three modes of spreading, local, neighbourhood and global to capture the worm's spreading behaviour. The parameters of the model are inferred directly from network data obtained during the first day of the Conifcker epidemic. The model is then used to explore the trade-off between spreading modes in determining the worm's effectiveness. Our results show that the Conficker epidemic is an example of a critically hybrid epidemic, in which the different modes of spreading in isolation do not lead to successful epidemics. Such hybrid spreading strategies may be used beneficially to provide the most effective strategies for promulgating information across a large population. When used maliciously, however, they can present a dangerous challenge to current internet security protocols

Networks and the epidemiology of infectious disease

The science of networks has revolutionised research into the dynamics of interacting elements. It could be argued that epidemiology in particular has embraced the potential of network theory more than any other discipline. Here we review the growing body of research concerning the spread of infectious diseases on networks, focusing on the interplay between network theory and epidemiology. The review is split into four main sections, which examine: the types of network relevant to epidemiology; the multitude of ways these networks can be characterised; the statistical methods that can be applied to infer the epidemiological parameters on a realised network; and finally simulation and analytical methods to determine epidemic dynamics on a given network. Given the breadth of areas covered and the ever-expanding number of publications, a comprehensive review of all work is impossible. Instead, we provide a personalised overview into the areas of network epidemiology that have seen the greatest progress in recent years or have the greatest potential to provide novel insights. As such, considerable importance is placed on analytical approaches and statistical methods which are both rapidly expanding fields. Throughout this review we restrict our attention to epidemiological issues

Impact of spatially constrained sampling of temporal contact networks on the evaluation of the epidemic risk

The ability to directly record human face-to-face interactions increasingly enables the development of detailed data-driven models for the spread of directly transmitted infectious diseases at the scale of individuals. Complete coverage of the contacts occurring in a population is however generally unattainable, due for instance to limited participation rates or experimental constraints in spatial coverage. Here, we study the impact of spatially constrained sampling on our ability to estimate the epidemic risk in a population using such detailed data-driven models. The epidemic risk is quantified by the epidemic threshold of the susceptible-infectious-recovered-susceptible model for the propagation of communicable diseases, i.e. the critical value of disease transmissibility above which the disease turns endemic. We verify for both synthetic and empirical data of human interactions that the use of incomplete data sets due to spatial sampling leads to the underestimation of the epidemic risk. The bias is however smaller than the one obtained by uniformly sampling the same fraction of contacts: it depends nonlinearly on the fraction of contacts that are recorded and becomes negligible if this fraction is large enough. Moreover, it depends on the interplay between the timescales of population and spreading dynamics.Comment: 21 pages, 7 figure

Correlations between stochastic endemic infection in multiple interacting subpopulations.

Heterogeneity plays an important role in the emergence, persistence and control of infectious diseases. Metapopulation models are often used to describe spatial heterogeneity, and the transition from random- to heterogeneous-mixing is made by incorporating the interaction, or coupling, within and between subpopulations. However, such couplings are difficult to measure explicitly; instead, their action through the correlations between subpopulations is often all that can be observed. We use moment-closure methods to investigate how the coupling and resulting correlation are related, considering systems of multiple identical interacting populations on highly symmetric complex networks: the complete network, the k-regular tree network, and the star network. We show that the correlation between the prevalence of infection takes a relatively simple form and can be written in terms of the coupling, network parameters and epidemiological parameters only. These results provide insight into the effect of metapopulation network structure on endemic disease dynamics, and suggest that detailed case-reporting data alone may be sufficient to infer the strength of between population interaction and hence lead to more accurate mathematical descriptions of infectious disease behaviour