Arrival Time Statistics in Global Disease Spread

Metapopulation models describing cities with different populations coupled by the travel of individuals are of great importance in the understanding of disease spread on a large scale. An important example is the Rvachev-Longini model [{\it Math. Biosci.} {\bf 75}, 3-22 (1985)] which is widely used in computational epidemiology. Few analytical results are however available and in particular little is known about paths followed by epidemics and disease arrival times. We study the arrival time of a disease in a city as a function of the starting seed of the epidemics. We propose an analytical Ansatz, test it in the case of a spreading on the world wide air transportation network, and show that it predicts accurately the arrival order of a disease in world-wide cities

Variability of Contact Process in Complex Networks

We study numerically how the structures of distinct networks influence the epidemic dynamics in contact process. We first find that the variability difference between homogeneous and heterogeneous networks is very narrow, although the heterogeneous structures can induce the lighter prevalence. Contrary to non-community networks, strong community structures can cause the secondary outbreak of prevalence and two peaks of variability appeared. Especially in the local community, the extraordinarily large variability in early stage of the outbreak makes the prediction of epidemic spreading hard. Importantly, the bridgeness plays a significant role in the predictability, meaning the further distance of the initial seed to the bridgeness, the less accurate the predictability is. Also, we investigate the effect of different disease reaction mechanisms on variability, and find that the different reaction mechanisms will result in the distinct variabilities at the end of epidemic spreading.Comment: 6 pages, 4 figure

Fluctuation effects in metapopulation models: percolation and pandemic threshold

Metapopulation models provide the theoretical framework for describing disease spread between different populations connected by a network. In particular, these models are at the basis of most simulations of pandemic spread. They are usually studied at the mean-field level by neglecting fluctuations. Here we include fluctuations in the models by adopting fully stochastic descriptions of the corresponding processes. This level of description allows to address analytically, in the SIS and SIR cases, problems such as the existence and the calculation of an effective threshold for the spread of a disease at a global level. We show that the possibility of the spread at the global level is described in terms of (bond) percolation on the network. This mapping enables us to give an estimate (lower bound) for the pandemic threshold in the SIR case for all values of the model parameters and for all possible networks.Comment: 14 pages, 13 figures, final versio

Temporal networks of face-to-face human interactions

The ever increasing adoption of mobile technologies and ubiquitous services allows to sense human behavior at unprecedented levels of details and scale. Wearable sensors are opening up a new window on human mobility and proximity at the finest resolution of face-to-face proximity. As a consequence, empirical data describing social and behavioral networks are acquiring a longitudinal dimension that brings forth new challenges for analysis and modeling. Here we review recent work on the representation and analysis of temporal networks of face-to-face human proximity, based on large-scale datasets collected in the context of the SocioPatterns collaboration. We show that the raw behavioral data can be studied at various levels of coarse-graining, which turn out to be complementary to one another, with each level exposing different features of the underlying system. We briefly review a generative model of temporal contact networks that reproduces some statistical observables. Then, we shift our focus from surface statistical features to dynamical processes on empirical temporal networks. We discuss how simple dynamical processes can be used as probes to expose important features of the interaction patterns, such as burstiness and causal constraints. We show that simulating dynamical processes on empirical temporal networks can unveil differences between datasets that would otherwise look statistically similar. Moreover, we argue that, due to the temporal heterogeneity of human dynamics, in order to investigate the temporal properties of spreading processes it may be necessary to abandon the notion of wall-clock time in favour of an intrinsic notion of time for each individual node, defined in terms of its activity level. We conclude highlighting several open research questions raised by the nature of the data at hand.Comment: Chapter of the book "Temporal Networks", Springer, 2013. Series: Understanding Complex Systems. Holme, Petter; Saram\"aki, Jari (Eds.

Characterising two-pathogen competition in spatially structured environments

Different pathogens spreading in the same host population often generate complex co-circulation dynamics because of the many possible interactions between the pathogens and the host immune system, the host life cycle, and the space structure of the population. Here we focus on the competition between two acute infections and we address the role of host mobility and cross-immunity in shaping possible dominance/co-dominance regimes. Host mobility is modelled as a network of traveling flows connecting nodes of a metapopulation, and the two-pathogen dynamics is simulated with a stochastic mechanistic approach. Results depict a complex scenario where, according to the relation among the epidemiological parameters of the two pathogens, mobility can either be non-influential for the competition dynamics or play a critical role in selecting the dominant pathogen. The characterisation of the parameter space can be explained in terms of the trade-off between pathogen's spreading velocity and its ability to diffuse in a sparse environment. Variations in the cross-immunity level induce a transition between presence and absence of competition. The present study disentangles the role of the relevant biological and ecological factors in the competition dynamics, and provides relevant insights into the spatial ecology of infectious diseases.Comment: 30 pages, 6 figures, 1 table. Final version accepted for publication in Scientific Report

Fractional diffusion emulates a human mobility network during a simulated disease outbreak

From footpaths to flight routes, human mobility networks facilitate the spread of communicable diseases. Control and elimination efforts depend on characterizing these networks in terms of connections and flux rates of individuals between contact nodes. In some cases, transport can be parameterized with gravity-type models or approximated by a diffusive random walk. As a alternative, we have isolated intranational commercial air traffic as a case study for the utility of non-diffusive, heavy-tailed transport models. We implemented new stochastic simulations of a prototypical influenza-like infection, focusing on the dense, highly-connected United States air travel network. We show that mobility on this network can be described mainly by a power law, in agreement with previous studies. Remarkably, we find that the global evolution of an outbreak on this network is accurately reproduced by a two-parameter space-fractional diffusion equation, such that those parameters are determined by the air travel network.Comment: 26 pages, 4 figure