Analytical computation of the epidemic threshold on temporal networks

The time variation of contacts in a networked system may fundamentally alter the properties of spreading processes and affect the condition for large-scale propagation, as encoded in the epidemic threshold. Despite the great interest in the problem for the physics, applied mathematics, computer science and epidemiology communities, a full theoretical understanding is still missing and currently limited to the cases where the time-scale separation holds between spreading and network dynamics or to specific temporal network models. We consider a Markov chain description of the Susceptible-Infectious-Susceptible process on an arbitrary temporal network. By adopting a multilayer perspective, we develop a general analytical derivation of the epidemic threshold in terms of the spectral radius of a matrix that encodes both network structure and disease dynamics. The accuracy of the approach is confirmed on a set of temporal models and empirical networks and against numerical results. In addition, we explore how the threshold changes when varying the overall time of observation of the temporal network, so as to provide insights on the optimal time window for data collection of empirical temporal networked systems. Our framework is both of fundamental and practical interest, as it offers novel understanding of the interplay between temporal networks and spreading dynamics.Comment: 22 pages, 6 figure

Epidemic Threshold in Continuous-Time Evolving Networks

Current understanding of the critical outbreak condition on temporal networks relies on approximations (time scale separation, discretization) that may bias the results. We propose a theoretical framework to compute the epidemic threshold in continuous time through the infection propagator approach. We introduce the {\em weak commutation} condition allowing the interpretation of annealed networks, activity-driven networks, and time scale separation into one formalism. Our work provides a coherent connection between discrete and continuous time representations applicable to realistic scenarios.Comment: 13 pages, 2 figure

Predicting epidemic risk from past temporal contact data

Understanding how epidemics spread in a system is a crucial step to prevent and control outbreaks, with broad implications on the system's functioning, health, and associated costs. This can be achieved by identifying the elements at higher risk of infection and implementing targeted surveillance and control measures. One important ingredient to consider is the pattern of disease-transmission contacts among the elements, however lack of data or delays in providing updated records may hinder its use, especially for time-varying patterns. Here we explore to what extent it is possible to use past temporal data of a system's pattern of contacts to predict the risk of infection of its elements during an emerging outbreak, in absence of updated data. We focus on two real-world temporal systems; a livestock displacements trade network among animal holdings, and a network of sexual encounters in high-end prostitution. We define the node's loyalty as a local measure of its tendency to maintain contacts with the same elements over time, and uncover important non-trivial correlations with the node's epidemic risk. We show that a risk assessment analysis incorporating this knowledge and based on past structural and temporal pattern properties provides accurate predictions for both systems. Its generalizability is tested by introducing a theoretical model for generating synthetic temporal networks. High accuracy of our predictions is recovered across different settings, while the amount of possible predictions is system-specific. The proposed method can provide crucial information for the setup of targeted intervention strategies.Comment: 24 pages, 5 figures + SI (18 pages, 15 figures

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

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

Human mobility networks and persistence of rapidly mutating pathogens

Rapidly mutating pathogens may be able to persist in the population and reach an endemic equilibrium by escaping hosts' acquired immunity. For such diseases, multiple biological, environmental and population-level mechanisms determine the dynamics of the outbreak, including pathogen's epidemiological traits (e.g. transmissibility, infectious period and duration of immunity), seasonality, interaction with other circulating strains and hosts' mixing and spatial fragmentation. Here, we study a susceptible-infected-recovered-susceptible model on a metapopulation where individuals are distributed in subpopulations connected via a network of mobility flows. Through extensive numerical simulations, we explore the phase space of pathogen's persistence and map the dynamical regimes of the pathogen following emergence. Our results show that spatial fragmentation and mobility play a key role in the persistence of the disease whose maximum is reached at intermediate mobility values. We describe the occurrence of different phenomena including local extinction and emergence of epidemic waves, and assess the conditions for large scale spreading. Findings are highlighted in reference to previous works and to real scenarios. Our work uncovers the crucial role of hosts' mobility on the ecological dynamics of rapidly mutating pathogens, opening the path for further studies on disease ecology in the presence of a complex and heterogeneous environment.Comment: 29 pages, 7 figures. Submitted for publicatio

Metapopulation epidemic models with heterogeneous mixing and travel behaviour.

BACKGROUND: Determining the pandemic potential of an emerging infectious disease and how it depends on the various epidemic and population aspects is critical for the preparation of an adequate response aimed at its control. The complex interplay between population movements in space and non-homogeneous mixing patterns have so far hindered the fundamental understanding of the conditions for spatial invasion through a general theoretical framework. To address this issue, we present an analytical modelling approach taking into account such interplay under general conditions of mobility and interactions, in the simplifying assumption of two population classes. METHODS: We describe a spatially structured population with non-homogeneous mixing and travel behaviour through a multi-host stochastic epidemic metapopulation model. Different population partitions, mixing patterns and mobility structures are considered, along with a specific application for the study of the role of age partition in the early spread of the 2009 H1N1 pandemic influenza. RESULTS: We provide a complete mathematical formulation of the model and derive a semi-analytical expression of the threshold condition for global invasion of an emerging infectious disease in the metapopulation system. A rich solution space is found that depends on the social partition of the population, the pattern of contacts across groups and their relative social activity, the travel attitude of each class, and the topological and traffic features of the mobility network. Reducing the activity of the less social group and reducing the cross-group mixing are predicted to be the most efficient strategies for controlling the pandemic potential in the case the less active group constitutes the majority of travellers. If instead traveling is dominated by the more social class, our model predicts the existence of an optimal across-groups mixing that maximises the pandemic potential of the disease, whereas the impact of variations in the activity of each group is less important. CONCLUSIONS: The proposed modelling approach introduces a theoretical framework for the study of infectious diseases spread in a population with two layers of heterogeneity relevant for the local transmission and the spatial propagation of the disease. It can be used for pandemic preparedness studies to identify adequate interventions and quantitatively estimate the corresponding required effort, as well as in an emerging epidemic situation to assess the pandemic potential of the pathogen from population and early outbreak data

Dynamics of new strain emergence on a temporal network

Multi-strain competition on networks is observed in many contexts, including infectious disease ecology, information dissemination or behavioral adaptation to epidemics. Despite a substantial body of research has been developed considering static, time-aggregated networks, it remains a challenge to understand the transmission of concurrent strains when links of the network are created and destroyed over time. Here we analyze how network dynamics shapes the outcome of the competition between an initially endemic strain and an emerging one, when both strains follow a susceptible-infected-susceptible dynamics, and spread at time scales comparable with the network evolution one. Using time-resolved data of close-proximity interactions between patients admitted to a hospital and medical health care workers, we analyze the impact of temporal patterns and initial conditions on the dominance diagram and coexistence time. We find that strong variations in activity volume cause the probability that the emerging strain replaces the endemic one to be highly sensitive to the time of emergence. The temporal structure of the network shapes the dominance diagram, with significant variations in the replacement probability (for a given set of epidemiological parameters) observed from the empirical network and a randomized version of it. Our work contributes towards the description of the complex interplay between competing pathogens on temporal networks.Comment: 9 pages, 4 figure

Human Mobility Networks, Travel Restrictions, and the Global Spread of 2009 H1N1 Pandemic

After the emergence of the H1N1 influenza in 2009, some countries responded with travel-related controls during the early stage of the outbreak in an attempt to contain or slow down its international spread. These controls along with self-imposed travel limitations contributed to a decline of about 40% in international air traffic to/from Mexico following the international alert. However, no containment was achieved by such restrictions and the virus was able to reach pandemic proportions in a short time. When gauging the value and efficacy of mobility and travel restrictions it is crucial to rely on epidemic models that integrate the wide range of features characterizing human mobility and the many options available to public health organizations for responding to a pandemic. Here we present a comprehensive computational and theoretical study of the role of travel restrictions in halting and delaying pandemics by using a model that explicitly integrates air travel and short-range mobility data with high-resolution demographic data across the world and that is validated by the accumulation of data from the 2009 H1N1 pandemic. We explore alternative scenarios for the 2009 H1N1 pandemic by assessing the potential impact of mobility restrictions that vary with respect to their magnitude and their position in the pandemic timeline. We provide a quantitative discussion of the delay obtained by different mobility restrictions and the likelihood of containing outbreaks of infectious diseases at their source, confirming the limited value and feasibility of international travel restrictions. These results are rationalized in the theoretical framework characterizing the invasion dynamics of the epidemics at the metapopulation level