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Register a new userSome aspects of the Markovian SIRS epidemic on networks and its mean-field approximation
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We study the spread of an SIRS-type epidemic with vaccination on network. Starting from an exact Markov description of the model, we investigate the mean epidemic lifetime by providing a sufficient condition for fast extinction that depends on the model parameters and the topology of the network. Then, we pass to consider a firstorder mean-field approximation of the exact model and its stability properties, by relying on the graph-theoretical notion of equitable partition. In the case of graphs possessing this kind of partition, we prove that the endemic equilibrium can be computed by using a lower-dimensional dynamical system. Finally, in the special case of regular graphs, we investigate the domain of attraction of the endemic equilibrium.
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Clustering is the propensity of nodes that share a common neighbour to be connected. It is ubiquitous in many networks but poses many modelling challenges. Clustering typically manifests itself by a higher than expected frequency of triangles, and this has led to the principle of constructing networks from such building blocks. This approach has been generalised to networks being constructed from a set of more exotic subgraphs. As long as these are fully connected, it is then possible to derive mean-field models that approximate epidemic dynamics well. However, there are virtually no results for non-fully connected subgraphs. In this paper, we provide a general and automated approach to deriving a set of ordinary differential equations, or mean-field model, that describes, to a high degree of accuracy, the expected values of system-level quantities, such as the prevalence of infection. Our approach offers a previously unattainable degree of control over the arrangement of subgraphs and network characteristics such as classical node degree, variance and clustering. The combination of these features makes it possible to generate families of networks with different subgraph compositions while keeping classical network metrics constant. Using our approach, we show that higher-order structure realised either through the introduction of loops of different sizes or by generating clustered networks based on different subgraphs, leads to significant differences in epidemic dynamics despite controlling for basic network metrics.
The concept of square-mean almost automorphy for stochastic processes is introduced. The existence and uniqueness of square-mean almost automorphic solutions to some linear and non-linear stochastic differential equations are established provided the coefficients satisfy some conditions. The asymptotic stability of the unique square-mean almost automorphic solution in square-mean sense is discussed.
Networks are widely used to model the contact structure within a population and in the resulting models of disease spread. While networks provide a high degree of realism, the analysis of the exact model is out of reach and even numerical methods fail for modest network size. Hence, mean-field models (e.g. pairwise) focusing on describing the evolution of some summary statistics from the exact model gained a lot of traction over the last few decades. In this paper we revisit the problem of deriving triple closures for pairwise models and we investigate in detail the assumptions behind some of the well-known closures as well as their validity. Using a top-down approach we start at the level of the entire graph and work down to the level of triples and combine this with information around nodes and pairs. We use our approach to derive many of the existing closures and propose new ones and theoretically connect the two well-studied models of multinomial link and Poisson link selection. The theoretical work is backed up by numerical examples to highlight where the commonly used assumptions may fail and provide some recommendations for how to choose the most appropriate closure when using graphs with no or modest degree heterogeneity.
In this letter, a generalization of pairwise models to non-Markovian epidemics on networks is presented. For the case of infectious periods of fixed length, the resulting pairwise model is a system of delay differential equations (DDEs), which shows excellent agreement with results based on explicit stochastic simulations of non-Markovian epidemics on networks. Furthermore, we analytically compute a new R0-like threshold quantity and an implicit analytical relation between this and the final epidemic size. In addition we show that the pairwise model and the analytic calculations can be generalized in terms of integro-differential equations to any distribution of the infectious period, and we illustrate this by presenting a closed form expression for the final epidemic size. By showing the rigorous mathematical link between non-Markovian network epidemics and pairwise DDEs, we provide the framework for a deeper and more rigorous understanding of the impact of non-Markovian dynamics with explicit results for final epidemic size and threshold quantities.
Time-varying network topologies can deeply influence dynamical processes mediated by them. Memory effects in the pattern of interactions among individuals are also known to affect how diffusive and spreading phenomena take place. In this paper we analyze the combined effect of these two ingredients on epidemic dynamics on networks. We study the susceptible-infected-susceptible (SIS) and the susceptible-infected-removed (SIR) models on the recently introduced activity-driven networks with memory. By means of an activity-based mean-field approach we derive, in the long time limit, analytical predictions for the epidemic threshold as a function of the parameters describing the distribution of activities and the strength of the memory effects. Our results show that memory reduces the threshold, which is the same for SIS and SIR dynamics, therefore favouring epidemic spreading. The theoretical approach perfectly agrees with numerical simulations in the long time asymptotic regime. Strong aging effects are present in the preasymptotic regime and the epidemic threshold is deeply affected by the starting time of the epidemics. We discuss in detail the origin of the model-dependent preasymptotic corrections, whose understanding could potentially allow for epidemic control on correlated temporal networks.
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