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.
In this paper we provide the derivation of a super compact pairwise model with only 4 equations in the context of describing susceptible-infected-susceptible (SIS) epidemic dynamics on heterogenous networks. The super compact model is based on a new
closure relation that involves not only the average degree but also the second and third moments of the degree distribution. Its derivation uses an a priori approximation of the degree distribution of susceptible nodes in terms of the degree distribution of the network. The new closure gives excellent agreement with heterogeneous pairwise models that contain significantly more differential equations.
Non-Markovian processes are widespread in natural and human-made systems, yet explicit model- ling and analysis of such systems is underdeveloped. We consider a non-Markovian dynamic network with random link activation and deletion (RLAD) and heavy t
ailed Mittag-Leffler distribution for the inter-event times. We derive an analytically and computationally tractable system of Kolmogorov- like forward equations utilising the Caputo derivative for the probability of having a given number of active links in the network and solve them. Simulations for the RLAD are also studied for power-law inter-event times and we show excellent agreement with the Mittag-Leffler model. This agreement holds even when the RLAD network dynamics is coupled with the susceptible-infected-susceptible (SIS) spreading dynamics. Thus, the analytically solvable Mittag-Leffler model provides an excel- lent approximation to the case when the network dynamics is characterised by power-law distributed inter-event times. We further discuss possible generalizations of our result.
An adaptive network model using SIS epidemic propagation with link-type dependent link activation and deletion is considered. Bifurcation analysis of the pairwise ODE approximation and the network-based stochastic simulation is carried out, showing t
hat three typical behaviours may occur; namely, oscillations can be observed besides disease-free or endemic steady states. The oscillatory behaviour in the stochastic simulations is studied using Fourier analysis, as well as through analysing the exact master equations of the stochastic model. A compact pairwise approximation for the dynamic network case is also developed and, for the case of link-type independent rewiring, the outcome of epidemics and changes in network structure are concurrently presented in a single bifurcation diagram. By going beyond simply comparing simulation results to mean-field models, our approach yields deeper insights into the observed phenomena and help better understand and map out the limitations of mean-field models.
The existence of a die-out threshold (different from the classic disease-invasion one) defining a region of slow extinction of an epidemic has been proved elsewhere for susceptible-aware-infectious-susceptible models without awareness decay, through
bifurcation analysis. By means of an equivalent mean-field model defined on regular random networks, we interpret the dynamics of the system in this region and prove that the existence of bifurcation for this second epidemic threshold crucially depends on the absence of awareness decay. We show that the continuum of equilibria that characterizes the slow die-out dynamics collapses into a unique equilibrium when a constant rate of awareness decay is assumed, no matter how small, and that the resulting bifurcation from the disease-free equilibrium is equivalent to that of standard epidemic models. We illustrate these findings with continuous-time stochastic simulations on regular random networks with different degrees. Finally, the behaviour of solutions with and without decay in awareness is compared around the second epidemic threshold for a small rate of awareness decay.
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 th
is 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.
