Continuous-time Markov process models of contagions are widely studied, not least because of their utility in predicting the evolution of real-world contagions and in formulating control measures. It is often the case, however, that discrete-time approaches are employed to analyze such models or to simulate them numerically. In such cases, time is discretized into uniform steps and transition rates between states are replaced by transition probabilities. In this paper, we illustrate potential limitations to this approach. We show how discretizing time leads to a restriction on the values of the model parameters that can accurately be studied. We examine numerical simulation schemes employed in the literature, showing how synchronous-type updating schemes can bias discrete-time formalisms when compared against continuous-time formalisms. Event-based simulations, such as the Gillespie algorithm, are proposed as optimal simulation schemes both in terms of replicating the continuous-time process and computational speed. Finally, we show how discretizing time can affect the value of the epidemic threshold for large values of the infection rate and the recovery rate, even if the ratio between the former and the latter is small.

Citation:O 'Sullivan DJP, O'Keeffe GJ, Fennell PG and Gleeson JP (2015) Mathematical modeling of complex contagion on clustered networks. Front. Phys. 3:71. doi: 10.3389/fphy.2015.00071 Mathematical modeling of complex contagion on clustered networks The spreading of behavior, such as the adoption of a new innovation, is influenced by the structure of social networks that interconnect the population. In the experiments of Centola [15], adoption of new behavior was shown to spread further and faster across clustered-lattice networks than across corresponding random networks. This implies that the "complex contagion" effects of social reinforcement are important in such diffusion, in contrast to "simple" contagion models of disease-spread which predict that epidemics would grow more efficiently on random networks than on clustered networks. To accurately model complex contagion on clustered networks remains a challenge because the usual assumptions (e.g., of mean-field theory) regarding tree-like networks are invalidated by the presence of triangles in the network; the triangles are, however, crucial to the social reinforcement mechanism, which posits an increased probability of a person adopting behavior that has been adopted by two or more neighbors. In this paper we modify the analytical approach that was introduced by Hébert-Dufresne et al. [19], to study disease-spread on clustered networks. We show how the approximation method can be adapted to a complex contagion model, and confirm the accuracy of the method with numerical simulations. The analytical results of the model enable us to quantify the level of social reinforcement that is required to observe-as in Centola's experiments-faster diffusion on clustered topologies than on random networks.

Multistate dynamical processes on networks, where nodes can occupy one of a multitude of discrete states, are gaining widespread use because of their ability to recreate realistic, complex behaviour that cannot be adequately captured by simpler binary-state models. In epidemiology, multistate models are employed to predict the evolution of real epidemics, while multistate models are used in the social sciences to study diverse opinions and complex phenomena such as segregation. In this paper, we introduce generalized approximation frameworks for the study and analysis of multistate dynamical processes on networks. These frameworks are degree-based, allowing for the analysis of the effect of network connectivity structures on dynamical processes. We illustrate the utility of our approach with the analysis of two specific dynamical processes from the epidemiological and physical sciences. The approximation frameworks that we develop, along with open-source numerical solvers, provide a unifying framework and a valuable suite of tools for the interdisciplinary study of multistate dynamical processes on networks.

Networks facilitate the spread of cascades, allowing a local perturbation to percolate via interactions between nodes and their neighbors. We investigate how network structure affects the dynamics of a spreading cascade. By accounting for the joint degree distribution of a network within a generating function framework, we can quantify how degree correlations affect both the onset of global cascades and the propensity of nodes of specific degree class to trigger large cascades. However, not all degree correlations are equally important in a spreading process. We introduce a new measure of degree assortativity that accounts for correlations among nodes relevant to a spreading cascade. We show that the critical point defining the onset of global cascades has a monotone relationship to this new assortativity measure. In addition, we show that the choice of nodes to seed the largest cascades is strongly affected by degree correlations. Contrary to traditional wisdom, when degree assortativity is positive, low degree nodes are more likely to generate largest cascades. Our work suggests that it may be possible to tailor spreading processes by manipulating the higher-order structure of networks.