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Register a new userA multi-type branching process method for modelling complex contagion on clustered networks
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Complex contagion adoption dynamics are characterised by a node being more likely to adopt after multiple network neighbours have adopted. We show how to construct multi-type branching processes to approximate complex contagion adoption dynamics on networks with clique-based clustering. This involves tracking the evolution of a cascade via different classes of clique motifs that account for the different numbers of active, inactive and removed nodes. This description allows for extensive Monte Carlo simulations (which are faster than network-based simulations), accurate analytical calculation of cascade sizes, determination of critical behaviour and other quantities of interest.
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The threshold model has been widely adopted as a classic model for studying contagion processes on social networks. We consider asymmetric individual interactions in social networks and introduce a persuasion mechanism into the threshold model. Specifically, we study a combination of adoption and persuasion in cascading processes on complex networks. It is found that with the introduction of the persuasion mechanism, the system may become more vulnerable to global cascades, and the effects of persuasion tend to be more significant in heterogeneous networks than those in homogeneous networks: a comparison between heterogeneous and homogeneous networks shows that under weak persuasion, heterogeneous networks tend to be more robust against random shocks than homogeneous networks; whereas under strong persuasion, homogeneous networks are more stable. Finally, we study the effects of adoption and persuasion threshold heterogeneity on systemic stability. Though both heterogeneities give rise to global cascades, the adoption heterogeneity has an overwhelmingly stronger impact than the persuasion heterogeneity when the network connectivity is sufficiently dense.
Forecasting the evolution of contagion dynamics is still an open problem to which mechanistic models only offer a partial answer. To remain mathematically or computationally tractable, these models must rely on simplifying assumptions, thereby limiting the quantitative accuracy of their predictions and the complexity of the dynamics they can model. Here, we propose a complementary approach based on deep learning where the effective local mechanisms governing a dynamic on a network are learned from time series data. Our graph neural network architecture makes very few assumptions about the dynamics, and we demonstrate its accuracy using different contagion dynamics of increasing complexity. By allowing simulations on arbitrary network structures, our approach makes it possible to explore the properties of the learned dynamics beyond the training data. Finally, we illustrate the applicability of our approach using real data of the COVID-19 outbreak in Spain. Our results demonstrate how deep learning offers a new and complementary perspective to build effective models of contagion dynamics on networks.
Brute-force simulations for dynamics on very large networks are quite expensive. While phenomenological treatments may capture some macroscopic properties, they often ignore important microscopic details. Fortunately, one may be only interested in the property of local part and not in the whole network. Here, we propose a hybrid multiscale coarse-grained(HMCG) method which combines a fine Monte Carlo(MC) simulation on the part of nodes of interest with a more coarse Langevin dynamics on the rest part. We demonstrate the validity of our method by analyzing the equilibrium Ising model and the nonequilibrium susceptible-infected-susceptible model. It is found that HMCG not only works very well in reproducing the phase transitions and critical phenomena of the microscopic models, but also accelerates the evaluation of dynamics with significant computational savings compared to microscopic MC simulations directly for the whole networks. The proposed method is general and can be applied to a wide variety of networked systems just adopting appropriate microscopic simulation methods and coarse graining approaches.
The quadratic contact process (QCP) is a natural extension of the well studied linear contact process where infected (1) individuals infect susceptible (0) neighbors at rate $lambda$ and infected individuals recover ($1 longrightarrow 0$) at rate 1. In the QCP, a combination of two 1s is required to effect a $0 longrightarrow 1$ change. We extend the study of the QCP, which so far has been limited to lattices, to complex networks. comment{as a model for the change in a population through sexual reproduction and death.} We define t
Contagion, broadly construed, refers to anything that can spread infectiously from peer to peer. Examples include communicable diseases, rumors, misinformation, ideas, innovations, bank failures, and electrical blackouts. Sometimes, as in the 1918 Spanish flu epidemic, a contagion mutates at some point as it spreads through a network. Here, using a simple susceptible-infected (SI) model of contagion, we explore the downstream impact of a single mutation event. Assuming that this mutation occurs at a random node in the contact network, we calculate the distribution of the number of descendants, $d$, downstream from the initial Patient Zero mutant. We find that the tail of the distribution decays as $d^{-2}$ for complete graphs, random graphs, small-world networks, networks with block-like structure, and other infinite-dimensional networks. This prediction agrees with the observed statistics of memes propagating and mutating on Facebook, and is expected to hold for other effectively infinite-dimensional networks, such as the global human contact network. In a wider context, our approach suggests a possible starting point for a mesoscopic theory of contagion. Such a theory would focus on the paths traced by a spreading contagion, thereby furnishing an intermediate level of description between that of individual nodes and the total infected population. We anticipate that contagion pathways will hold valuable lessons, given their role as the conduits through which single mutations, innovations, or failures can sweep through a network as a whole.
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