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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.
By incorporating delayed epidemic information and self-restricted travel behavior into the SIS model, we have investigated the coupled effects of timely and accurate epidemic information and peoples sensitivity to the epidemic information on contagio
In this paper, we propose a continuous-time stochastic intensity model, namely, two-phase dynamic contagion process(2P-DCP), for modelling the epidemic contagion of COVID-19 and investigating the lockdown effect based on the dynamic contagion model i
Albeit epidemic models have evolved into powerful predictive tools for the spread of diseases and opinions, most assume memoryless agents and independent transmission channels. We develop an infection mechanism that is endowed with memory of past exp
In this study, we develop the mathematical model to understand the coupling between the spreading dynamics of infectious diseases and the mobility dynamics through urban transportation systems. We first describe the mobility dynamics of the urban pop
The ongoing COVID-19 pandemic has created a global crisis of massive scale. Prior research indicates that human mobility is one of the key factors involved in viral spreading. Indeed, in a connected planet, rapid world-wide spread is enabled by long-