Macroscopic patterns of interacting contagions are indistinguishable from social reinforcement

Abstract

From fake news to innovative technologies, many contagions spread via a process of social reinforcement, where multiple exposures are distinct from prolonged exposure to a single source. Contrarily, biological agents such as Ebola or measles are typically thought to spread as simple contagions. Here, we demonstrate that interacting simple contagions are indistinguishable from complex contagions. In the social context, our results highlight the challenge of identifying and quantifying mechanisms, such as social reinforcement, in a world where an innumerable amount of ideas, memes and behaviors interact. In the biological context, this parallel allows the use of complex contagions to effectively quantify the non-trivial interactions of infectious diseases.On September 27th 2016, the World Health Organization (WHO) declared that measles had been eliminated from the Americas [1]. Less than two years later, an outbreak of the disease in Venezuela sparked an epidemic across South America, which is ongoing and has sickened tens-of-thousands [2][3][4]. Concurrently, the number of measles cases has increased in all but one of the WHO regions [5], over 80,000 cases (with a hospitalisation rate >60%) occurred in the European Union [6], and the United States of America experienced 17 measles outbreaks [2,7]. The majority of these cases occurred in unvaccinated individuals [8][9][10]. From collapsing public health infrastructure [11] and lack of access to vaccines [4] to non-medical exemptions, e.g., religious beliefs [12,13], and the spread of fraudulent science [14-16], the precise reason individuals go unvaccinated are myriad; however, underlying all these mechanisms is the coupled transmission of two contagions, one biological and one-or more-social.Clearly, contagions never occur in a vacuum, instead pathogens and ideas interact with each other and with externalities such as host connectivity, behaviour, and mobility. Nevertheless, many biological contagions are still considered to be "simple", where infectious individuals transmit to susceptible individuals independently of anything else occurring around the individuals, susceptible and/or infectious, in question [17]. In complex contagions, however, the spreading mechanism explicitly depends on the context of transmission events, usually via the neighbourhood of the susceptible individuals, such that pairwise information becomes insufficient to model the transmission process [18,19]. For example, social reinforcement can lead to a transmission rate effectively proportional to the number of different infectious contacts to which a susceptible individual is exposed [20]. This mechanistic difference creates a false dichotomy, forcing us to choose the mechanism we think best describe the reality of a given contagion. In practice, the context of transmission events always matters.When modeling a contagion, the choice of mechanism is critical because simple and complex contagions tend to induce substantially different dynamics and can lead to incompatible conclusions about i...

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“…Specifically, we must remember that distributions of secondary cases, just like R 0 itself, are just as much a product of a pathogen as of the population in which it spreads. For example, aspects of the social contact network [27], metapopulation structure [28,29], mobility [30,31], adaptive behavior [32,33], higher-order contact structure [34,35], and even other pathogens [36,37], all interact to cause complex patterns of disease emergence, spread, and persistence. Therefore, great care must be taken when using any of these tools to compare outbreaks or to inform current events with past data.…”

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