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Register a new userDynamics of beneficial epidemics
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Pathogens can spread epidemically through populations. Beneficial contagions, such as viruses that enhance host survival or technological innovations that improve quality of life, also have the potential to spread epidemically. How do the dynamics of beneficial biological and social epidemics differ from those of detrimental epidemics? We investigate this question using three theoretical approaches. First, in the context of population genetics, we show that a horizontally-transmissible element that increases fitness, such as viral DNA, spreads superexponentially through a population, more quickly than a beneficial mutation. Second, in the context of behavioral epidemiology, we show that infections that cause increased connectivity lead to superexponential fixation in the population. Third, in the context of dynamic social networks, we find that preferences for increased global infection accelerate spread and produce superexponential fixation, but preferences for local assortativity halt epidemics by disconnecting the infected from the susceptible. We conclude that the dynamics of beneficial biological and social epidemics are characterized by the rapid spread of beneficial elements, which is facilitated in biological systems by horizontal transmission and in social systems by active spreading behavior of infected individuals.
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Online social networks (OSN) are prime examples of socio-technical systems in which individuals interact via a technical platform. OSN are very volatile because users enter and exit and frequently change their interactions. This makes the robustness of such systems difficult to measure and to control. To quantify robustness, we propose a coreness value obtained from the directed interaction network. We study the emergence of large drop-out cascades of users leaving the OSN by means of an agent-based model. For agents, we define a utility function that depends on their relative reputation and their costs for interactions. The decision of agents to leave the OSN depends on this utility. Our aim is to prevent drop-out cascades by influencing specific agents with low utility. We identify strategies to control agents in the core and the periphery of the OSN such that drop-out cascades are significantly reduced, and the robustness of the OSN is increased.
We consider the emergent behavior of viral spread when agents in a large population interact with each other over a contact network. When the number of agents is large and the contact network is a complete graph, it is well known that the population behavior -- that is, the fraction of susceptible, infected and recovered agents -- converges to the solution of an ordinary differential equation (ODE) known as the classical SIR model as the population size approaches infinity. In contrast, we study interactions over contact networks with generic topologies and derive conditions under which the population behavior concentrates around either the classic SIR model or other deterministic models. Specifically, we show that when most vertex degrees in the contact network are sufficiently large, the population behavior concentrates around an ODE known as the network SIR model. We then study the short and intermediate-term evolution of the network SIR model and show that if the contact network has an expander-type property or the initial set of infections is well-mixed in the population, the network SIR model reduces to the classical SIR model. To complement these results, we illustrate through simulations that the two models can yield drastically different predictions, hence use of the classical SIR model can be misleading in certain cases.
We investigate a multi-agent model of firms in an R&D network. Each firm is characterized by its knowledge stock $x_{i}(t)$, which follows a non-linear dynamics. It can grow with the input from other firms, i.e., by knowledge transfer, and decays otherwise. Maintaining interactions is costly. Firms can leave the network if their expected knowledge growth is not realized, which may cause other firms to also leave the network. The paper discusses two bottom-up intervention scenarios to prevent, reduce, or delay cascades of firms leaving. The first one is based on the formalism of network controllability, in which driver nodes are identified and subsequently incentivized, by reducing their costs. The second one combines node interventions and network interventions. It proposes the controlled removal of a single firm and the random replacement of firms leaving. This allows to generate small cascades, which prevents the occurrence of large cascades. We find that both approaches successfully mitigate cascades and thus improve the resilience of the R&D network.
The flow of information reaching us via the online media platforms is optimized not by the information content or relevance but by popularity and proximity to the target. This is typically performed in order to maximise platform usage. As a side effect, this introduces an algorithmic bias that is believed to enhance polarization of the societal debate. To study this phenomenon, we modify the well-known continuous opinion dynamics model of bounded confidence in order to account for the algorithmic bias and investigate its consequences. In the simplest version of the original model the pairs of discussion participants are chosen at random and their opinions get closer to each other if they are within a fixed tolerance level. We modify the selection rule of the discussion partners: there is an enhanced probability to choose individuals whose opinions are already close to each other, thus mimicking the behavior of online media which suggest interaction with similar peers. As a result we observe: a) an increased tendency towards polarization, which emerges also in conditions where the original model would predict convergence, and b) a dramatic slowing down of the speed at which the convergence at the asymptotic state is reached, which makes the system highly unstable. Polarization is augmented by a fragmented initial population.
A simple generative model of a foraging society generates significant wealth inequalities from identical agents on an equal opportunity landscape. These inequalities arise in both equilibrium and non-equilibrium regimes with some societies essentially never reaching equilibrium. Reproduction costs mitigate inequality beyond their affect on intrinsic growth rate. The highest levels of inequality are found during non-equilibrium regimes. Inequality in dynamic regimes is driven by factors different than those driving steady state inequality.
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