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Register a new userCommon group dynamic drives modern epidemics across social, financial and biological domains
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We show that qualitatively different epidemic-like processes from distinct societal domains (finance, social and commercial blockbusters, epidemiology) can be quantitatively understood using the same unifying conceptual framework taking into account the interplay between the timescales of the grouping and fragmentation of social groups together with typical epidemic transmission processes. Different domain-specific empirical infection profiles, featuring multiple resurgences and abnormal decay times, are reproduced simply by varying the timescales for group formation and individual transmission. Our model emphasizes the need to account for the dynamic evolution of multi-connected networks. Our results reveal a new minimally-invasive dynamical method for controlling such outbreaks, help fill a gap in existing epidemiological theory, and offer a new understanding of complex system response functions.
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Quantifying human group dynamics represents a unique challenge. Unlike animals and other biological systems, humans form groups in both real (offline) and virtual (online) spaces -- from potentially dangerous street gangs populated mostly by disaffected male youths, through to the massive global guilds in online role-playing games for which membership currently exceeds tens of millions of people from all possible backgrounds, age-groups and genders. We have compiled and analyzed data for these two seemingly unrelated offline and online human activities, and have uncovered an unexpected quantitative link between them. Although their overall dynamics differ visibly, we find that a common team-based model can accurately reproduce the quantitative features of each simply by adjusting the average tolerance level and attribute range for each population. By contrast, we find no evidence to support a version of the model based on like-seeking-like (i.e. kinship or `homophily).
To evaluate the effectiveness of the containment on the epidemic spreading of the new Coronavirus disease 2019, we carry on an analysis of the time evolution of the infection in a selected number of different Countries, by considering well-known macroscopic growth laws, the Gompertz law, and the logistic law. We also propose here a generalization of Gompertz law. Our data analysis permits an evaluation of the maximum number of infected individuals. The daily data must be compared with the obtained fits, to verify if the spreading is under control. From our analysis it appears that the spreading reached saturation in China, due to the strong containment policy of the national government. In Singapore a large growth rate, recently observed, suggests the start of a new strong spreading. For South Korea and Italy, instead, the next data on new infections will be crucial to understand if the saturation will be reached for lower or higher numbers of infected individuals.
In a social network, the number of links of a node, or node degree, is often assumed as a proxy for the nodes importance or prominence within the network. It is known that social networks exhibit the (first-order) assortative mixing, i.e. if two nodes are connected, they tend to have similar node degrees, suggesting that people tend to mix with those of comparable prominence. In this paper, we report the second-order assortative mixing in social networks. If two nodes are connected, we measure the degree correlation between their most prominent neighbours, rather than between the two nodes themselves. We observe very strong second-order assortative mixing in social networks, often significantly stronger than the first-order assortative mixing. This suggests that if two people interact in a social network, then the importance of the most prominent person each knows is very likely to be the same. This is also true if we measure the average prominence of neighbours of the two people. This property is weaker or negative in non-social networks. We investigate a number of possible explanations for this property. However, none of them was found to provide an adequate explanation. We therefore conclude that second-order assortative mixing is a new property of social networks.
In this letter, a generalization of pairwise models to non-Markovian epidemics on networks is presented. For the case of infectious periods of fixed length, the resulting pairwise model is a system of delay differential equations (DDEs), which shows excellent agreement with results based on explicit stochastic simulations of non-Markovian epidemics on networks. Furthermore, we analytically compute a new R0-like threshold quantity and an implicit analytical relation between this and the final epidemic size. In addition we show that the pairwise model and the analytic calculations can be generalized in terms of integro-differential equations to any distribution of the infectious period, and we illustrate this by presenting a closed form expression for the final epidemic size. By showing the rigorous mathematical link between non-Markovian network epidemics and pairwise DDEs, we provide the framework for a deeper and more rigorous understanding of the impact of non-Markovian dynamics with explicit results for final epidemic size and threshold quantities.
The compartmental models used to study epidemic spreading often assume the same susceptibility for all individuals, and are therefore, agnostic about the effects that differences in susceptibility can have on epidemic spreading. Here we show that--for the SIS model--differential susceptibility can make networks more vulnerable to the spread of diseases when the correlation between a nodes degree and susceptibility are positive, and less vulnerable when this correlation is negative. Moreover, we show that networks become more likely to contain a pocket of infection when individuals are more likely to connect with others that have similar susceptibility (the network is segregated). These results show that the failure to include differential susceptibility to epidemic models can lead to a systematic over/under estimation of fundamental epidemic parameters when the structure of the networks is not independent from the susceptibility of the nodes or when there are correlations between the susceptibility of connected individuals.
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