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Register a new userAn Epidemiological Approach to the Spread of Political Third Parties
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Third political parties are influential in shaping American politics. In this work we study the spread of a third party ideology in a voting population where we assume that party members/activists are more influential in recruiting new third party voters than non-member third party voters. The study uses an epidemiological metaphor to develop a theoretical model with nonlinear ordinary differential equations as applied to a case study, the Green Party. Considering long-term behavior, we identify three threshold parameters in our model that describe the different possible scenarios for the political party and its spread. We also apply the model to the study of the Green Partys growth using voting and registration data in six states and the District of Columbia to identify and explain trends over the past decade. Our system produces a backward bifurcation that helps identify conditions under which a sufficiently dedicated activist core can enable a third party to thrive, under conditions which would not normally allow it to arise. Our results explain the critical role activists play in sustaining grassroots movements under adverse conditions.
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We formulate a generalized susceptible exposed infectious recovered (SEIR) model on a graph, describing the population dynamics of an open crowded place with an arbitrary topology. As a sample calculation, we discuss three simple cases, both analytically, and numerically, by means of a cellular automata simulation of the individual dynamics in the system. As a result, we provide the infection ratio in the system as a function of controllable parameters, which allows for quantifying how acting on the human behavior may effectively lower the disease spread throughout the system.
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-distance air-, land- and sea-transportation among countries and continents, and subsequently fostered by commuting trips within densely populated cities. While early travel restrictions contribute to delayed disease spread, their utility is much reduced if the disease has a long incubation period or if there is asymptomatic transmission. Given the lack of vaccines, public health officials have mainly relied on non-pharmaceutical interventions, including social distancing measures, curfews, and stay-at-home orders. Here we study the impact of city organization on its susceptibility to disease spread, and amenability to interventions. Cities can be classified according to their mobility in a spectrum between compact-hierarchical and decentralized-sprawled. Our results show that even though hierarchical cities are more susceptible to the rapid spread of epidemics, their organization makes mobility restrictions quite effective. Conversely, sprawled cities are characterized by a much slower initial spread, but are less responsive to mobility restrictions. These findings hold globally across cities in diverse geographical locations and a broad range of sizes. Our empirical measurements are confirmed by a simulation of COVID-19 spread in urban areas through a compartmental model. These results suggest that investing resources on early monitoring and prompt ad-hoc interventions in more vulnerable cities may prove most helpful in containing and reducing the impact of present and future pandemics.
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 population as the process of leaving from home, traveling to and from the activity locations, and engaging in activities. We then embed the susceptible-exposed-infectious-recovered (SEIR) process over the mobility dynamics and develops the spatial SEIR model with travel contagion (Trans-SEIR), which explicitly accounts for contagions both during travel and during daily activities. We investigate the theoretical properties of the proposed model and show how activity contagion and travel contagion contribute to the average number of secondary infections. In the numerical experiments, we explore how the urban transportation system may alter the fundamental dynamics of the infectious disease, change the number of secondary infections, promote the synchronization of the disease across the city, and affect the peak of the disease outbreaks. The Trans-SEIR model is further applied to the understand the disease dynamics during the COVID-19 outbreak in New York City, where we show how the activity and travel contagion may be distributed and how effective travel control can be implemented with only limited resources. The Trans-SEIR model along with the findings in our study may have significant contributions to improving our understanding of the coupling between urban transportation and disease dynamics, the development of quarantine and control measures of disease system, and promoting the idea of disease-resilient urban transportation networks.
Most models of epidemic spread, including many designed specifically for COVID-19, implicitly assume that social networks are undirected, i.e., that the infection is equally likely to spread in either direction whenever a contact occurs. In particular, this assumption implies that the individuals most likely to spread the disease are also the most likely to receive it from others. Here, we review results from the theory of random directed graphs which show that many important quantities, including the reproductive number and the epidemic size, depend sensitively on the joint distribution of in- and out-degrees (risk and spread), including their heterogeneity and the correlation between them. By considering joint distributions of various kinds we elucidate why some types of heterogeneity cause a deviation from the standard Kermack-McKendrick analysis of SIR models, i.e., so called mass-action models where contacts are homogeneous and random, and some do not. We also show that some structured SIR models informed by complex contact patterns among types of individuals (age or activity) are simply mixtures of Poisson processes and tend not to deviate significantly from the simplest mass-action model. Finally, we point out some possible policy implications of this directed structure, both for contact tracing strategy and for interventions designed to prevent superspreading events. In particular, directed networks have a forward and backward version of the classic friendship paradox -- forward links tend to lead to individuals with high risk, while backward links lead to individuals with high spread -- such that a combination of both forward and backward contact tracing is necessary to find superspreading events and prevent future cascades of infection.
Travel restrictions have often been used as a measure to combat the spread of disease -- in particular, they have been extensively applied in 2020 against coronavirus disease 2019 (COVID-19). How to best restrict travel, however, is unclear. Most studies and policies simply constrain the distance r individuals may travel from their home or neighbourhood. However, the epidemic risk is related not only to distance travelled, but also to frequency of contacts, which is proxied by the frequency f with which individuals revisit locations over a given reference period. Inspired by recent literature that uncovers a clear universality pattern on how r and f interact in routine human mobility, this paper addresses the following question: does this universal relation between r and f carry over to epidemic spreading, so that the risk associated with human movement can be modeled by a single, unifying variable r * f? To answer this question, we use two large-scale datasets of individual human mobility to simulate disease spread. Results show that a universal relation between r and f indeed exists in the context of epidemic spread: in both of the datasets, the final size and the spatial distribution of the infected population depends on the product r * f more directly than on the individual values of r and f. The important implication here is that restricting r (where you can go), but not f (how frequently), could be unproductive: high frequency trips to nearby locations can be as dangerous for disease spread as low frequency trips to distant locations. This counter-intuitive discovery could explain the modest effectiveness of distance-based travel restrictions and could inform future policies on COVID-19 and other epidemics.
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