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Register a new userModeling the spread of infectious disease in urban areas with travel contagion
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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.
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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.
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.
Infectious diseases are a significant threat to human society which was over sighted before the incidence of COVID-19, although according to the report of the World Health Organisation (WHO) about 4.2 million people die annually due to infectious disease. Due to recent COVID-19 pandemic, more than 2 million people died during 2020 and 96.2 million people got affected by this devastating disease. Recent research shows that applying individual interactions and movements data could help managing the pandemic though modelling the spread of infectious diseases on social contact networks. Infectious disease spreading can be explained with the theories and methods of diffusion processes where a dynamic phenomena evolves on networked systems. In the modelling of diffusion process, it is assumed that contagious items spread out in the networked system through the inter-node interactions. This resembles spreading of infectious virus, e.g. spread of COVID-19, within a population through individual social interactions. The evolution behaviours of the diffusion process are strongly influenced by the characteristics of the underlying system and the mechanism of the diffusion process itself. Thus, spreading of infectious disease can be explained how people interact with each other and by the characteristics of the disease itself. This paper presenters the relevant theories and methodologies of diffusion process that can be used to model the spread of infectious diseases.
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 exposures and simultaneously incorporates the joint effect of multiple infectious sources. Analytic equations and simulations of the susceptible-infected-susceptible model in unstructured substrates reveal the emergence of an additional phase that separates the usual healthy and endemic ones. This intermediate phase shows fundamentally distinct characteristics, and the system exhibits either excitability or an exotic variant of bistability. Moreover, the transition to endemicity presents hybrid aspects. These features are the product of an intricate balance between two memory modes and indicate that non-Markovian effects significantly alter the properties of spreading processes.
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.
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