Multiscale mobility networks and the spatial spreading of infectious diseases.
Ontology highlight
ABSTRACT:
SUBMITTER: Balcan D
PROVIDER: S-EPMC2793313 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Current modeling of infectious diseases allows for the study of realistic scenarios that include population heterogeneity, social structures, and mobility processes down to the individual level. The advances in the realism of epidemic description call for the explicit modeling of individual behavioral responses to the presence of disease within modeling frameworks. Here we formulate and analyze a metapopulation model that incorporates several scenarios of self-initiated behavioral changes into the mobility patterns of individuals. We find that prevalence-based travel limitations do not alter the epidemic invasion threshold. Strikingly, we observe in both synthetic and data-driven numerical simulations that when travelers decide to avoid locations with high levels of prevalence, this self-initiated behavioral change may enhance disease spreading. Our results point out that the real-time availability of information on the disease and the ensuing behavioral changes in the population may produce a negative impact on disease containment and mitigation.
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Project description:We propose a theoretical framework for the study of spreading processes in structured metapopulations, with heterogeneous agents, subjected to different recurrent mobility patterns. We propose to represent the heterogeneity in the composition of the metapopulations as layers in a multiplex network, where nodes would correspond to geographical areas and layers account for the mobility patterns of agents of the same class. We analyze classical epidemic models within this framework and obtain an excellent agreement with extensive Monte Carlo simulations. This agreement allows us to derive analytical expressions of the epidemic threshold and to face the challenge of characterizing a real multiplex metapopulation, the city of Medellín in Colombia, where different recurrent mobility patterns are observed depending on the socioeconomic class of the agents. Our framework allows us to unveil the geographical location of those patches that trigger the epidemic state at the critical point. A careful exploration reveals that social mixing between classes and mobility crucially determines these critical patches and, more importantly, it can produce abrupt changes of the critical properties of the epidemic onset. Summary The spread of disease is strongly driven by how humans move and segregate across cities, regions, and countries. Understanding how epidemics arise from the interplay of these behaviors is crucial for implementing efficient containment and prevention policies. In this work, we propose a theoretical framework for the spread of pathogens that incorporates the real patterns of mobility, demographics, and human diversity observed in urban environments. Our framework represents various populations in a community as layers in a multiplex network, where nodes correspond to geographical areas and layers account for movement patterns. With this framework, we analyze a real urban system, the city of Medellin in Colombia, considering the interplay between six socioeconomic classes displaying disparate demographic segregation and mobility habits. Our framework can identify those neighborhoods and classes that trigger epidemic outbreaks. Remarkably, we observe that small changes to both mobility and social mixing among these subpopulations can trigger abrupt changes. As a consequence, containment strategies targeting a certain neighborhood can quickly change from efficient to useless. Finally, we provide a physical interpretation of the abrupt changes of those patches driving the unfolding of epidemics based on the effective number of contacts of agents. Our framework provides a reliable, time-saving platform for analyzing the spread of pathogens among various populations, allowing researchers to identify areas critical to the unfolding of diseases. With further improvements, our formalism could be extended to accommodate more sophisticated commuting patterns and epidemic models.
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Project description:We consider multiple diseases spreading in a static configuration model network. We make standard assumptions that infection transmits from neighbor to neighbor at a disease-specific rate and infected individuals recover at a disease-specific rate. Infection by one disease confers immediate and permanent immunity to infection by any disease. Under these assumptions, we find a simple, low-dimensional ordinary differential equations model which captures the global dynamics of the infection. The dynamics depend strongly on initial conditions. Although we motivate this Rapid Communication with infectious disease, the model may be adapted to the spread of other infectious agents such as competing political beliefs, or adoption of new technologies if these are influenced by contacts. As an example, we demonstrate how to model an infectious disease which can be prevented by a behavior change.
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Project description:Control of animal-born diseases is a major challenge faced by applied ecologists and public health managers. To improve cost-effectiveness, the effort required to control such pathogens needs to be predicted as accurately as possible. In this context, we reviewed the anti-rabies vaccination schemes applied around the world during the past 25 years.We contrasted predictions from classic approaches based on theoretical population ecology (which governs rabies control to date) with a newly developed individual-based model. Our spatially explicit approach allowed for the reproduction of pattern formation emerging from a pathogen's spread through its host population.We suggest that a much lower management effort could eliminate the disease than that currently in operation. This is supported by empirical evidence from historic field data. Adapting control measures to the new prediction would save one-third of resources in future control programmes.The reason for the lower prediction is the spatial structure formed by spreading infections in spatially arranged host populations. It is not the result of technical differences between models.Synthesis and applications. For diseases predominantly transmitted by neighbourhood interaction, our findings suggest that the emergence of spatial structures facilitates eradication. This may have substantial implications for the cost-effectiveness of existing disease management schemes, and suggests that when planning management strategies consideration must be given to methods that reflect the spatial nature of the pathogen-host system.
| S-EPMC2326892 | biostudies-literature
Project description:Computational models for large, resurgent epidemics are recognized as a crucial tool for predicting the spread of infectious diseases. It is widely agreed, that such models can be augmented with realistic multiscale population models and by incorporating human mobility patterns. Nevertheless, a large proportion of recent studies, aimed at better understanding global epidemics, like influenza, measles, H1N1, SARS, and COVID-19, underestimate the role of heterogeneous mixing in populations, characterized by strong social structures and geography. Motivated by the reduced tractability of studies employing homogeneous mixing, which make conclusions hard to deduce, we propose a new, very fine-grained model incorporating the spatial distribution of population into geographical settlements, with a hierarchical organization down to the level of households (inside which we assume homogeneous mixing). In addition, population is organized heterogeneously outside households, and we model the movement of individuals using travel distance and frequency parameters for inter- and intra-settlement movement. Discrete event simulation, employing an adapted SIR model with relapse, reproduces important qualitative characteristics of real epidemics, like high variation in size and temporal heterogeneity (e.g., waves), that are challenging to reproduce and to quantify with existing measures. Our results pinpoint an important aspect, that epidemic size is more sensitive to the increase in distance of travel, rather that the frequency of travel. Finally, we discuss implications for the control of epidemics by integrating human mobility restrictions, as well as progressive vaccination of individuals.
| S-EPMC8275763 | biostudies-literature
Project description:Infectious diseases caused by pathogens, including viruses, bacteria and parasites, pose a serious threat to human health worldwide. Frequent changes in the pattern of infection mechanisms and the emergence of multidrug-resistant strains among pathogens have weakened the current treatment regimen. This necessitates the development of new therapeutic interventions to prevent and control such diseases. To cater to the need, analysis of protein interaction networks (PINs) has gained importance as one of the promising strategies. The present review aims to discuss various computational approaches to analyse the PINs in context to infectious diseases. Topology and modularity analysis of the network with their biological relevance, and the scenario till date about host-pathogen and intra-pathogenic protein interaction studies were delineated. This would provide useful insights to the research community, thereby enabling them to design novel biomedicine against such infectious diseases.
| S-EPMC7110031 | biostudies-literature
Project description:International mobility facilitates the exchange of scientific, institutional and cultural knowledge. Yet whether globalization and advances in virtual communication technologies have altered the impact of researcher mobility is a relevant and open question that we address by analysing a broad international set of 26 170 physicists from 1980 to 2009, focusing on the 10-year period centred around each mobility event to assess the impact of mobility on research outcomes. We account for secular globalization trends by splitting the analysis into three periods, measuring for each period the effect of mobility on researchers' citation impact, research topic diversity, collaboration networks and geographical coordination. In order to identify causal effects we leverage statistical matching methods that pair mobile researchers with non-mobile researchers that are similar in research profile attributes prior the mobility event. We find that mobile researchers gain up to a 17% increase in citations relative to their non-mobile counterparts, which can be explained by the simultaneous increase in their diversity of co-authors, topics and geographical coordination in the period immediately following migration. Nevertheless, we also observe that researcher's completely curtail prior collaborations with their source country in 11% of the cross-border mobility events. As such, these individual-level perturbations fuel multiscale churning in scientific networks, e.g. rewiring the connectivity of individuals and ideas and affecting international integration. Together these results provide additional clarity on the complex relationship between human capital mobility and the dynamics of social capital investment, with implications for immigration and national innovation system policy.
| S-EPMC6170771 | biostudies-literature
Project description:We suggest a novel mathematical framework for the in-homogeneous spatial spreading of an infectious disease in human population, with particular attention to COVID-19. Common epidemiological models, e.g., the well-known susceptible-exposed-infectious-recovered (SEIR) model, implicitly assume uniform (random) encounters between the infectious and susceptible sub-populations, resulting in homogeneous spatial distributions. However, in human population, especially under different levels of mobility restrictions, this assumption is likely to fail. Splitting the geographic region under study into areal nodes, and assuming infection kinetics within nodes and between nearest-neighbor nodes, we arrive into a continuous, "reaction-diffusion", spatial model. To account for COVID-19, the model includes five different sub-populations, in which the infectious sub-population is split into pre-symptomatic and symptomatic. Our model accounts for the spreading evolution of infectious population domains from initial epicenters, leading to different regimes of sub-exponential (e.g., power-law) growth. Importantly, we also account for the variable geographic density of the population, that can strongly enhance or suppress infection spreading. For instance, we show how weakly infected regions surrounding a densely populated area can cause rapid migration of the infection towards the populated area. Predicted infection "heat-maps" show remarkable similarity to publicly available heat-maps, e.g., from South Carolina. We further demonstrate how localized lockdown/quarantine conditions can slow down the spreading of disease from epicenters. Application of our model in different countries can provide a useful predictive tool for the authorities, in particular, for planning strong lockdown measures in localized areas-such as those underway in a few countries.
| S-EPMC7894958 | biostudies-literature
Project description:Infectious diseases are the leading cause of death, particularly in developing countries. Although many drugs are available for treating the most common infectious diseases, in many cases the mechanism of action of these drugs or even their targets in the pathogen remain unknown. In addition, the key factors or processes in pathogens that facilitate infection and disease progression are often not well understood. Since proteins do not work in isolation, understanding biological systems requires a better understanding of the interconnectivity between proteins in different pathways and processes, which includes both physical and other functional interactions. Such biological networks can be generated within organisms or between organisms sharing a common environment using experimental data and computational predictions. Though different data sources provide different levels of accuracy, confidence in interactions can be measured using interaction scores. Connections between interacting proteins in biological networks can be represented as graphs and edges, and thus studied using existing algorithms and tools from graph theory. There are many different applications of biological networks, and here we discuss three such applications, specifically applied to the infectious disease tuberculosis, with its causative agent Mycobacterium tuberculosis and host, Homo sapiens. The applications include the use of the networks for function prediction, comparison of networks for evolutionary studies, and the generation and use of host-pathogen interaction networks.
| S-EPMC4212278 | biostudies-literature
Project description:BackgroundOutbreaks of infectious diseases would cause great losses to the human society. Source identification in networks has drawn considerable interest in order to understand and control the infectious disease propagation processes. Unsatisfactory accuracy and high time complexity are major obstacles to practical applications under various real-world situations for existing source identification algorithms.MethodsThis study attempts to measure the possibility for nodes to become the infection source through label ranking. A unified Label Ranking framework for source identification with complete observation and snapshot is proposed. Firstly, a basic label ranking algorithm with complete observation of the network considering both infected and uninfected nodes is designed. Our inferred infection source node with the highest label ranking tends to have more infected nodes surrounding it, which makes it likely to be in the center of infection subgraph and far from the uninfected frontier. A two-stage algorithm for source identification via semi-supervised learning and label ranking is further proposed to address the source identification issue with snapshot.ResultsExtensive experiments are conducted on both synthetic and real-world network datasets. It turns out that the proposed label ranking algorithms are capable of identifying the propagation source under different situations fairly accurately with acceptable computational complexity without knowing the underlying model of infection propagation.ConclusionsThe effectiveness and efficiency of the label ranking algorithms proposed in this study make them be of practical value for infection source identification.
| S-EPMC7808631 | biostudies-literature