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Competing activation mechanisms in epidemics on networks

In contrast to previous common wisdom that epidemic activity in heterogeneous networks is dominated by the hubs with the largest number of connections, recent research has pointed out the role that the innermost, dense core of the network plays in sustaining epidemic processes. Here we show that the...

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Detalles Bibliográficos
Autores principales: Castellano, Claudio, Pastor-Satorras, Romualdo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3330633/
https://www.ncbi.nlm.nih.gov/pubmed/22523634
http://dx.doi.org/10.1038/srep00371
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author Castellano, Claudio
Pastor-Satorras, Romualdo
author_facet Castellano, Claudio
Pastor-Satorras, Romualdo
author_sort Castellano, Claudio
collection PubMed
description In contrast to previous common wisdom that epidemic activity in heterogeneous networks is dominated by the hubs with the largest number of connections, recent research has pointed out the role that the innermost, dense core of the network plays in sustaining epidemic processes. Here we show that the mechanism responsible of spreading depends on the nature of the process. Epidemics with a transient state are boosted by the innermost core. Contrarily, epidemics allowing a steady state present a dual scenario, where either the hub independently sustains activity and propagates it to the rest of the system, or, alternatively, the innermost network core collectively turns into the active state, maintaining it globally. In uncorrelated networks the former mechanism dominates if the degree distribution decays with an exponent larger than 5/2, and the latter otherwise. Topological correlations, rife in real networks, may perturb this picture, mixing the role of both mechanisms.
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spelling pubmed-33306332012-04-20 Competing activation mechanisms in epidemics on networks Castellano, Claudio Pastor-Satorras, Romualdo Sci Rep Article In contrast to previous common wisdom that epidemic activity in heterogeneous networks is dominated by the hubs with the largest number of connections, recent research has pointed out the role that the innermost, dense core of the network plays in sustaining epidemic processes. Here we show that the mechanism responsible of spreading depends on the nature of the process. Epidemics with a transient state are boosted by the innermost core. Contrarily, epidemics allowing a steady state present a dual scenario, where either the hub independently sustains activity and propagates it to the rest of the system, or, alternatively, the innermost network core collectively turns into the active state, maintaining it globally. In uncorrelated networks the former mechanism dominates if the degree distribution decays with an exponent larger than 5/2, and the latter otherwise. Topological correlations, rife in real networks, may perturb this picture, mixing the role of both mechanisms. Nature Publishing Group 2012-04-20 /pmc/articles/PMC3330633/ /pubmed/22523634 http://dx.doi.org/10.1038/srep00371 Text en Copyright © 2012, Macmillan Publishers Limited. All rights reserved http://creativecommons.org/licenses/by-nc-sa/3.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-ShareALike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/
spellingShingle Article
Castellano, Claudio
Pastor-Satorras, Romualdo
Competing activation mechanisms in epidemics on networks
title Competing activation mechanisms in epidemics on networks
title_full Competing activation mechanisms in epidemics on networks
title_fullStr Competing activation mechanisms in epidemics on networks
title_full_unstemmed Competing activation mechanisms in epidemics on networks
title_short Competing activation mechanisms in epidemics on networks
title_sort competing activation mechanisms in epidemics on networks
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3330633/
https://www.ncbi.nlm.nih.gov/pubmed/22523634
http://dx.doi.org/10.1038/srep00371
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