Epidemic percolation networks, epidemic outcomes, and interventions.
Ontology highlight
ABSTRACT:
SUBMITTER: Kenah E
PROVIDER: S-EPMC3062991 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:We consider cumulative merging percolation (CMP), a long-range percolation process describing the iterative merging of clusters in networks, depending on their mass and mutual distance. For a specific class of CMP processes, which represents a generalization of degree-ordered percolation, we derive a scaling solution on uncorrelated complex networks, unveiling the existence of diverse mechanisms leading to the formation of a percolating cluster. The scaling solution accurately reproduces universal properties of the transition. This finding is used to infer the critical properties of the susceptible-infected-susceptible model for epidemics in infinite and finite power-law distributed networks. Here, discrepancies between analytical approaches and numerical results regarding the finite-size scaling of the epidemic threshold are a crucial open issue in the literature. We find that the scaling exponent assumes a nontrivial value during a long preasymptotic regime. We calculate this value, finding good agreement with numerical evidence. We also show that the crossover to the true asymptotic regime occurs for sizes much beyond currently feasible simulations. Our findings allow us to rationalize and reconcile all previously published results (both analytical and numerical), thus ending a long-standing debate. Summary Complex networks represent the interaction pattern for many real-world phenomena such as epidemic spreading. The simplest and most fundamental model for the diffusion of infectious diseases without acquired immunity predicts a vanishing epidemic threshold in the limit of large systems. In other words, no matter how small the infectiousness of the disease, there is always a finite fraction of the overall population which is infected for long times. So far, the detailed mechanism underlying this phenomenology has remained unclear. Here, we provide a complete and quantitative understanding of the model’s behavior. While the role of hubs (individuals with high connectivity) was already believed to be important, we fully clarify its nature, pointing out the highly nontrivial interplay among hubs. Each hub acts as an infection hotbed and the global epidemic emerges from hubs reinfecting each other. Surprisingly, this mechanism is at work even when the hubs are not in direct mutual contact but transmit the infection through chains of low-connectivity individuals. The survival of the epidemic is then a manifestation of a novel, long-range, percolation process among distant hubs, whose properties explain the behavior of the epidemic model. These findings rationalize and reconcile previously published results and point out long-range indirect interactions as potentially crucial ingredients for other collective phenomena in networked systems.
| S-EPMC7226907 | biostudies-literature
Project description:Human to human transmissible infectious diseases spread in a population using human interactions as its transmission vector. The early stages of such an outbreak can be modeled by a graph whose edges encode these interactions between individuals, the vertices. This article attempts to account for the case when each individual entails in different kinds of interactions which have therefore different probabilities of transmitting the disease. The majority of these results can be also stated in the language of percolation theory. The main contributions of the article are: (1) Extend to this setting some results which were previously known in the case when each individual has only one kind of interactions. (2) Find an explicit formula for the basic reproduction number [Formula: see text] which depends only on the probabilities of transmitting the disease along the different edges and the first two moments of the degree distributions of the associated graphs. (3) Motivated by the recent Covid-19 pandemic, we use the framework developed to compute the [Formula: see text] of a model disease spreading in populations whose trees and degree distributions are adjusted to several different countries. In this setting, we shall also compute the probability that the outbreak will not lead to an epidemic. In all cases we find such probability to be very low if no interventions are put in place.
| S-EPMC7499022 | biostudies-literature
Project description:Optimal percolation is the problem of finding the minimal set of nodes whose removal from a network fragments the system into non-extensive disconnected clusters. The solution to this problem is important for strategies of immunization in disease spreading, and influence maximization in opinion dynamics. Optimal percolation has received considerable attention in the context of isolated networks. However, its generalization to multiplex networks has not yet been considered. Here we show that approximating the solution of the optimal percolation problem on a multiplex network with solutions valid for single-layer networks extracted from the multiplex may have serious consequences in the characterization of the true robustness of the system. We reach this conclusion by extending many of the methods for finding approximate solutions of the optimal percolation problem from single-layer to multiplex networks, and performing a systematic analysis on synthetic and real-world multiplex networks.
| S-EPMC5691044 | biostudies-literature
Project description:Bootstrap percolation is a general representation of some networked activation process, which has found applications in explaining many important social phenomena, such as the propagation of information. Inspired by some recent findings on spatial structure of online social networks, here we study bootstrap percolation on undirected spatial networks, with the probability density function of long-range links' lengths being a power law with tunable exponent. Setting the size of the giant active component as the order parameter, we find a parameter-dependent critical value for the power-law exponent, above which there is a double phase transition, mixed of a second-order phase transition and a hybrid phase transition with two varying critical points, otherwise there is only a second-order phase transition. We further find a parameter-independent critical value around -1, about which the two critical points for the double phase transition are almost constant. To our surprise, this critical value -1 is just equal or very close to the values of many real online social networks, including LiveJournal, HP Labs email network, Belgian mobile phone network, etc. This work helps us in better understanding the self-organization of spatial structure of online social networks, in terms of the effective function for information spreading.
| S-EPMC4589777 | biostudies-literature
Project description:The structure of interconnected systems and its impact on the system dynamics is a much-studied cross-disciplinary topic. Although various critical phenomena have been found in different models, study of the connections between different percolation transitions is still lacking. Here we propose a unified framework to study the origins of the discontinuous transitions of the percolation process on interacting networks. The model evolves in generations with the result of the present percolation depending on the previous state, and thus is history-dependent. Both theoretical analysis and Monte Carlo simulations reveal that the nature of the transition remains the same at finite generations but exhibits an abrupt change for the infinite generation. We use brain functional correlation and morphological similarity data to show that our model also provides a general method to explore the network structure and can contribute to many practical applications, such as detecting the abnormal structures of human brain networks.
| S-EPMC8288926 | biostudies-literature
Project description:Percolation is a process that impairs network connectedness by deactivating links or nodes. This process features a phase transition that resembles paradigmatic critical transitions in epidemic spreading, biological networks, traffic and transportation systems. Some biological systems, such as networks of neural cells, actively respond to percolation-like damage, which enables these structures to maintain their function after degradation and aging. Here we study percolation in networks that actively respond to link damage by adopting a mechanism resembling synaptic scaling in neurons. We explain critical transitions in such active networks and show that these structures are more resilient to damage as they are able to maintain a stronger connectedness and ability to spread information. Moreover, we uncover the role of local rescaling strategies in biological networks and indicate a possibility of designing smart infrastructures with improved robustness to perturbations.
| S-EPMC8748765 | biostudies-literature
Project description:In this work, we study the evolution of the susceptible individuals during the spread of an epidemic modeled by the susceptible-infected-recovered (SIR) process spreading on the top of complex networks. Using an edge-based compartmental approach and percolation tools, we find that a time-dependent quantity ?S(t), namely, the probability that a given neighbor of a node is susceptible at time t, is the control parameter of a node void percolation process involving those nodes on the network not-reached by the disease. We show that there exists a critical time t(c) above which the giant susceptible component is destroyed. As a consequence, in order to preserve a macroscopic connected fraction of the network composed by healthy individuals which guarantee its functionality, any mitigation strategy should be implemented before this critical time t(c). Our theoretical results are confirmed by extensive simulations of the SIR process.
| S-EPMC3441612 | biostudies-literature
Project description:Actin networks are essential for living cells to move, reproduce, and sense their environments. The dynamic and rheological behavior of actin networks is modulated by actin-binding proteins such as α-actinin, Arp2/3, and myosin. There is experimental evidence that actin-binding proteins modulate the cooperation of myosin motors by connecting the actin network. In this work, we present an analytical mean field model, using the Flory-Stockmayer theory of gelation, to understand how different actin-binding proteins change the connectivity of the actin filaments as the networks are formed. We follow the kinetics of the networks and estimate the concentrations of actin-binding proteins that are needed to reach connectivity percolation as well as to reach rigidity percolation. We find that Arp2/3 increases the actomyosin connectivity in the network in a non-monotonic way. We also describe how changing the connectivity of actomyosin networks modulates the ability of motors to exert forces, leading to three possible phases of the networks with distinctive dynamical characteristics: a sol phase, a gel phase, and an active phase. Thus, changes in the concentration and activity of actin-binding proteins in cells lead to a phase transition of the actin network, allowing the cells to perform active contraction and change their rheological properties.
| S-EPMC9119625 | biostudies-literature
Project description:Percolation in complex networks is a process that mimics network degradation and a tool that reveals peculiarities of the network structure. During the course of percolation, the emergent properties of networks undergo non-trivial transformations, which include a phase transition in the connectivity, and in some special cases, multiple phase transitions. Such global transformations are caused by only subtle changes in the degree distribution, which locally describe the network. Here we establish a generic analytic theory that describes how structure and sizes of all connected components in the network are affected by simple and colour-dependent bond percolations. This theory predicts locations of the phase transitions, existence of wide critical regimes that do not vanish in the thermodynamic limit, and a phenomenon of colour switching in small components. These results may be used to design percolation-like processes, optimise network response to percolation, and detect subtle signals preceding network collapse.
| S-EPMC6345799 | biostudies-other
Project description:The stochastic addition of either vertices or connections in a network leads to the observation of the percolation transition, a structural change with the appearance of a connected component encompassing a finite fraction of the system. Percolation has always been regarded as a substrate-dependent but model-independent process, in the sense that the critical exponents of the transition are determined by the geometry of the system, but they are identical for the bond and site percolation models. Here, we report a violation of such assumption. We provide analytical and numerical evidence of a difference in the values of the critical exponents between the bond and site percolation models in networks with null percolation thresholds, such as scale-free graphs with diverging second moment of the degree distribution. We discuss possible implications of our results in real networks, and provide additional insights on the anomalous nature of the percolation transition with null threshold.
| S-EPMC4682156 | biostudies-literature