arXiv subjects

I. Z. Kiss

Publications and source records attributed to I. Z. Kiss.

10 recordsLinked to original sources

arXiv2021

A unified and automated approach to attractor reconstruction

We present a fully automated method for the optimal state space reconstruction from univariate and multivariate time series. The proposed methodology generalizes the time delay embedding procedure by unifying two promising ideas in a symbiotic fashion. Using non-uniform delays allows the successful reconstruction of systems inheriting different time scales. In contrast to the established methods, the minimization of an appropriate cost function determines the embedding dimension without using a threshold parameter. Moreover, the method is capable of detecting stochastic time series and, thus, can handle noise contaminated input without adjusting parameters. The superiority of the proposed method is shown on some paradigmatic models and experimental data from chaotic chemical oscillators.

physics.data-an↗

arXiv2019

Network Inference from Population-Level Observation of Epidemics

Using the continuous-time susceptible-infected-susceptible (SIS) model on networks, we investigate the problem of inferring the class of the underlying network when epidemic data is only available at population-level (i.e. the number of infected individuals at a finite set of discrete times of a single realisation of the epidemic), the only information likely to be available in real world settings. To tackle this, epidemics on networks are approximated by a Birth-and-Death process which keeps track of the number of infected nodes at population level. The rates of this surrogate model encode both the structure of the underlying network and disease dynamics. We use extensive simulations over Regular, Erdős-Rényi and Barabási-Albert networks to build network class-specific priors for these rates. % show that different well-known network classes map onto distinct regions of the parameter space of this model. We then use Bayesian model selection to recover the most likely underlying network class, based only on a single realisation of the epidemic. We show that the proposed methodology yields good results on both synthetic and real-world networks.

q-bio.PE↗

arXiv2018

Consistent Approximation of Epidemic Dynamics on Degree-heterogeneous Clustered Networks

Realistic human contact networks capable of spreading infectious disease, for example studied in social contact surveys, exhibit both significant degree heterogeneity and clustering, both of which greatly affect epidemic dynamics. To understand the joint effects of these two network properties on epidemic dynamics, the effective degree model of Lindquist et al. is reformulated with a new moment closure to apply to highly clustered networks. A simulation study comparing alternative ODE models and stochastic simulations is performed for SIR (Susceptible-Infected-Removed) epidemic dynamics, including a test for the conjectured error behaviour in Pellis et al., providing evidence that this novel model can be a more accurate approximation to epidemic dynamics on complex networks than existing approaches.

q-bio.PE↗

arXiv2018

Bursting endemic bubbles in an adaptive network

The spread of an infectious disease is known to change people's behavior, which in turn affects the spread of disease. Adaptive network models that account for both epidemic and behavior change have found oscillations, but in an extremely narrow region of the parameter space, which contrasts with intuition and available data. In this paper we propose a simple SIS epidemic model on an adaptive network with time-delayed rewiring, and show that oscillatory solutions are now present in a wide region of the parameter space. Altering the transmission or rewiring rates reveals the presence of an endemic bubble - an enclosed region of the parameter space where oscillations are observed.

q-bio.QM↗

arXiv2016

Self-Organized Stationary Patterns in Networks of Bistable Chemical Reactions

Experiments with networks of discrete reactive bistable electrochemical elements organized in regular and nonregular tree networks are presented to confirm an alternative to the Turing mechanism for the formation of self-organized stationary patterns. The results show that the pattern formation can be described by the identification of domains that can be activated individually or in combinations. The method also enabled the localization of chemical reactions to network substructures and the identification of critical sites whose activation results in complete activation of the system. Although the experiments were performed with a specific nickel electrodissolution system, they reproduced all the salient dynamic behavior of a general network model with a single nonlinearity parameter. Thus, the considered pattern-formation mechanism is very robust, and similar behavior can be expected in other natural or engineered networked systems that exhibit, at least locally, a treelike structure.

nlin.PS↗

arXiv2016

Mean-field models for non-Markovian epidemics on networks: from edge-based compartmental to pairwise models

This paper presents a novel extension of the edge-based compartmental model for epidemics with arbitrary distributions of transmission and recovery times. Using the message passing approach we also derive a new pairwise-like model for epidemics with Markovian transmission and an arbitrary recovery period. The new pairwise-like model allows one to formally prove that the message passing and edge-based compartmental models are equivalent in the case of Markovian transmission and arbitrary recovery processes. The edge-based and message passing models are conjectured to also be equivalent for arbitrary transmission processes; we show the first step of a full proof of this. The new pairwise-like model encompasses many existing well-known models that can be obtained by appropriate reductions. It is also amenable to a relatively straightforward numerical implementation. We test the theoretical results by comparing the numerical solutions of the various pairwise-like models to results based on explicit stochastic network simulations.

q-bio.QM↗

arXiv2016

Pairwise approximation for SIR type network epidemics with non-Markovian recovery

We present the generalised mean-field and pairwise models for non-Markovian epidemics on networks with arbitrary recovery time distributions. First we consider a hyperbolic system, where the population of infective nodes and links are structured by age since infection. By solving the partial differential equations, the model is transformed into a system of integro-differential equations, which is analysed both from a mathematical and numerical point of view. We analytically study the asymptotic behaviour of the generalised model and provide a rigorous mathematical proof of the conjecture on the functional form of the final epidemic size and pairwise reproduction number. As an illustration of the applicability of the general model we recover known results for the exponentially distributed and fixed recovery time cases and obtain new pairwise models with gamma and uniformly distributed infectious period. The general framework that we proposed shows a more complete picture of the impact of non-Markovian recovery on network epidemics.

math.DS↗

arXiv2016

Compact pairwise models for epidemics with multiple infectious stages on degree heterogeneous and clustered networks

This paper presents a compact pairwise model that describes the spread of multi-stage epidemics on networks. The multi-stage model corresponds to a gamma-distributed infectious period which interpolates between the classical Markovian models with exponentially distributed infectious period and epidemics with a constant infectious period. We show how the compact approach leads to a system of equations whose size is independent of the range of node degrees, thus significantly reducing the complexity of the model. Network clustering is incorporated into the model to provide a more accurate representation of realistic contact networks, and the accuracy of proposed closures is analysed for different levels of clustering and number of infection stages. Our results support recent findings that standard closure techniques are likely to perform better when the infectious period is constant.

q-bio.PE↗

arXiv2015

Dynamics of multi-stage infections on networks

This paper investigates the dynamics of infectious diseases with a non-exponentially distributed infectious period. This is achieved by considering a multi-stage infection model on networks. Using pairwise approximation with a standard closure, a number of important characteristics of disease dynamics are derived analytically, including the final size of an epidemic and a threshold for epidemic outbreaks, and it is shown how these quantities depend on disease characteristics, as well as the number of disease stages. Stochastic simulations of dynamics on networks are performed and compared to the results of pairwise models for several realistic examples of infectious diseases to illustrate the role played by the number of stages in the disease dynamics. These results show that a higher number of disease stages results in faster epidemic outbreaks with a higher peak prevalence and a larger final size of the epidemic. The agreement between the pairwise and simulation methods is excellent in the cases we consider.

physics.soc-ph↗

arXiv2014

The impact of constrained rewiring on network structure and node dynamics

In this paper, we study an adaptive spatial network. We consider an SIS (susceptible-infectedsusceptible) epidemic on the network, with a link/contact rewiring process constrained by spatial proximity. In particular, we assume that susceptible nodes break links with infected nodes independently of distance, and reconnect at random to susceptible nodes available within a given radius. By systematically manipulating this radius we investigate the impact of rewiring on the structure of the network and characteristics of the epidemic. We adopt a step-by-step approach whereby we first study the impact of rewiring on the network structure in the absence of an epidemic, then with nodes assigned a disease status but without disease dynamics, and finally running network and epidemic dynamics simultaneously. In the case of no labelling and no epidemic dynamics, we provide both analytic and semi-analytic formulas for the value of clustering achieved in the network. Our results also show that the rewiring radius and the network's initial structure have a pronounced effect on the endemic equilibrium, with increasingly large rewiring radiuses yielding smaller disease prevalence.

q-bio.PE↗