arXiv subjects

Istvan Z. Kiss

Publications and source records attributed to Istvan Z. Kiss.

At least 19 recordsLinked to original sources

arXiv2026

Likelihood-based inference for birth-death processes with composite birth mechanisms

We develop a likelihood-based inference for finite-state birth-death processes with composite birth rates, in which multiple distinct mechanisms contribute additively to the total birth intensity. Our main motivating example is an SIS epidemic model with pairwise and higher-order transmission. The process is observed through a single aggregate trajectory, and in the main setting of interest, birth events are unmarked. This creates a deconvolution problem in event space: the state is one-dimensional, but the mechanism underlying each birth is latent. We formulate the inference under a Doob $h$-transformed $Q$-process, which is time-homogeneous and ergodic and which provides a time-homogeneous asymptotic surrogate for the law of the original process conditioned on long survival. We derive the corresponding conditional likelihood and study both the conditional maximum likelihood estimator and a quasi-maximum likelihood estimator which is based on a simplified working score. Under the Doob-transform law, we prove consistency and asymptotic normality for both estimators, with asymptotic covariance determined by the inverse Fisher and inverse Godambe information matrices, respectively. We also showcase a practical one-dimensional test for the presence of a specific higher-order birth mechanism.

math.ST↗

arXiv2022

Necessary and sufficient conditions for exact closures of epidemic equations on configuration model networks

We prove that the exact closure of SIR pairwise epidemic equations on a configuration model network is possible if and only if the degree distribution is Poisson, Binomial, or Negative Binomial. The proof relies on establishing, for these specific degree distributions, the equivalence of the closed pairwise model and the so-called dynamical survival analysis (DSA) edge-based model which was previously shown to be exact. Indeed, as we show here, the DSA model is equivalent to the well-known edge-based Volz model. We use this result to provide reductions of the closed pairwise and Volz models to the same single equation involving only susceptibles, which has a useful statistical interpretation in terms of the times to infection. We illustrate our findings with some numerical examples.

q-bio.PE↗

arXiv2022

Dynamic Survival Analysis for non-Markovian Epidemic Models

We present a new method for analyzing stochastic epidemic models under minimal assumptions. The method, dubbed DSA, is based on a simple yet powerful observation, namely that population-level mean-field trajectories described by a system of PDE may also approximate individual-level times of infection and recovery. This idea gives rise to a certain non-Markovian agent-based model and provides an agent-level likelihood function for a random sample of infection and/or recovery times. Extensive numerical analyses on both synthetic and real epidemic data from the FMD in the United Kingdom and the COVID-19 in India show good accuracy and confirm method's versatility in likelihood-based parameter estimation. The accompanying software package gives prospective users a practical tool for modeling, analyzing and interpreting epidemic data with the help of the DSA approach.

q-bio.PE↗

arXiv2021

Probabilistic predictions of SIS epidemics on networks based on population-level observations

We predict the future course of ongoing susceptible-infected-susceptible (SIS) epidemics on regular, Erdős-Rényi and Barabási-Albert networks. It is known that the contact network influences the spread of an epidemic within a population. Therefore, observations of an epidemic, in this case at the population-level, contain information about the underlying network. This information, in turn, is useful for predicting the future course of an ongoing epidemic. To exploit this in a prediction framework, the exact high-dimensional stochastic model of an SIS epidemic on a network is approximated by a lower-dimensional surrogate model. The surrogate model is based on a birth-and-death process; the effect of the underlying network is described by a parametric model for the birth rates. We demonstrate empirically that the surrogate model captures the intrinsic stochasticity of the epidemic once it reaches a point from which it will not die out. Bayesian parameter inference allows for uncertainty about the model parameters and the class of the underlying network to be incorporated directly into probabilistic predictions. An evaluation of a number of scenarios shows that in most cases the resulting prediction intervals adequately quantify the prediction uncertainty. As long as the population-level data is available over a long-enough period, even if not sampled frequently, the model leads to excellent predictions where the underlying network is correctly identified and prediction uncertainty mainly reflects the intrinsic stochasticity of the spreading epidemic. For predictions inferred from shorter observational periods, uncertainty about parameters and network class dominate prediction uncertainty. The proposed method relies on minimal data and is numerically efficient, which makes it attractive either as a standalone inference and prediction scheme or in conjunction with other methods.

q-bio.PE↗

arXiv2021

Coherent Dynamics Enhanced by Uncorrelated Noise

Synchronization is a widespread phenomenon observed in physical, biological, and social networks, which persists even under the influence of strong noise. Previous research on oscillators subject to common noise has shown that noise can actually facilitate synchronization, as correlations in the dynamics can be inherited from the noise itself. However, in many spatially distributed networks, such as the mammalian circadian system, the noise that different oscillators experience can be effectively uncorrelated. Here, we show that uncorrelated noise can in fact enhance synchronization when the oscillators are coupled. Strikingly, our analysis also shows that uncorrelated noise can be more effective than common noise in enhancing synchronization. We first establish these results theoretically for phase and phase-amplitude oscillators subject to either or both additive and multiplicative noise. We then confirm the predictions through experiments on coupled electrochemical oscillators. Our findings suggest that uncorrelated noise can promote rather than inhibit coherence in natural systems and that the same effect can be harnessed in engineered systems.

nlin.AO↗

arXiv2020

Beyond COVID-19: Network science and sustainable exit strategies

On May $28^{th}$ and $29^{th}$, a two day workshop was held virtually, facilitated by the Beyond Center at ASU and Moogsoft Inc. The aim was to bring together leading scientists with an interest in Network Science and Epidemiology to attempt to inform public policy in response to the COVID-19 pandemic. Epidemics are at their core a process that progresses dynamically upon a network, and are a key area of study in Network Science. In the course of the workshop a wide survey of the state of the subject was conducted. We summarize in this paper a series of perspectives of the subject, and where the authors believe fruitful areas for future research are to be found.

physics.soc-ph↗

arXiv2020

Braess's paradox and programmable behaviour in microfluidic networks

Microfluidic systems are now being designed with precision to execute increasingly complex tasks. However, their operation often requires numerous external control devices due to the typically linear nature of microscale flows, which has hampered the development of integrated control mechanisms. We address this difficulty by designing microfluidic networks that exhibit a nonlinear relation between applied pressure and flow rate, which can be harnessed to switch the direction of internal flows solely by manipulating input and/or output pressures. We show that these networks exhibit an experimentally-supported fluid analog of Braess's paradox, in which closing an intermediate channel results in a higher, rather than lower, total flow rate. The harnessed behavior is scalable and can be used to implement flow routing with multiple switches. These findings have the potential to advance development of built-in control mechanisms in microfluidic networks, thereby facilitating the creation of portable systems that may one day be as controllable as microelectronic circuits.

physics.flu-dyn↗

arXiv2015

Solvable non-Markovian dynamic network

Non-Markovian processes are widespread in natural and human-made systems, yet explicit model- ling and analysis of such systems is underdeveloped. We consider a non-Markovian dynamic network with random link activation and deletion (RLAD) and heavy tailed Mittag-Leffler distribution for the inter-event times. We derive an analytically and computationally tractable system of Kolmogorov- like forward equations utilising the Caputo derivative for the probability of having a given number of active links in the network and solve them. Simulations for the RLAD are also studied for power-law inter-event times and we show excellent agreement with the Mittag-Leffler model. This agreement holds even when the RLAD network dynamics is coupled with the susceptible-infected-susceptible (SIS) spreading dynamics. Thus, the analytically solvable Mittag-Leffler model provides an excel- lent approximation to the case when the network dynamics is characterised by power-law distributed inter-event times. We further discuss possible generalizations of our result.

math.PR↗

arXiv2015

Pairwise-like models for non-Markovian epidemics on networks

In this letter, a generalization of pairwise models to non-Markovian epidemics on networks is presented. For the case of infectious periods of fixed length, the resulting pairwise model is a system of delay differential equations (DDEs), which shows excellent agreement with results based on explicit stochastic simulations of non-Markovian epidemics on networks. Furthermore, we analytically compute a new R0-like threshold quantity and an implicit analytical relation between this and the final epidemic size. In addition we show that the pairwise model and the analytic calculations can be generalized in terms of integro-differential equations to any distribution of the infectious period, and we illustrate this by presenting a closed form expression for the final epidemic size. By showing the rigorous mathematical link between non-Markovian network epidemics and pairwise DDEs, we provide the framework for a deeper and more rigorous understanding of the impact of non-Markovian dynamics with explicit results for final epidemic size and threshold quantities.

physics.soc-ph↗

arXiv2015

Super compact pairwise model for SIS epidemic on heterogeneous networks

In this paper we provide the derivation of a super compact pairwise model with only 4 equations in the context of describing susceptible-infected-susceptible (SIS) epidemic dynamics on heterogenous networks. The super compact model is based on a new closure relation that involves not only the average degree but also the second and third moments of the degree distribution. Its derivation uses an a priori approximation of the degree distribution of susceptible nodes in terms of the degree distribution of the network. The new closure gives excellent agreement with heterogeneous pairwise models that contain significantly more differential equations.

math.DS↗

arXiv2014

Analysis of an epidemic model with awareness decay on regular random networks

The existence of a die-out threshold (different from the classic disease-invasion one) defining a region of slow extinction of an epidemic has been proved elsewhere for susceptible-aware-infectious-susceptible models without awareness decay, through bifurcation analysis. By means of an equivalent mean-field model defined on regular random networks, we interpret the dynamics of the system in this region and prove that the existence of bifurcation for this second epidemic threshold crucially depends on the absence of awareness decay. We show that the continuum of equilibria that characterizes the slow die-out dynamics collapses into a unique equilibrium when a constant rate of awareness decay is assumed, no matter how small, and that the resulting bifurcation from the disease-free equilibrium is equivalent to that of standard epidemic models. We illustrate these findings with continuous-time stochastic simulations on regular random networks with different degrees. Finally, the behaviour of solutions with and without decay in awareness is compared around the second epidemic threshold for a small rate of awareness decay.

q-bio.QM↗

arXiv2014

Beyond clustering: Mean-field dynamics on networks with arbitrary subgraph composition

Clustering is the propensity of nodes that share a common neighbour to be connected. It is ubiquitous in many networks but poses many modelling challenges. Clustering typically manifests itself by a higher than expected frequency of triangles, and this has led to the principle of constructing networks from such building blocks. This approach has been generalised to networks being constructed from a set of more exotic subgraphs. As long as these are fully connected, it is then possible to derive mean-field models that approximate epidemic dynamics well. However, there are virtually no results for non-fully connected subgraphs. In this paper, we provide a general and automated approach to deriving a set of ordinary differential equations, or mean-field model, that describes, to a high degree of accuracy, the expected values of system-level quantities, such as the prevalence of infection. Our approach offers a previously unattainable degree of control over the arrangement of subgraphs and network characteristics such as classical node degree, variance and clustering. The combination of these features makes it possible to generate families of networks with different subgraph compositions while keeping classical network metrics constant. Using our approach, we show that higher-order structure realised either through the introduction of loops of different sizes or by generating clustered networks based on different subgraphs, leads to significant differences in epidemic dynamics despite controlling for basic network metrics.

math.DS↗

arXiv2014

Oscillating epidemics in a dynamic network model: stochastic and mean-field analysis

An adaptive network model using SIS epidemic propagation with link-type dependent link activation and deletion is considered. Bifurcation analysis of the pairwise ODE approximation and the network-based stochastic simulation is carried out, showing that three typical behaviours may occur; namely, oscillations can be observed besides disease-free or endemic steady states. The oscillatory behaviour in the stochastic simulations is studied using Fourier analysis, as well as through analysing the exact master equations of the stochastic model. A compact pairwise approximation for the dynamic network case is also developed and, for the case of link-type independent rewiring, the outcome of epidemics and changes in network structure are concurrently presented in a single bifurcation diagram. By going beyond simply comparing simulation results to mean-field models, our approach yields deeper insights into the observed phenomena and help better understand and map out the limitations of mean-field models.

math.PR↗

arXiv2014

Dynamic control of modern, network-based epidemic models

In this paper we make the first steps to bridge the gap between classic control theory and modern, network-based epidemic models. In particular, we apply nonlinear model predictive control (NMPC) to a pairwise ODE model which we use to model a susceptible-infectious-susceptible (SIS) epidemic on non-trivial contact structures. While classic control of epidemics concentrates on aspects such as vaccination, quarantine and fast diagnosis, our novel setup allows us to deliver control by altering the contact network within the population. Moreover, the ideal outcome of control is to eradicate the disease while keeping the network well connected. The paper gives a thorough and detailed numerical investigation of the impact and interaction of system and control parameters on the controllability of the system. The analysis reveals, that for certain set parameters it is possible to identify critical control bounds above which the system is controllable. We foresee, that our approach can be extended to even more realistic or simulation-based models with the aim to apply these to real-world situations.

math.CA↗

arXiv2013

Exact equations for SIR epidemics on tree graphs

We consider Markovian susceptible-infectious-removed (SIR) dynamics on time-invariant weighted contact networks where the infection and removal processes are Poisson and where network links may be directed or undirected. We prove that a particular pair-based moment closure representation generates the expected infectious time series for networks with no cycles in the underlying graph. Moreover, this ``deterministic'' representation of the expected behaviour of a complex heterogeneous and finite Markovian system is straightforward to evaluate numerically.

q-bio.PE↗

arXiv2013

Higher-order structure and epidemic dynamics in clustered networks

Clustering is typically measured by the ratio of triangles to all triples, open or closed. Generating clustered networks, and how clustering affects dynamics on networks, is reasonably well understood for certain classes of networks \cite{vmclust, karrerclust2010}, e.g., networks composed of lines and non-overlapping triangles. In this paper we show that it is possible to generate networks which, despite having the same degree distribution and equal clustering, exhibit different higher-order structure, specifically, overlapping triangles and other order-four (a closed network motif composed of four nodes) structures. To distinguish and quantify these additional structural features, we develop a new network metric capable of measuring order-four structure which, when used alongside traditional network metrics, allows us to more accurately describe a network's topology. Three network generation algorithms are considered: a modified configuration model and two rewiring algorithms. By generating homogeneous networks with equal clustering we study and quantify their structural differences, and using SIS (Susceptible-Infected-Susceptible) and SIR (Susceptible-Infected-Recovered) dynamics we investigate computationally how differences in higher-order structure impact on epidemic threshold, final epidemic or prevalence levels and time evolution of epidemics. Our results suggest that characterising and measuring higher-order network structure is needed to advance our understanding of the impact of network topology on dynamics unfolding on the networks.

physics.soc-ph↗

arXiv2013

Exact deterministic representation of Markovian SIR epidemics on networks with and without loops

In a previous paper Sharkey et al. [13] proved the exactness of closures at the level of triples for Markovian SIR (susceptible-infected-removed) dynamics on tree-like networks. This resulted in a deterministic representation of the epidemic dynamics on the network that can be numerically evaluated. In this paper, we extend this modelling framework to certain classes of networks exhibiting loops. We show that closures where the loops are kept intact are exact, and lead to a simplified and numerically solvable system of ODEs (ordinary-differential-equations). The findings of the paper lead us to a generalisation of closures that are based on partitioning the network around nodes that are cut-vertices (i.e. the removal of such a node leads to the network breaking down into at least two disjointed components or subnetworks). Exploiting this structural property of the network yields some natural closures, where the evolution of a particular state can typically be exactly given in terms of the corresponding or projected sates on the subnetworks and the cut-vertex. A byproduct of this analysis is an alternative probabilistic proof of the exactness of the closures for tree-like networks presented in Sharkey et al. [13]. In this paper we also elaborate on how the main result can be applied to more realistic networks, for which we write down the ODEs explicitly and compare output from these to results from simulation. Furthermore, we give a general, recipe-like method of how to apply the reduction by closures technique for arbitrary networks, and give an upper bound on the maximum number of equations needed for an exact representation.

math.PR↗

arXiv2012

A class of pairwise models for epidemic dynamics on weighted networks

In this paper, we study the $SIS$ (susceptible-infected-susceptible) and $SIR$ (susceptible-infected-removed) epidemic models on undirected, weighted networks by deriving pairwise-type approximate models coupled with individual-based network simulation. Two different types of theoretical/synthetic weighted network models are considered. Both models start from non-weighted networks with fixed topology followed by the allocation of link weights in either (i) random or (ii) fixed/deterministic way. The pairwise models are formulated for a general discrete distribution of weights, and these models are then used in conjunction with network simulation to evaluate the impact of different weight distributions on epidemic threshold and dynamics in general. For the $SIR$ dynamics, the basic reproductive ratio $R_0$ is computed, and we show that (i) for both network models $R_{0}$ is maximised if all weights are equal, and (ii) when the two models are equally matched, the networks with a random weight distribution give rise to a higher $R_0$ value. The models are also used to explore the agreement between the pairwise and simulation models for different parameter combinations.

math.DS↗