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Register a new userComplete hierarchies of SIR models on arbitrary networks with exact and approximate moment closure
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We first generalise ideas discussed by Kiss et al. (2015) to prove a theorem for generating exact closures (here expressing joint probabilities in terms of their constituent marginal probabilities) for susceptible-infectious-removed (SIR) dynamics on arbitrary graphs (networks). For Poisson transmission and removal processes, this enables us to obtain a systematic reduction in the number of differential equations needed for an exact `moment closure representation of the underlying stochastic model. We define `transmission blocks as a possible extension of the block concept in graph theory and show that the order at which the exact moment closure representation is curtailed is the size of the largest transmission block. More generally, approximate closures of the hierarchy of moment equations for these dynamics are typically defined for the first and second order yielding mean-field and pairwise models respectively. It is frequently implied that, in principle, closed models can be written down at arbitrary order if only we had the time and patience to do this. However, for epidemic dynamics on networks, these higher-order models have not been defined explicitly. Here we unambiguously define hierarchies of approximate closed models that can utilise subsystem states of any order, and show how well-known models are special cases of these hierarchies.
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Stochastic epidemic models on networks are inherently high-dimensional and the resulting exact models are intractable numerically even for modest network sizes. Mean-field models provide an alternative but can only capture average quantities, thus offering little or no information about variability in the outcome of the exact process. In this paper we conjecture and numerically prove that it is possible to construct PDE-limits of the exact stochastic SIS epidemics on regular and ErdH{o}s-Renyi networks. To do this we first approximate the exact stochastic process at population level by a Birth-and-Death process (BD) (with a state space of $O(N)$ rather than $O(2^N)$) whose coefficients are determined numerically from Gillespie simulations of the exact epidemic on explicit networks. We numerically demonstrate that the coefficients of the resulting BD process are density-dependent, a crucial condition for the existence of a PDE limit. Extensive numerical tests for Regular and ErdH{o}s-Renyi networks show excellent agreement between the outcome of simulations and the numerical solution of the Fokker-Planck equations. Apart from a significant reduction in dimensionality, the PDE also provides the means to derive the epidemic outbreak threshold linking network and disease dynamics parameters, albeit in an implicit way. Perhaps more importantly, it enables the formulation and numerical evaluation of likelihoods for epidemic and network inference as illustrated in a worked out example.
Amidst the current COVID-19 pandemic, quantifying the effects of strategies that mitigate the spread of infectious diseases is critical. This article presents a compartmental model that addresses the role of random viral testing, follow-up contact tracing, and subsequent isolation of infectious individuals to stabilize the spread of a disease. We propose a branching model and an individual (or agent) based model, both of which capture the stochastic, heterogeneous nature of interactions within a community. The branching model is used to derive new analytical results for the trade-offs between the different mitigation strategies, with the surprising result that a communitys resilience to disease outbreaks is independent of its underlying network structure.
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We present an efficient and flexible method for computing likelihoods of phenotypic traits on a phylogeny. The method does not resort to Monte-Carlo computation but instead blends Felsensteins discrete character pruning algorithm with methods for numerical quadrature. It is not limited to Gaussian models and adapts readily to model uncertainty in the observed trait values. We demonstrate the framework by developing efficient algorithms for likelihood calculation and ancestral state reconstruction under Wrights threshold model, applying our methods to a dataset of trait data for extrafloral nectaries (EFNs) across a phylogeny of 839 Labales species.
Models of codon evolution are commonly used to identify positive selection. Positive selection is typically a heterogeneous process, i.e., it acts on some branches of the evolutionary tree and not others. Previous work on DNA models showed that when evolution occurs under a heterogeneous process it is important to consider the property of model closure, because non-closed models can give biased estimates of evolutionary processes. The existing codon models that account for the genetic code are not closed; to establish this it is enough to show that they are not linear (meaning that the sum of two codon rate matrices in the model is not a matrix in the model). This raises the concern that a single codon model fit to a heterogeneous process might mis-estimate both the effect of selection and branch lengths. Codon models are typically constructed by choosing an underlying DNA model (e.g., HKY) that acts identically and independently at each codon position, and then applying the genetic code via the parameter $omega$ to modify the rate of transitions between codons that code for different amino acids. Here we use simulation to investigate the accuracy of estimation of both the selection parameter $omega$ and branch lengths in cases where the underlying DNA process is heterogeneous but $omega$ is constant. We find that both $omega$ and branch lengths can be mis-estimated in these scenarios. Errors in $omega$ were usually less than 2% but could be as high as 17%. We also assessed if choosing different underlying DNA models had any affect on accuracy, in particular we assessed if using closed DNA models gave any advantage. However, a DNA model being closed does not imply that the codon model constructed from it is closed, and in general we found that using closed DNA models did not decrease errors in the estimation of $omega$.
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