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Simulation of four respiratory viruses and inference of epidemiological parameters.

ABSTRACT: While influenza has been simulated extensively to better understand its behavior and predict future outbreaks, most other respiratory viruses have seldom been simulated. In this study, we provide an overview of four common respiratory viral infections: respiratory syncytial virus (RSV), respiratory adenovirus, rhinovirus and parainfluenza, present specimen data collected 2004-2014, and simulate outbreaks in 19 overlapping regions in the United States. Pairing a compartmental model and data assimilation methods, we infer key epidemiological parameters governing transmission: the basic reproductive number R 0 and length of infection D. RSV had been previously simulated, and our mean estimate of D and R 0 of 5.2 days and 2.8, respectively, are within published clinical and modeling estimates. Among the four virus groupings, mean estimates of R 0 range from 2.3 to 3.0, with a lower and upper quartile range of 2.0-2.8 and 2.6-3.2, respectively. As rapid PCR testing becomes more common, estimates of the observed virulence and duration of infection for these viruses could inform decision making by clinicians and officials for managing patient treatment and response.

SUBMITTER: Reis J

PROVIDER: S-EPMC6326234 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Project description:The rate of adaptive evolution depends on the rate at which beneficial mutations are introduced into a population and the fitness effects of those mutations. The rate of beneficial mutations and their expected fitness effects is often difficult to empirically quantify. As these 2 parameters determine the pace of evolutionary change in a population, the dynamics of adaptive evolution may enable inference of their values. Copy number variants (CNVs) are a pervasive source of heritable variation that can facilitate rapid adaptive evolution. Previously, we developed a locus-specific fluorescent CNV reporter to quantify CNV dynamics in evolving populations maintained in nutrient-limiting conditions using chemostats. Here, we use CNV adaptation dynamics to estimate the rate at which beneficial CNVs are introduced through de novo mutation and their fitness effects using simulation-based likelihood-free inference approaches. We tested the suitability of 2 evolutionary models: a standard Wright-Fisher model and a chemostat model. We evaluated 2 likelihood-free inference algorithms: the well-established Approximate Bayesian Computation with Sequential Monte Carlo (ABC-SMC) algorithm, and the recently developed Neural Posterior Estimation (NPE) algorithm, which applies an artificial neural network to directly estimate the posterior distribution. By systematically evaluating the suitability of different inference methods and models, we show that NPE has several advantages over ABC-SMC and that a Wright-Fisher evolutionary model suffices in most cases. Using our validated inference framework, we estimate the CNV formation rate at the GAP1 locus in the yeast Saccharomyces cerevisiae to be 10-4.7 to 10-4 CNVs per cell division and a fitness coefficient of 0.04 to 0.1 per generation for GAP1 CNVs in glutamine-limited chemostats. We experimentally validated our inference-based estimates using 2 distinct experimental methods-barcode lineage tracking and pairwise fitness assays-which provide independent confirmation of the accuracy of our approach. Our results are consistent with a beneficial CNV supply rate that is 10-fold greater than the estimated rates of beneficial single-nucleotide mutations, explaining the outsized importance of CNVs in rapid adaptive evolution. More generally, our study demonstrates the utility of novel neural network-based likelihood-free inference methods for inferring the rates and effects of evolutionary processes from empirical data with possible applications ranging from tumor to viral evolution.

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Simulation of four respiratory viruses and inference of epidemiological parameters.

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