No Arabic abstract
The fundamental models of epidemiology describe the progression of an infectious disease through a population using compartmentalized differential equations, but do not incorporate population-level heterogeneity in infection susceptibility. We show that variation strongly influences the rate of infection, while the infection process simultaneously sculpts the susceptibility distribution. These joint dynamics influence the force of infection and are, in turn, influenced by the shape of the initial variability. Intriguingly, we find that certain susceptibility distributions (the exponential and the gamma) are unchanged through the course of the outbreak, and lead naturally to power-law behavior in the force of infection; other distributions often tend towards these eigen-distributions through the process of contagion. The power-law behavior fundamentally alters predictions of the long-term infection rate, and suggests that first-order epidemic models that are parameterized in the exponential-like phase may systematically and significantly over-estimate the final severity of the outbreak.
In this work we demonstrate how to automate parts of the infectious disease-control policy-making process via performing inference in existing epidemiological models. The kind of inference tasks undertaken include computing the posterior distribution over controllable, via direct policy-making choices, simulation model parameters that give rise to acceptable disease progression outcomes. Among other things, we illustrate the use of a probabilistic programming language that automates inference in existing simulators. Neither the full capabilities of this tool for automating inference nor its utility for planning is widely disseminated at the current time. Timely gains in understanding about how such simulation-based models and inference automation tools applied in support of policymaking could lead to less economically damaging policy prescriptions, particularly during the current COVID-19 pandemic.
Several analytical models have been used in this work to describe the evolution of death cases arising from coronavirus (COVID-19). The Death or `D model is a simplified version of the SIR (susceptible-infected-recovered) model, which assumes no recovery over time, and allows for the transmission-dynamics equations to be solved analytically. The D-model can be extended to describe various focuses of infection, which may account for the original pandemic (D1), the lockdown (D2) and other effects (Dn). The evolution of the COVID-19 pandemic in several countries (China, Spain, Italy, France, UK, Iran, USA and Germany) shows a similar behavior in concord with the D-model trend, characterized by a rapid increase of death cases followed by a slow decline, which are affected by the earliness and efficiency of the lockdown effect. These results are in agreement with more accurate calculations using the extended SIR model with a parametrized solution and more sophisticated Monte Carlo grid simulations, which predict similar trends and indicate a common evolution of the pandemic with universal parameters.
We propose a physical theory underlying the temporal evolution of competing virus variants that relies on the existence of (quasi) fixed points capturing the large time scale invariance of the dynamics. To motivate our result we first modify the time-honoured compartmental models of the SIR type to account for the existence of competing variants and then show how their evolution can be naturally re-phrased in terms of flow equations ending at quasi fixed points. As the natural next step we employ (near) scale invariance to organise the time evolution of the competing variants within the effective description of the epidemic Renormalization Group framework. We test the resulting theory against the time evolution of COVID-19 virus variants that validate the theory empirically.
To better predict the dynamics of spread of COVID-19 epidemics, it is important not only to investigate the network of local and long-range contagious contacts, but also to understand the temporal dynamics of infectiousness and detectable symptoms. Here we present a model of infection spread in a well-mixed group of individuals, which usually corresponds to a node in large-scale epidemiological networks. The model uses delay equations that take into account the duration of infection and is based on experimentally-derived time courses of viral load, virus shedding, severity and detectability of symptoms. We show that because of an early onset of infectiousness, which is reported to be synchronous or even precede the onset of detectable symptoms, the tracing and immediate testing of everyone who came in contact with the detected infected individual reduces the spread of epidemics, hospital load, and fatality rate. We hope that this more precise node dynamics could be incorporated into complex large-scale epidemiological models to improve the accuracy and credibility of predictions.
We revisit the modeling of the diauxic growth of a pure microorganism on two distinct sugars which was first described by Monod. Most available models are deterministic and make the assumption that all cells of the microbial ecosystem behave homogeneously with respect to both sugars, all consuming the first one and then switching to the second when the first is exhausted. We propose here a stochastic model which describes what is called metabolic heterogeneity. It allows to consider small populations as in microfluidics as well as large populations where billions of individuals coexist in the medium in a batch or chemostat. We highlight the link between the stochastic model and the deterministic behavior in real large cultures using a large population approximation. Then the influence of model parameter values on model dynamics is studied, notably with respect to the lag-phase observed in real systems depending on the sugars on which the microorganism grows. It is shown that both metabolic parameters as well as initial conditions play a crucial role on system dynamics.