No Arabic abstract
This technical report describes a dynamic causal model of the spread of coronavirus through a population. The model is based upon ensemble or population dynamics that generate outcomes, like new cases and deaths over time. The purpose of this model is to quantify the uncertainty that attends predictions of relevant outcomes. By assuming suitable conditional dependencies, one can model the effects of interventions (e.g., social distancing) and differences among populations (e.g., herd immunity) to predict what might happen in different circumstances. Technically, this model leverages state-of-the-art variational (Bayesian) model inversion and comparison procedures, originally developed to characterise the responses of neuronal ensembles to perturbations. Here, this modelling is applied to epidemiological populations to illustrate the kind of inferences that are supported and how the model per se can be optimised given timeseries data. Although the purpose of this paper is to describe a modelling protocol, the results illustrate some interesting perspectives on the current pandemic; for example, the nonlinear effects of herd immunity that speak to a self-organised mitigation process.
This technical report addresses a pressing issue in the trajectory of the coronavirus outbreak; namely, the rate at which effective immunity is lost following the first wave of the pandemic. This is a crucial epidemiological parameter that speaks to both the consequences of relaxing lockdown and the propensity for a second wave of infections. Using a dynamic causal model of reported cases and deaths from multiple countries, we evaluated the evidence models of progressively longer periods of immunity. The results speak to an effective population immunity of about three months that, under the model, defers any second wave for approximately six months in most countries. This may have implications for the window of opportunity for tracking and tracing, as well as for developing vaccination programmes, and other therapeutic interventions.
We recently described a dynamic causal model of a COVID-19 outbreak within a single region. Here, we combine several of these (epidemic) models to create a (pandemic) model of viral spread among regions. Our focus is on a second wave of new cases that may result from loss of immunity--and the exchange of people between regions--and how mortality rates can be ameliorated under different strategic responses. In particular, we consider hard or soft social distancing strategies predicated on national (Federal) or regional (State) estimates of the prevalence of infection in the population. The modelling is demonstrated using timeseries of new cases and deaths from the United States to estimate the parameters of a factorial (compartmental) epidemiological model of each State and, crucially, coupling between States. Using Bayesian model reduction, we identify the effective connectivity between States that best explains the initial phases of the outbreak in the United States. Using the ensuing posterior parameter estimates, we then evaluate the likely outcomes of different policies in terms of mortality, working days lost due to lockdown and demands upon critical care. The provisional results of this modelling suggest that social distancing and loss of immunity are the two key factors that underwrite a return to endemic equilibrium.
One of the key indicators used in tracking the evolution of an infectious disease isthe reproduction number. This quantity is usually computed using the reportednumber of cases, but ignoring that many more individuals may be infected (e.g.asymptomatics). We propose a statistical procedure to quantify the impact of un-detected infectious cases on the determination of the effective reproduction number. Our approach is stochastic, data-driven and not relying on any compartmentalmodel. It is applied to the COVID-19 case in eight different countries and all Italianregions, showing that the effect of undetected cases leads to estimates of the effective reproduction numbers larger than those obtained only with the reported cases by factors ranging from two to ten. Our findings urge caution about deciding when and how to relax containment measures based on the value of the reproduction number.
The COVID-19 has caused more than three million infections and over two hundred thousand deaths by April 20201. Limiting socioeconomic activities (SA) is among the most adopted governmental mitigating efforts to combat the transmission of the virus, though the degree varies dramatically among different regimes2. This study aims to quantify the contribution from the SA and weather conditions to the transmission of COVID-19 at global scale. Ruling out the unobservable factors including medical facilities and other control policies (MOC) through region-by-time fixed effects3,4, we show that the limiting SA has a leading contribution to lower the reproductive number by 18.3%, while weather conditions, including ultraviolet, relative humidity, and wind explain a smaller amount of variation. Temperature might have a non-monotonic impact on the transmission. We further show that in developed countries5 and China, the SA effect is more pronounced whereas the weather effect is significantly downplayed possibly because people tend to stay indoors most of the time with a controlled climate. We finally estimate the reduced reproductive number and the population spared from infections due to restricting SA at 40,964, 180,336, 174,494, in China, United States, and Europe respectively. From late January to mid-April, all regions, except for China, Australia, and south Korea show a steep upward trend of spared infections due to restricting SA. US and Europe, in particular, show far steeper upward trends of spared infections in the analyzed timeframe, signaling a greater risk of reopening the economy too soon.
By characterising the time evolution of COVID-19 in term of its velocity (log of the new cases per day) and its rate of variation, or acceleration, we show that in many countries there has been a deceleration even before lockdowns were issued. This feature, possibly due to the increase of social awareness, can be rationalised by a susceptible-hidden-infected-recovered (SHIR) model introduced by Barnes, in which a hidden (isolated from the virus) compartment $H$ is gradually populated by susceptible people, thus reducing the effectiveness of the virus spreading. By introducing a partial hiding mechanism, for instance due to the impossibility for a fraction of the population to enter the hidden state, we obtain a model that, although still sufficiently simple, faithfully reproduces the different deceleration trends observed in several major countries.