No Arabic abstract
We estimate the growth in demand for ICU beds in Chicago during the emerging COVID-19 epidemic, using state-of-the-art computer simulations calibrated for the SARS-CoV-2 virus. The questions we address are these: (1) Will the ICU capacity in Chicago be exceeded, and if so by how much? (2) Can strong mitigation strategies, such as lockdown or shelter in place order, prevent the overflow of capacity? (3) When should such strategies be implemented? Our answers are as follows: (1) The ICU capacity may be exceeded by a large amount, probably by a factor of ten. (2) Strong mitigation can avert this emergency situation potentially, but even that will not work if implemented too late. (3) If the strong mitigation precedes April 1st, then the growth of COVID-19 can be controlled and the ICU capacity could be adequate. The earlier the strong mitigation is implemented, the greater the probability that it will be successful. After around April 1 2020, any strong mitigation will not avert the emergency situation. In Italy, the lockdown occurred too late and the number of deaths is still doubling every 2.3 days. It is difficult to be sure about the precise dates for this window of opportunity, due to the inherent uncertainties in computer simulation. But there is high confidence in the main conclusion that it exists and will soon be closed. Our conclusion is that, being fully cognizant of the societal trade-offs, there is a rapidly closing window of opportunity to avert a worst-case scenario in Chicago, but only with strong mitigation/lockdown implemented in the next week at the latest. If this window is missed, the epidemic will get worse and then strong mitigation/lockdown will be required after all, but it will be too late.
Epidemics generally spread through a succession of waves that reflect factors on multiple timescales. On short timescales, super-spreading events lead to burstiness and overdispersion, while long-term persistent heterogeneity in susceptibility is expected to lead to a reduction in the infection peak and the herd immunity threshold (HIT). Here, we develop a general approach to encompass both timescales, including time variations in individual social activity, and demonstrate how to incorporate them phenomenologically into a wide class of epidemiological models through parameterization. We derive a non-linear dependence of the effective reproduction number Re on the susceptible population fraction S. We show that a state of transient collective immunity (TCI) emerges well below the HIT during early, high-paced stages of the epidemic. However, this is a fragile state that wanes over time due to changing levels of social activity, and so the infection peak is not an indication of herd immunity: subsequent waves can and will emerge due to behavioral changes in the population, driven (e.g.) by seasonal factors. Transient and long-term levels of heterogeneity are estimated by using empirical data from the COVID-19 epidemic as well as from real-life face-to-face contact networks. These results suggest that the hardest-hit areas, such as NYC, have achieved TCI following the first wave of the epidemic, but likely remain below the long-term HIT. Thus, in contrast to some previous claims, these regions can still experience subsequent waves.
We present modeling of the COVID-19 epidemic in Illinois, USA, capturing the implementation of a Stay-at-Home order and scenarios for its eventual release. We use a non-Markovian age-of-infection model that is capable of handling long and variable time delays without changing its model topology. Bayesian estimation of model parameters is carried out using Markov Chain Monte Carlo (MCMC) methods. This framework allows us to treat all available input information, including both the previously published parameters of the epidemic and available local data, in a uniform manner. To accurately model deaths as well as demand on the healthcare system, we calibrate our predictions to total and in-hospital deaths as well as hospital and ICU bed occupancy by COVID-19 patients. We apply this model not only to the state as a whole but also its sub-regions in order to account for the wide disparities in population size and density. Without prior information on non-pharmaceutical interventions (NPIs), the model independently reproduces a mitigation trend closely matching mobility data reported by Google and Unacast. Forward predictions of the model provide robust estimates of the peak position and severity and also enable forecasting the regional-dependent results of releasing Stay-at-Home orders. The resulting highly constrained narrative of the epidemic is able to provide estimates of its unseen progression and inform scenarios for sustainable monitoring and control of the epidemic.
It is well recognized that population heterogeneity plays an important role in the spread of epidemics. While individual variations in social activity are often assumed to be persistent, i.e. constant in time, here we discuss the consequences of dynamic heterogeneity. By integrating the stochastic dynamics of social activity into traditional epidemiological models we demonstrate the emergence of a new long timescale governing the epidemic in broad agreement with empirical data. Our model captures multiple features of real-life epidemics such as COVID-19, including prolonged plateaus and multiple waves, which are transiently suppressed due to the dynamic nature of social activity. The existence of the long timescale due to the interplay between epidemic and social dynamics provides a unifying picture of how a fast-paced epidemic typically will transition to the endemic state.
SARS-CoV-2 has disrupted the life of billions of people around the world since the first outbreak was officially declared in China at the beginning of 2020. Yet, important questions such as how deadly it is or its degree of spread within different countries remain unanswered. In this work, we exploit the `universal growth of the mortality rate with age observed in different countries since the beginning of their respective outbreaks, combined with the results of the antibody prevalence tests in the population of Spain, to unveil both unknowns. We validate these results with an analogous antibody rate survey in the canton of Geneva, Switzerland. We also argue that the official number of deaths over 70 years old is importantly underestimated in most of the countries, and we use the comparison between the official records with the number of deaths mentioning COVID-19 in the death certificates to quantify by how much. Using this information, we estimate the fatality infection ratio (IFR) for the different age segments and the fraction of the population infected in different countries assuming a uniform exposure to the virus in all age segments. We also give estimations for the non-uniform IFR using the sero-epidemiological results of Spain, showing a very similar growth of the fatality ratio with age. Only for Spain, we estimate the probability (if infected) of being identified as a case, being hospitalized or admitted in the intensive care units as function of age. In general, we observe a nearly exponential growth of the fatality ratio with age, which anticipates large differences in total IFR in countries with different demographic distributions, with numbers that range from 1.82% in Italy, to 0.62% in China or even 0.14% in middle Africa.
Timely estimation of the current value for COVID-19 reproduction factor $R$ has become a key aim of efforts to inform management strategies. $R$ is an important metric used by policy-makers in setting mitigation levels and is also important for accurate modelling of epidemic progression. This brief paper introduces a method for estimating $R$ from biased case testing data. Using testing data, rather than hospitalisation or death data, provides a much earlier metric along the symptomatic progression scale. This can be hugely important when fighting the exponential nature of an epidemic. We develop a practical estimator and apply it to Scottish case testing data to infer a current (20 May 2020) $R$ value of $0.74$ with $95%$ confidence interval $[0.48 - 0.86]$.