No Arabic abstract
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.
We study a simple realistic model for describing the diffusion of an infectious disease on a population of individuals. The dynamics is governed by a single functional delay differential equation, which, in the case of a large population, can be solved exactly, even in the presence of a time-dependent infection rate. This delay model has a higher degree of accuracy than that of the so-called SIR model, commonly used in epidemiology, which, instead, is formulated in terms of ordinary differential equations. We apply this model to describe the outbreak of the new infectious disease, Covid-19, in Italy, taking into account the containment measures implemented by the government in order to mitigate the spreading of the virus and the social costs for the population.
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.
Within a short period of time, COVID-19 grew into a world-wide pandemic. Transmission by pre-symptomatic and asymptomatic viral carriers rendered intervention and containment of the disease extremely challenging. Based on reported infection case studies, we construct an epidemiological model that focuses on transmission around the symptom onset. The model is calibrated against incubation period and pairwise transmission statistics during the initial outbreaks of the pandemic outside Wuhan with minimal non-pharmaceutical interventions. Mathematical treatment of the model yields explicit expressions for the size of latent and pre-symptomatic subpopulations during the exponential growth phase, with the local epidemic growth rate as input. We then explore reduction of the basic reproduction number R_0 through specific disease control measures such as contact tracing, testing, social distancing, wearing masks and sheltering in place. When these measures are implemented in combination, their effects on R_0 multiply. We also compare our model behaviour to the first wave of the COVID-19 spreading in various affected regions and highlight generic and less generic features of the pandemic development.
In all Countries the political decisions aim to achieve an almost stable configuration with a small number of new infected individuals per day due to Covid-19. When such a condition is reached, the containment effort is usually reduced in favor of a gradual reopening of the social life and of the various economical sectors. However, in this new phase, the infection spread restarts and a quantitative analysis of the regrowth is very useful. We discuss a macroscopic approach which, on the basis of the collected data in the first lockdown, after few days from the beginning of the new phase, outlines different scenarios of the Covid-19 diffusion for longer time. The purpose of this paper is a demonstration-of-concept: one takes simple growth models, considers the available data and shows how the future trend of the spread can be obtained. The method applies a time dependent carrying capacity, analogously to many macroscopic growth laws in biology, economics and population dynamics. The illustrative cases of Singapore, France, Spain and Italy are analyzed.
India has been hit by a huge second wave of Covid-19 that started in mid-February 2021. Mumbai was amongst the first cities to see the increase. In this report, we use our agent based simulator to computationally study the second wave in Mumbai. We build upon our earlier analysis, where projections were made from November 2020 onwards. We use our simulator to conduct an extensive scenario analysis - we play out many plausible scenarios through varying economic activity, reinfection levels, population compliance, infectiveness, prevalence and lethality of the possible variant strains, and infection spread via local trains to arrive at those that may better explain the second wave fatality numbers. We observe and highlight that timings of peak and valley of the fatalities in the second wave are robust to many plausible scenarios, suggesting that they are likely to be accurate projections for Mumbai. During the second wave, the observed fatalities were low in February and mid-March and saw a phase change or a steep increase in the growth rate after around late March. We conduct extensive experiments to replicate this observed sharp convexity. This is not an easy phenomena to replicate, and we find that explanations such as increased laxity in the population, increased reinfections, increased intensity of infections in Mumbai transportation, increased lethality in the virus, or a combination amongst them, generally do a poor job of matching this pattern. We find that the most likely explanation is presence of small amount of extremely infective variant on February 1 that grows rapidly thereafter and becomes a dominant strain by Mid-March. From a prescriptive view, this points to an urgent need for extensive and continuous genome sequencing to establish existence and prevalence of different virus strains in Mumbai and in India, as they evolve over time.