No Arabic abstract
Coronavirus disease 2019 (CoViD-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Among many symptoms, cough, fever and tiredness are the most common. People over 60 years old and with associated comorbidities are most likely to develop a worsening health condition. This paper proposes a non-integer order model to describe the dynamics of CoViD-19 in a standard population. The model incorporates the reinfection rate in the individuals recovered from the disease. Numerical simulations are performed for different values of the order of the fractional derivative and of reinfection rate. The results are discussed from a biological point of view.
We propose a qualitative analysis of a recent fractional-order COVID-19 model. We start by showing that the model is mathematically and biologically well posed. Then, we give a proof on the global stability of the disease free equilibrium point. Finally, some numerical simulations are performed to ensure stability and convergence of the disease free equilibrium point.
The Covid-19 pandemic is ongoing worldwide, and the damage it has caused is unprecedented. For prevention, South Korea has adopted a local quarantine strategy rather than a global lockdown. This approach not only minimizes economic damage, but it also efficiently prevents the spread of the disease. In this work, the spread of COVID-19 under local quarantine measures is modeled using the Susceptible-Exposed-Infected-Recovered model on complex networks. In this network approach, the links connected to isolated people are disconnected and then reinstated when they are released. This link dynamics leads to time-dependent reproduction number. Numerical simulations are performed on networks with reaction rates estimated from empirical data. The temporal pattern of the cumulative number of confirmed cases is then reproduced. The results show that a large number of asymptomatic infected patients are detected as they are quarantined together with infected patients. Additionally, possible consequences of the breakdowns of local quarantine measures and social distancing are considered.
Mathematical models describing SARS-CoV-2 dynamics and the corresponding immune responses in patients with COVID-19 can be critical to evaluate possible clinical outcomes of antiviral treatments. In this work, based on the concept of virus spreadability in the host, antiviral effectiveness thresholds are determined to establish whether or not a treatment will be able to clear the infection. In addition, the virus dynamic in the host -- including the time-to-peak and the final monotonically decreasing behavior -- is chracterized as a function of the treatment initial time. Simulation results, based on nine real patient data, show the potential clinical benefits of a treatment classification according to patient critical parameters. This study is aimed at paving the way for the different antivirals being developed to tackle SARS-CoV-2.
In this paper, we propose a continuous-time stochastic intensity model, namely, two-phase dynamic contagion process(2P-DCP), for modelling the epidemic contagion of COVID-19 and investigating the lockdown effect based on the dynamic contagion model introduced by Dassios and Zhao (2011). It allows randomness to the infectivity of individuals rather than a constant reproduction number as assumed by standard models. Key epidemiological quantities, such as the distribution of final epidemic size and expected epidemic duration, are derived and estimated based on real data for various regions and countries. The associated time lag of the effect of intervention in each country or region is estimated. Our results are consistent with the incubation time of COVID-19 found by recent medical study. We demonstrate that our model could potentially be a valuable tool in the modeling of COVID-19. More importantly, the proposed model of 2P-DCP could also be used as an important tool in epidemiological modelling as this type of contagion models with very simple structures is adequate to describe the evolution of regional epidemic and worldwide pandemic.
We study the epidemic spreading on spatial networks where the probability that two nodes are connected decays with their distance as a power law. As the exponent of the distance dependence grows, model networks smoothly transition from the random network limit to the regular lattice limit. We show that despite keeping the average number of contacts constant, the increasing exponent hampers the epidemic spreading by making long-distance connections less frequent. The spreading dynamics is influenced by the distance-dependence exponent as well and changes from exponential growth to power-law growth. The observed power-law growth is compatible with recent analyses of empirical data on the spreading of COVID-19 in numerous countries.