ABSTRACT
India was the second highest COVID-19 affected country in the world with 2.1 million cases by 11th August. This study focused on the spatial transmission of the pandemic among the 640 districts in India over time, and aimed to understand the urban-centric nature of the infection. The connectivity context was emphasized that possibly had inflicted the outbreak. Using the modes of transmission data for the available cases, the diffusion of this disease was explained. Metropolitans contributed three-fourths of total cases from the beginning. The transport networks attributed significantly in transmitting the virus from the urban containment zones. Later, there was a gradual shift of infections from urban to rural areas; however, the numbers kept increasing in the former. The massive reverse migration after lockdown spiked the infected cases further. Districts with airports reported more with influx of international passengers. A profound east-west division in April with higher infections in the southern and western districts existed. By mid-May eastern India saw a steep rise in active cases. Moran's I analysis showed a low autocorrelation initially which increased over time. Hotspot clustering was observed in western Maharashtra, eastern Tamil Nadu, Gujarat and around Kolkata by the second week of August. The diffusion was due to travel, exposure to infected individuals and among the frontline workers. Spatial regression models confirmed that urbanization was positively correlated with higher incidences of infections. Transit mediums, especially rail and aviation were positively associated. These models validated the crucial role of spatial proximity in diffusion of the pandemic.
ABSTRACT
Mathematical modeling is crucial to investigating tthe ongoing coronavirus disease 2019 (COVID-19) pandemic. The primary target area of the SARS-CoV-2 virus is epithelial cells in the human lower respiratory tract. During this viral infection, infected cells can activate innate and adaptive immune responses to viral infection. Immune response in COVID-19 infection can lead to longer recovery time and more severe secondary complications. We formulate a micro-level mathematical model by incorporating a saturation term for SARS-CoV-2-infected epithelial cell loss reliant on infected cell levels. Forward and backward bifurcation between disease-free and endemic equilibrium points have been analyzed. Global stability of both disease-free and endemic equilibrium is provided. We have seen that the disease-free equilibrium is globally stable for R0<1, and endemic equilibrium exists and is globally stable for R0>1. Impulsive application of drug dosing has been applied for the treatment of COVID-19 patients. Additionally, the dynamics of the impulsive system are discussed when a patient takes drug holidays. Numerical simulations support the analytical findings and the dynamical regimes in the systems.