Abstract

The new coronavirus disease 2019 (COVID-19) has been emerged as a rapidly spreading pandemic. The disease is thought to spread mainly from person-to-person through respiratory droplets produced when an infected person coughs, sneezes, or talks. The pathogen of COVID-19 is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It infects the cells binding to the angiotensin-converting enzyme 2 receptor (ACE2) which is expressed by cells throughout the airways as targets for cellular entry. Although the majority of persons infected with SARS-CoV-2 experience symptoms of mild upper respiratory tract infection, in some people infections of the acinar airways result in severe, potentially fatal pneumonia. However, the induction of COVID-19 pneumonia requires that SARS-CoV-2 reaches the acinar airways. While huge efforts have been made to understand the spread of the disease as well as the pathogenesis following cellular entry, much less attention is paid to how SARS-CoV-2 from the environment reach the receptors of the target cells. The aim of the present study is to characterize the deposition distribution of SARS-CoV-2 in the airways upon exposure to cough-generated droplets and aerosol particles. For this purpose, the Stochastic Lung Deposition Model has been applied. Particle size distribution, breathing parameters supposing normal breathing through the nose, and viral loads were taken from the literature. We found that the probability of direct infection of the acinar airways due to inhalation of particles emitted by a bystander cough is very low. As the number of viruses deposited in the extrathoracic airways is about 7 times higher than in the acinar airways, we concluded that in most cases COVID-19 pneumonia must be preceded by SARS-CoV-2 infection of the upper airways. Our results suggest that without the enhancement of viral load in the upper airways, COVID-19 would be much less dangerous. The period between the onset of initial symptoms and the potential clinical deterioration could provide an opportunity for prevention of pneumonia by blocking or significantly reducing the transport of viruses towards the acinar airways. Therefore, even non-specific treatment forms like disinfection of the throat and nasal and oral mucosa may effectively keep the viral load of the upper airways low enough to avoid or prolong the progression of the disease. In addition, using a tissue or cloth in order to absorb droplets and aerosol particles emitted by own coughs of infected patients before re-inhalation is highly recommended even if they are alone in quarantine.

Highlights

  • COVID-19, and there is great uncertainty regarding its mechanism of ­spread[3]

  • The majority of persons infected with SARS-CoV-2 experience symptoms of mild upper respiratory tract infection, in some people infections of the acinar airways result in severe pneumonia potentially leading to significant hypoxia with acute respiratory distress syndrome (ARDS) and death

  • As the infection with SARS-CoV-2 causes very different symptoms depending on the infected region, first we focus on the regional deposition distribution of particles emitted by coughing

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Summary

Introduction

COVID-19, and there is great uncertainty regarding its mechanism of ­spread[3]. the disease is thought to spread (1) mainly from person-to-person, (2) mainly through respiratory droplets produced when an infected person coughs, sneezes or talks (3) which can land in the mouths or noses of people who are nearby or possibly be inhaled into the l­ungs[4]. The pathogen of COVID 19 is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)[6], which infects the cells binding to the angiotensin-converting enzyme 2 receptor (ACE2)[7] primarily in the respiratory system. The majority of persons infected with SARS-CoV-2 experience symptoms of mild upper respiratory tract infection, in some people infections of the acinar airways result in severe pneumonia potentially leading to significant hypoxia with acute respiratory distress syndrome (ARDS) and death. The induction of COVID-19 pneumonia and ARDS requires that SARS-CoV-2 reaches the lower airways. While huge efforts have been made to understand the spread of COVID-19 disease as well as its pathogenesis following cellular entry of SARS-CoV-2, much less attention is paid to how viruses from the environment reach the receptors of the target cells in the respiratory system. The aims of the present study are to quantify the deposition distribution of cough-generated droplets and aerosol particles carrying SARS-CoV-2, to estimate the amount of deposited SARS-CoV-2 in different parts of the human airways upon exposure to cough generated droplets and aerosol particles, and to discuss its consequences on the pathogenesis of COVID-19

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