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. 2020 Dec 31;10(1):22430.
doi: 10.1038/s41598-020-79985-6.

Deposition distribution of the new coronavirus (SARS-CoV-2) in the human airways upon exposure to cough-generated droplets and aerosol particles

Affiliations

Deposition distribution of the new coronavirus (SARS-CoV-2) in the human airways upon exposure to cough-generated droplets and aerosol particles

Balázs G Madas et al. Sci Rep. .

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.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
Mass size distribution of particles emitted by coughing of patients with influenza. This mass size distribution was used as input of the Stochastic Lung Deposition Model.
Figure 2
Figure 2
Mass deposition fraction of inhaled particles (left axis) and deposited mass from a single inhalation (right axis) in the extrathoracic, bronchial and acinar regions of the lungs upon exposure to cough-generated droplets and aerosol particles. The insert shows the subdivisions of the intrathoracic airways.
Figure 3
Figure 3
Mass deposition fraction of inhaled particles (left axis) and deposited mass from a single inhalation (right axis) in the large, small, and peripheral airways upon exposure to cough-generated droplets and aerosol particles. See also the insert in Fig. 2 for the definitions of large, small, and peripheral airways.
Figure 4
Figure 4
Mass deposition fraction of inhaled particles (left axis) and deposited mass from a single inhalation (right axis) upon exposure to cough-generated droplets and aerosol particles as the function of airway generation number.
Figure 5
Figure 5
The average number of RNA copies of the virus in one particle (left axis and dash lines) and the probability that a particle contains at least one RNA copy (right axis and solid lines) as the function of particle size in case of different initial viral loads (in RNA copy per cm3) in the throat (different colors).

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