Abstract
Background: While the nasopharynx is initially the dominant upper airway infection site for SARS-CoV-2, the physiologic mechanism launching the infection at the lower airway is still not well-understood. Based on the rapidity of infection progression to the lungs, it has been hypothesized that the nasopharynx may be acting as the primary seeding zone for subsequent contamination of the lower airway via aspiration of virus-laden boluses of nasopharyngeal fluids. Methodology: To examine the plausibility of the aspiration-driven mechanism, we have computationally tracked the inhalation process in three anatomic airway reconstructions and have quantified the nasopharyngeal liquid volume transmitted to the lower airspace during each aspiration. Results: Extending the numerical trends on aspiration volume to earlier records on aspiration frequencies indicates a total aspirated nasopharyngeal liquid volume of 0.3 – 0.76 ml/day. Subsequently, for mean sputum viral load, our modeling projects that the number of virions reaching the lower airway will range over 2.1×106 – 5.3×106 /day; for peak viral load, the corresponding number hovers between 7.1×108 – 1.8×109. Conclusions: The virion transmission findings fill in a key piece of the mechanistic puzzle on the systemic progression of SARS-CoV-2, and subjectively point to health conditions like dysphagia, with proclivity to increased aspiration, as some of the potential underlying risk factors for aggressive lung infections.
Highlights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent for coronavirus disease 2019 (COVID-19), has been linked[1,2] to a remarkable pattern of relatively high infectivity in ciliated epithelial cells along the nasal passage lining in the upper airway, moderate infectivity in cells lining the throat and bronchia, and relatively low infectivity in lung cells
The virion transmission findings fill in a key piece of the mechanistic puzzle on the systemic progression of SARSCoV-2, and subjectively point to health conditions like dysphagia, with proclivity to increased aspiration, as some of the potential underlying risk factors for aggressive lung infections
Such viral trends are governed by the abundance of angiotensin-converting enzyme 2 (ACE2), a single-pass type I membrane protein that is exploited by viral spike protein binding as a gateway for cellular entry
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent for coronavirus disease 2019 (COVID-19), has been linked[1,2] to a remarkable pattern of relatively high infectivity in ciliated epithelial cells along the nasal passage lining in the upper airway, moderate infectivity in cells lining the throat and bronchia, and relatively low infectivity in lung cells. Such viral trends are governed by the abundance of angiotensin-converting enzyme 2 (ACE2), a single-pass type I membrane protein that is exploited by viral spike protein binding as a gateway for cellular entry. Based on the rapidity of infection progression to the lungs, it has been hypothesized that the nasopharynx may be acting as the primary seeding zone for subsequent contamination of the lower airway via aspiration of virus-laden boluses of nasopharyngeal fluids
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