This virus exits the cell using exocytosis after assembling golgi vesicles which contain the virus by fusing with the cell membrane.

In the case of infected pneumocytes, I imagine that the virus could then exit into the alveolus and infect other pneumocytes using again the interaction of the S protein with ACE2 or it could exit into the blood and spread to other pneumocytes in a 'miliary' fashion like TB. Is either or both the main mechanism of spread in the lung? Does lymphatic spread play any role?


We know that early CT scan of patients, even asymptomatic ones, show ground glass opacities and histology of resected lung segments in asymptomatic patients taken for lung cancer resection show alveloli filling with proteinaceous material. Patchy changes progress with time and if it were haematogenous spread then we would expect military like spread through the lung which is not what is being described.

The disease is spread by droplets full of virus, and it is likely that the patient in coughing is spreading the virus to other parts of the lung.

But this is speculative as the disease progression has not yet been fully characterised.

Pulmonary Pathology of Early-Phase 2019 Novel Coronavirus (COVID-19) Pneumonia in Two Patients With Lung Cancer https://www.jto.org/article/S1556-0864(20)30132-5/pdf

Temporal Changes of CT Findings in 90 Patients with COVID-19 Pneumonia: A Longitudinal Study https://pubs.rsna.org/doi/10.1148/radiol.2020200843

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