[katieHaylor (OP)]

Andrew says:

Recently it was suggested that the alveoli of Covid-infected lungs seem to become compromised in their ability to produce surfactant, essential for lung function. Earlier it had been observed that in some patients, viral infection establishes deeper in the respiratory system, and that these were the patients who became critically ill. Surfactants have the additional property of breaching the lipid bilayer containing the viral RNA, which is why soap nullifies the virus on hands.

Is it possible that for some susceptible patients, their alveoli were not producing enough surfactant even *before* they were infected, and that’s why their respiratory tracts are susceptible to deep infection?

What do you think?

[chris]

I gather that the SARS-CoV-2 coronavirus, which causes Covid-19, targets so-called type II pneumocytes, which produce surfactants. So affected parts of the lung can be robbed of surfacant, leading to terminal airway collapse and contributing to the hypoxia that characterises the disease.

We also published this article recently on why people lose their sense of smell and taste when they are infected with covid.

[Andrew Troup]

I gather that the SARS-CoV-2 coronavirus, which causes Covid-19, targets so-called type II pneumocytes, which produce surfactants. So affected parts of the lung can be robbed of surfactant, leading to terminal airway collapse and contributing to the hypoxia that characterises the disease.
.....

That's what I understand the conventional thinking to be, but I wondered if the arrow of causation might also point the other way. (IOW, have a point at both ends)

Hypothetically, a person with a surfactant deficiency prior to infection might be prone to having the viral particles colonise the air sacs, rather than (as more usual) just the nasal passages.
If borne out, this would explain why only some patients are susceptible to deep infection.

The infection deep in the respiratory system would create a positive feedback loop when the type II pneumocytes (such as they were) got further compromised.

I'm thinking of other situations where such loops exist, as in CO2 in the atmosphere, which can both cause, and be caused by, global warming, causing the potential for runaway warming.

[Andrew Troup]

Interesting: that article you kindly posted, Chris, mentioned the ACE-2 protein.

For some cryptic reason it reminded me I have read a paper linking constitutional susceptibility to  High Altitude Pulmonary Edema to polymorphisms in genes SP-A1 and SP-A2, where SP-A is the pulmonary surfactant protein.

Which in turn reminded me that in the early days of Covid-19, several intensivists reported that critically ill patients responded more like HAPE victims than like classic ARDS sufferers.

Hmmm.