I thought it was lowered expression of the receptors covid-19 binds to (known condition among smokers) ace-2... Because smokers have suppressed ace-2 while smoking but a higher baseline; they are protected from getting it because when they are in public they are likely smoking and protected but once they get it they get very severe COVID...

I mean it's all kind of a just-so story. Iirc Omeprazole which also depresses ace-2 failed as a prophylactic treatment

Cigarette smoking definitely does not provide with a better physical barrier, and does not "coat" the surface of your lungs with tar. There could be some effect from reduced surface area (see: emphysema, although typically patients with this condition, or even smokers generally, will have an increased risk of infection), but my bet is on some nicotine receptor effect. These are quite immunomodulatory.

Everything in a relative of mine who smokes house is coated with tar. They regularly burn out computers because they get so impacted with tar covered lint. I find it very likely their lungs are covered in tar as well - moreso I don’t understand how they could possibly not be.

This same relative has Crohn’s which is why I am here reading this.

That’s why I was so interested in the study of smokeless tobacco users.

Anyway, I don’t mean the tar is the physical barrier, inflammation response plus common changes to the extracellular matrix should both result in a physical barrier. The compensative increased respiratory rate seems like it would offset reduced surface area, but these changes are more complicated than that.

Also, it’s increased risk of detected infection, but patients without symptoms are rarely tested for viral disease at this scale. That makes comparisons very tricky.