So there would be no need to shine UV light directly into the lungs.
Medicine has often found treatments that works without any real understanding of why.
While he identified the mechanism of inoculation, my understanding is he theorized that it was due to the attenuated pathogen outcompeting the virulent one for nutrients rather than due to stimulation of the immune system.
I think I got that from a lecture by a science historian once. This idea seems to be glossed in the Wikipedia article on Pasteur here:
https://en.wikipedia.org/wiki/Louis_Pasteur#Anthrax
Do I have that right?
How could it outcompete the actual virus if the actual virus isn't there yet at the time of vaccination?
It does directly infects kidney cells, and kidney failure is one common cause of death.
Because of all the additional attention, it would be unsurprising for doctors to seemingly discover all kinds of previously unexamined phenomenon which have always been present, or to confuse increases in certain phenomenon as peculiar rather than simply reflecting the fact that you have a ton of patients with the same type of illness. For example, in one of the articles about blood clots a doctor is quoted as saying something to the effect of, "we're used to seeing these types of blood clots in the ICU, but only in 1 or 2 patients at a time, never in this number". For the sake of argument, maybe that's just because they've never had an entire ICU full of patients in viral-induced acute respiratory distress, that such blood clots happen to be more prevalent in such cases, and if you examined all such ICU patients over time (COVID, flu, w'ever), you'd see a similar pattern. (Because it's usually the elderly who die from respiratory infections, not alot of attention is paid to mechanisms of death. "Pneumonia" is something of a catch-all term, especially with an older cohort.) Maybe it's typical of anything that can incite such immune reactions--the article hinted that the mechanism may be related to how Ebola works, except with opposite outcomes (clots instead of bleeding out), which suggests the mechanism might be more a reflection of the severity of the distress than anything peculiar to the infectious agent, per se. Maybe younger cohorts are more likely to clot, but before COVID-19 they rarely died or had such severe symptoms, so nobody quantified prevalence. And if so, treating the clots might not significantly reduce fatality rates; or maybe it would, not just for COVID-19 but any similar viral ailment.
You could get UV light to the large bronchi but you couldn't get UV light into all the million little aveoli.
So you're off by a factor of 2 but are basically correct.
This may be somewhat different from the typical intubation case, for example prior to surgery. Where its a generally more healthy person who has not been hypoxic for hours or days and is not at the last of their reserves...
Biological systems are almost unimaginably complex. Unintuitive effects are not uncommon.
At least, that's how someone who researched rhinoviruses once explained it to me many years ago, but probably using more accurate terminology.
Also, AFAIU, these viruses have also evolved other exploits. It's no coincidence that cold viruses induce sneezing and other sinus irritations; the viral fragments themselves have evolved to trigger this behavior, which is why it can happen after a live infection is gone--your tissues are still shedding viral fragments.
Sars-Cov2 is a respiratory disease. I guess it maybe present in blood, but it doesn’t seem like removing it from blood would help with the respiratory issues it causes.
I can’t see how you would easily get UV light into the lungs. But maybe there’s a way... seems a bit far fetched.