So, to recap, in severe and critical cases, SARS-CoV-2 can cause bilateral viral pneumonia, lung fibrosis, myocarditis, myoglobinemia, acute kidney injury, liver injury, bacterial co-infections, autoimmune reactions, and cerebrovascular and medullary infections that manifest neurological symptoms like loss of automatic breathing, collapse, lethargy, seizures,
et cetera. In 80% of cases, symptoms are mild, but for 1 in 5, any of the above things can happen.
Many of the people dying are not dying from pneumonia. They're getting intubated, and then, the cardiomyopathy from their cardiac injuries is killing them. Even if they get enough oxygen, they die of heart attacks. The virus can attack the heart muscle, the myocardium. As the myocardium breaks down into the bloodstream, it causes myoglobinemia, which, in turn, attacks the kidneys, same as if you got rhabdo from crushing your leg flipping your ATV in the woods.
Someone with severe or critical COVID-19 doesn't just need intubation. They also need prophylactic antibiotics to keep the bacterial co-infections in check, dialysis to take the strain off their kidneys, antivirals to reduce viral load, antipyretics to manage fever, and they need constant lab work done to monitor their blood and their liver and adjust treatment as necessary. I don't know what you'd do about the nasty cytokine storms, sepsis, and clots. CytoSorb? Heparin? Steroids to try and keep the inflammation down? In Wuhan, they gave people methylprednisolone to manage the inflammation, but they kept dying, anyway, because some
managed inflammation is actually necessary to combat the virus. People who are already on steroids can be at risk because of immunosuppression.
Smokers, people with diabetes, people with hypertension, and people on angiotensin blockers may be especially susceptible. ARBs might protect cells from the virus, but they might also cause gene expression changes over time that make one more susceptible, so anyone who's already been on ARBs for a while may be at risk. Anything that increases ACE2 gene expression makes someone more vulnerable to COVID-19. Remdesivir and Chloroquine seem to be very effective at inhibiting SARS-CoV-2 replication.
The virus lingers in aerosols and can get in through your eyes, nose, and mouth, so you need both an N95 and skin-tight goggles at minimum. P100 full-face, even better. 40mm CBRN, better still.
It is shed in feces and urine, and patients' bedpans are very, very hazardous.
It's all in my (freshly-updated) notes:
As it turns out, SARS-CoV-2 can also be blocked by certain protease inhibitors. It needs transmembrane protease, serine 2, to enter cells. Block that, and you can block the virus:
https://www.cell.com/cell/fulltext/S0092-8674(20)30229-4?rss=yes
Tons of potential therapies are being investigated. This is just the beginning. The response from the scientific community has been incredibly comprehensive. They are basically waging war.
www.suomenmaa.fi
