China is now trying to blame us for this, exactly as I predicted they would:
As the crisis eases inside China, Beijing is trying to deflect blame and position itself as the world's coronavirus savior.
www.vice.com
What seems like a small outbreak can quickly go out of control due to exponential spread. That's why all of Italy is under quarantine right now.
I take this thing very,
very seriously. Which is why I sent this missive to my employer in response to a safety bulletin regarding the virus:
So, again, to recap, if you're one of the unlucky 1 in 5 infected who develops severe or critical COVID-19, this is what can happen to your body:
- Bilateral viral pneumonia with ground-glass lesions visible on CT scans
- Pulmonary fibrosis and permanent lung scarring, all the way up to hemorrhagic necrosis of lung tissue
- Hypoxemia precipitating injury of all organs, including the kidneys
- Myocarditis precipitating myoglobinemia and acute kidney injury
- Liver injury
- Possible male sterility
- Autoimmune reactions/cytokine release syndrome
- Severe bacterial co-infections
- Neurological symptoms including cerebrovascular or medullary infection, leading to collapses and seizures
You know what they do to severe and critical COVID-19 patients? They intubate them and they give them barely-tested cutting-edge antivirals, antibiotics, steroids, antipyretics, decongestants, and basically everything they can to keep them alive, while also monitoring their blood and liver labs and blood pressure. It's like running a marathon. Doctors and nurses are getting sick with this shit, too, treating patients day and night and collapsing from exhaustion, while also maintaining nearly inhuman infection control measures.
The exact mechanism by which SARS-CoV-2 causes all this insane inflammation is now known in great detail.
ACE2 normally converts Angiotensin II into Angiotensin 1-7, which, in turn, is a Mitochondrial assembly receptor agonist. The process has a blood pressure regulating and anti-inflammatory effect.
Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target
The virus uses ACE2 as its cell entry receptor, blocking Ang II from converting to Ang 1-7 and behaving as a MasR agonist. Ang II builds up, with a massive pro-inflammatory effect, damaging tissues and causing hypertension.
This is what I meant when I said weeks ago that the virus "dysregulates angiotensin".
For those who don't know what the RAAS system does, these vids do a good job of explaining it:
Most of the people dying of COVID-19 are not dying of respiratory issues. They're getting intubated, and they're getting sufficient air, and then, guess what? Heart failure out of the blue, and then they code in the ICU. Dead.
Anyone who is downplaying the seriousness of this virus does not know what they are talking about.