COVID-19 has been bullying the world since the winter. So far our public-health authorities have urged us to be scared and hide. They've ordered a quarantine, named in the 14th century but no doubt deployed millennia earlier. They'd like us to keep trying to hide from the virus until a safe, effective vaccine is developed. Like public health generally for the past half century, they blame us for dying. We didn't wear our masks right, or got too close to somebody positive.
Unfortunately, a safe and effective vaccine will take years unless significant corners are cut, enough to put an asterisk on the adjectives "safe" and "effective". But we seem to live in an asterisk world.
There has been almost no effort to develop oral treatments. Hydroxychloroquine, a drug known to prolong the Q-T interval on the electrocardiogram and possibly cause sudden death, failed many times. Dexamethasone helped a bit in the ICU. But the only way to treat COVID-19 is to beat it in the outpatient setting. Once a patient is hospitalized, the disease has done too much lasting damage.
Quercetin was suggested during the first SARS epidemic in 2003. Independently, I came to it in April 2020. First I'll tell you how my patient did, then I'll tell you my reasoning. The clinical outcome is much more valuable than the explanation, which will no doubt change with new knowledge.
My patient is an 18-year-old asthmatic who had failed standard asthma treatment: high-dose steroids, equivalent to the dexamethasone mentioned in the Oxford study above. I thought he was going to die. After two doses of oral quercetin, 1 gram each, 16 hours apart, he started breathing better, and within two days he felt better than he had in the previous month.
Now for the explanation, which is supported by my patient's dramatic response to quercetin. I know this reasoning is somewhat circular, and you don't have to believe it. The important thing in clinical medicine is that my patient actually got better. We can argue why until the cows come home.
In medicine, I have to add, one is either a "lumper" or a "splitter". Either you lump things together, in which case "splitters" accuse you of blurring the lines and ignoring important differences. Let me say at the outset that I'm proud to be a lumper. For example, I've already had my Abrahamic moment. I think that ACE, the angiotensin I-converting enzyme, is THE master disease gene. So let me get on with the story.
Lumpers would agree with me that viruses have many similarities. One problem they all have is packing their nucleic acid, be it DNA like the herpes viruses, or RNA like the SARS coronaviruses, inside a thin membrane made of fat. Nucleic acids have a strong negative charge because of their phosphate backbone. But lipids can't tolerate the charge. The charge has to be neutralized with a similarly strong positive charge. The virus's nucleic acid needs a protein blanket to keep it from touching the membrane directly. The blanket is called a nucleocapsid protein. It's the glue that holds the virus together.
Proteins are made of twenty possible amino acids. Some love lipids, others are charged. The nucleocapsid protein has a strong positive charge at one end. The other end of the nucleocapsid has a bunch of fat-loving amino acids that bury into the virus's lipid membrane. This happens to be the structure of a "basic secretagogue". (I owe this entire discussion to excellent articles in the medical literature.) Basic secretagogues are called this because they have a combination of a positive (basic) charge and a fat-loving region on the same molecule. They bind to a newly described receptor present only on the mast cell called the MRGPRX2 receptor.
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