The biochemistry of how COVID-19 attacks the body: a synopsis of the medical studies
The biochemistry of how COVID-19 attacks the body: a synopsis of the medical studies
“Our structural analyses confidently predict that the Wuhan coronavirus uses ACE2 as its host receptor,” the investigators wrote. That and several other structural details of the new virus are consistent with the ability of the Wuhan coronavirus to infect humans and with some capability to transmit among humans.”
BioQuick News: How SARS-CoV-2 (COVID-19) Gets into Respiratory Tissue — And How It May Exploit One of Our Anti-Viral Defenses; Interferon Boosts ACE2, Which Is Cell Surface Receptor That COVID-19 Binds To:
Nature: Infection prodeeds through as many as three phases: (1) an asymptomatic phase; if the body does not fight off the virus quickly enough, it proceeds to (2) a mildly symptomatic phase. If after about 10 days or so the body has still not fought off the virus, it proceeds to the devastating phase, including the oxygen transfer cells in the lungs, and also involving the blood cells themselves:
“ As the virus multiplies, an infected person may shed copious amounts of it, especially during the first week or so. Symptoms may be absent at this point. Or the virus’ new victim may develop a fever, dry cough, sore throat, loss of smell and taste, or head and body aches.“If the immune system doesn’t beat back SARS-CoV-2 during this initial phase, the virus then marches down the windpipe to attack the lungs, where it can turn deadly. The thinner, distant branches of the lung’s respiratory tree end in tiny air sacs called alveoli, each lined by a single layer of cells that are also rich in ACE2 receptors.“ Normally, oxygen crosses the alveoli into the capillaries, tiny blood vessels that lie beside the air sacs; the oxygen is then carried to the rest of the body. But as the immune system wars with the invader, the battle itself disrupts this healthy oxygen transfer. Front-line white blood cells release inflammatory molecules called chemokines, which in turn summon more immune cells that target and kill virus-infected cells, leaving a stew of fluid and dead cells—pus—behind. This is the underlying pathology of pneumonia, with its corresponding symptoms: coughing; fever; and rapid, shallow respiration (see graphic). Some COVID-19 patients recover, sometimes with no more support than oxygen breathed in through nasal prongs.
“ …. The disruption seems to extend to the blood itself. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one-third already had clots, according to a 10 April paper in Thrombosis Research. Blood clots can break apart and land in the lungs, blocking vital arteries—a condition known as pulmonary embolism, which has reportedly killed COVID-19 patients. Clots from arteries can also lodge in the brain, causing stroke. Many patients have “dramatically” high levels of D-dimer, a byproduct of blood clots, says Behnood Bikdeli, a cardiovascular medicine fellow at Columbia University Medical Center.”
ChemRxiv (pre-print server for chemistry studies): The virus seems to bind to the hemoglobin in red blood cells, preventing oxygen transfer to other cells in the body, and promoting clotting of the red blood cells themselves:
“The results showed the ORF8 and surface glycoprotein could bind to the porphyrin, r espectively. At the same time, orf1ab, ORF10, and ORF3a proteins could coordinate attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin. The attack will cause less and less hemoglobin that can carry oxygen and carbon dioxide. The lung cells have extremely intense poisoning and inflammatory due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images. The mechanism also interfered with the normal heme anabolic pathway of the human body, is expected to result in human disease.”
Thailand Medical News: More on the virus’s effect on red blood cells. It binds to the iron ion in the red blood cells. This is how it prevents oxygen transfer:
“The research discovered that some of these proteins are to hijack the red blod cells and remove the Iron ions from the heme groups (HBB) and replace themselves with it. This makes the hemoglobin unable to transport oxygen.
“As a result the lungs are stressed out and inflamed while the rest of the organs are also being affected. The so called ARDS and subsequent organ failure could be attributed to this.”
“The cells that the virus binds to using the ACE-2 receptor or three types: mucus producing cells; the alveoli in the lungs that hold oxygen; and nutrient absorbing cells in the intestines.[This probably explains why a large number of coronavirus infections begin with intestinal distress. The above two articles also explain why so many severe infections include strikingly low blood oxygen levels, and also why so much blood clotting is found in patients, including otherwise symptomatic patients who may suffer heart attacks or strokes.]
BioQuick News: How SARS-CoV-2 (COVID-19) Gets into Respiratory Tissue — And How It May Exploit One of Our Anti-Viral Defenses; Interferon Boosts ACE2, Which Is Cell Surface Receptor That COVID-19 Binds To:
“ Researchers from the New York Blood Centre and also from Fudan University in Shanghai have discovered that the SARS-CoV-2 coronavirus which causes the COVID-19 disease that often results severe acute respiratory syndrome also attacks the immune system’s T lymphocytes. The worrying findings highlight the destructive power of the novel coronavirus, which can destroy the immune system, leaving the patient vulnerable and unable to fight off the infection.
“ The researchers’ surprise discovery has shed light on the potency of the novel coronavirus is killing powerful immune cells, which are supposed to kill the virus instead.
“COVID-19, caused by the new pandemic coronavirus, is strangely—and tragically—selective. Only some infected people get sick, and although most of the critically ill are elderly or have complicating problems such as heart disease, some killed by the disease are previously healthy and even relatively young. Researchers are now gearing up to scour the patients’ genomes for DNA variations that explain this mystery. The findings could be used to identify those most at risk of serious illness and those who might be protected, and they might also guide the search for new treatments.
“ Ganna heads up a major effort to pool COVID-19 patients’ genetic data from around the world. The idea “came quite spontaneously” about 2 weeks ago when “everyone was sitting at their computers watching this crisis,” says Ganna, who is also affiliated with the Broad Institute, a U.S. genomic powerhouse.treatments.
The following study Impact of Diabetes on Ace/Ace2 Balance and Angiotensin II Type 1 Receptor Expression in db/db Diabetic Mice reports that ACE2 receptors increase in diabetes even without treatment drugs. It also found no effect of metformin on ACE2 receptors, although other studies have found that Metformin somewhat suppresses ACE2 receptors.
It is interesting that it took several months to get to this level of understanding. I suppose it is hard to figure out how to drain the swamp when one is up to one’s ass in alligators. Responding to incoming patients and ER codes doesn’t make it easy to figure out just what is going on.
P.S. A relation of mine died on a cruise ship off the coast of the Philippines back in January. COVID was not suspected as she was asymptomatic. It took some time before the ship finally found a port that would let the passengers disembark. Now, it is seems obvious that she was an early casualty of Trump’s Plague.
Wow! That’s a lot of info. Thanks for putting it all together and posting.
Fwiw, I tested positive for this disease. I likely got it mid-December, flared up the night of December 28th. Had a fever, really light green mucus. Some light problems breathing. Took about 2 weeks to fully get over it.
I will second Ken’s WOW!
The discussion of the “Angiotensin Receptor Blockers (ARBs or Sartans)” was very helpful.