Circulating on nursing forums, this is a better explanation of a possible mechanism for CoVid (summarizing various juried publications and pre-prints, as well as computer analysis of observations):
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"Might not even be a respiratory illness after all and that's just a byproduct of the wreckage it makes in blood haemoglobin (thus making ARDS a symptom not a cause).
I wish this would get more traction because if this computational analysis is correct, this could completely change the way we approach COVID, globally.
I will copy some summaries that explain this paper in layman's terms:
- Using computational analysis (modeling the behavior of a molecule in a computer), they've worked out the probable mechanism by which SARS-nCov-2 wreaks havoc on patients, as well as why chloroquine and favipiravir seem to work.
- Inside our red blood cells, there is a molecule called hemoglobin, which contains heme groups. Each heme group is a molecular "ring" (called a porphyrin) that can hold an iron (Fe) ion inside. Having an iron ion inside is what allows this heme to carry O2 (and CO2) in our blood. This is how our bodies move O2 to our tissues and remove CO2 waste products.
- The paper modeled these and found that the proteins produced when COVID replicates "collaborate" to knock iron ions out of heme groups (HBB) and replace them with one of the proteins. This makes the red blood cell unable to transport O2 and CO2!
- If the computer modeling is right, it shows that the virus hijacks our [red] blood [cells] and makes it unable to carry O2 to a patient's tissues/organs, and likewise unable to carry CO2 out of them. This would lead to organ and tissue death, roughly in the same way as if a patient were being suffocated. Even when a patient can breath (fill lungs with air), the oxygen isn't getting to the cells in their body.
- The inflammation in the lungs results from the lungs not being able to perform the oxygen/CO2 exchange, and would therefore appear to be a SECONDARY result of the hijacking of the blood. The lungs not working is a result of lack of O2 in blood, not the cause of it. Hence the "ground glass opacities".
- The paper models the behavior of chloroquine and faviparavir as well, which appear to bind to the non-structural viral proteins that hijack the heme groups, thus inhibiting them from knocking out the iron and wrecking the O2-carrying ability of the red blood cells.
- This also explains the observation made by various ER docs (incl this one in New Orleans) that patients tend to have elevated ferritin: ferritin is used to store excess iron. If a lot of iron is knocked out of heme groups and floating around, the body produces more ferritin
If true, this may mean a few things:
1. Starting drug treatment while symptoms are mild keeps virus from hijacking too much blood, enabling a still-healthy body to mount an immune response. Explains why early drug treatment (first week of symptoms) is often successful.
2. Drug treatment and intubation once patient is critical will rarely work because tissues/organs are already damaged, blood can't carry O2, and the body is too weak to produce new red blood cells able to carry Fe (and thus oxygen/CO2) even if drugs inhibit more hijacking.
3. Thus: start severe patients on drug treatment upon hospital intake to suppress further hijacking of blood by the virus, then give them a blood transfusion of new red blood cells immediately that are unhijacked. If all this is true, we would see rapid patient improvement.
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The problem is we have not yet had studies testing whether patients will respond well to blood transfusions from people who have not had COVID-19. Right now medical attention is focused on blood transfusions from those who have beat COVID and have antibodies. This needs to be looked at
This research ties in to the fact that weight/age/high blood pressure are such risk factor and why certain blood types are less afflicted than other
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