A large volume of evidence coming out of hospitals has shown that the COVID-19 virus has two stages to the infection of the body.

In the first phase, the virus inserts its spike protein into the ACE2 receptor, it sets off a chemical process that alters the structure of the receptor and allows the virus to infect. The spikes of the virus enables it to bind to heme groups in red blood cells.

The rate and effectivity at which this occurs can be mitigated by a strengthened immune system using the body’s internal defense mechanisms:

The lungs use vitamin C to protect against this attack via the epithelial surface which has a thin layer of fluid packed with high levels of antioxidant molecules. Vitamin C affects the immune system, for example the function of phagocytes, transformation of T lymphocytes and production of interferon. In particular, vitamin C increased the resistance of chick embryo tracheal organ cultures to infection caused by the coronavirus.

There are several mechanisms by which vitamin D activity is critical for immune defence: vitamin D acts to maintain tight junctions, promote the effect of antimicrobial peptides (i.e., cathelicidin and defensins), and moderate the inflammatory response.

Increased Zinc levels inhibit the virus’s spike protein from penetrating the ACE2 receptors.

Given that viruses are intracellular parasites that hijack cellular processes to replicate a virus’s genetic material, it is essential antiviral agents have the ability to enter

cells. An individual viral particle called a virion is able to produce about a million new virions once inside a cell. It would be critical for zinc to enter cells to destroy the virus, which makes the discovery of an ionophore as important as zinc’s primary role in infection control.

How does acute therapy with Hydroxychloroquine work?

The reason Hydroxychloroquine works for COVID-19 is by its ability to bind to DNA and interfere with the virus’s attack on haemoglobin by preventing the binding mechanism on haemoglobin.

By prophylactically introducing Hydroxychloroquine into the body, it interferes with the virus's ability to replicate in two ways. First, the drug enters compartments called endosomes within the cell membrane. Endosomes tend to be slightly acidic, but the chemical structure of the drug boosts their pH, making the compartments more basic. Many viruses, including SARS-CoV, acidify endosomes in order to breach the cell membrane, release their genetic material and begin replication; Hydroxychloroquine blocks this critical step. The drug also prevents SARS-CoV from plugging into a receptor called angiotensin-converting enzyme 2, or ACE2.

Prophylactic dosing with Hydroxychloroquine has been shown to undermine this process, and in turn, viral replication in general when treatment begins in an early enough phase.

Should the virus reach the second phase of infection before treatment, ie at the point of hospitalisation the process of infection accelerates in severity due to the following:

Your red blood cells carry oxygen from your lungs to all your organs and the rest of your body. Red blood cells can do this thanks to hemoglobin, which is a protein consisting of four “hemes”. Hemes have a special kind of iron ion, which is normally quite toxic in its free form, locked away in its center with a porphyrin acting as it’s ‘container’. In this way, the iron ion can be ‘caged’ and carried around safely by the hemoglobin, but used to bind to oxygen when it gets to your lungs.

When the red blood cell gets to the alveoli, or the little sacs in your lungs where all the gas exchange happens, that special little iron ion can flip between FE2+ and FE3+ states with electron exchange and bond to some oxygen, then it goes off on its little merry way to deliver O2 elsewhere.

Here’s where COVID-19 comes in. Its glycoproteins bond to the heme, and in doing so that special and toxic oxidative iron ion is “disassociated” (released). It’s basically let out of the cage and now freely roaming around on its own. This is bad for two reasons:

1) Without the iron ion, hemoglobin can no longer bind to oxygen. Once all the hemoglobin is impaired, the red blood cell is essentially turned into a Freightliner truck cab with no trailer and no ability to store its cargo.. it is useless and just running around with COVID-19 virus attached to its porphyrin. All these useless trucks running around not delivering oxygen is what starts to lead to desaturation, or watching the patient’s spO2 levels drop.

It is incorrect to assume traditional ARDS and in doing so, not offer the correct treatment. Think of it a lot like carbon monoxide poisoning, in which CO is bound to the hemoglobin, making it unable to carry oxygen. In those cases, ventilators aren’t treating the root cause; the patient’s lungs aren’t ‘tiring out’, they’re pumping just fine. The red blood cells just can’t carry O2, end of story.

Only in this case, unlike CO poisoning in which eventually the CO can break off, the affected hemoglobin is permanently stripped of its ability to carry O2 because it has lost its iron ion. The body compensates for this lack of O2 carrying capacity and deliveries by having your kidneys release hormones like erythropoietin, which tell your bone marrow factories to ramp up production on new red blood cells with freshly

made and fully functioning hemoglobin. This is the reason you find elevated haemoglobin and decreased blood oxygen saturation as one of the 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

2) That little iron ion, along with millions of its friends released from other hemes, are now floating through your blood freely. As I mentioned before, this type of iron ion is highly reactive and causes oxidative damage. It turns out that this happens to a limited extent naturally in our bodies and we have cleanup & defense mechanisms to keep the balance. The lungs, in particular, have 3 primary defenses to maintain “iron homeostasis”, 2 of which are in the alveoli, those little sacs in your lungs we talked about earlier. 

The first of the two are little macrophages that roam around and scavenge up any free radicals like this oxidative iron. The second is a lining on the walls) which has a thin layer of fluid packed with high levels of antioxidant molecules. Well, this is usually good enough for naturally occurring rogue iron ions but with COVID-19 running rampant your body is now basically like a progressive state letting out all the prisoners out of the prisons...

it’s just too much iron and it begins to overwhelm your lungs’ countermeasures, and thus begins the process of pulmonary oxidative stress. This leads to bilateral damage and inflammation which is atypical of ARDS, which leads to all that nasty stuff and damage you see in CT scans of COVID-19 patient lungs.

Once your body is now running out of control, with all your oxygen trucks running around without any freight, and tons of this toxic form of iron floating around in your bloodstream, other defences kick in. 

While your lungs are busy with all this oxidative stress they can’t handle, and your organs are being starved of o2 without their constant stream of deliveries from red blood cell’s haemoglobin  and your liver is attempting to do its best to remove the iron and store it in its ‘iron vault’.

Only it's getting overwhelmed too. It’s starved for oxygen and fighting a losing battle from all your hemoglobin letting its iron free, and starts crying out “help, I’m taking damage!” by releasing an enzyme called alanine aminotransferase (ALT). BOOM, there is your second of 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

COVID-19 causes prolonged and progressive hypoxia (starving your body of oxygen) by binding to the heme groups in hemoglobin in your red blood cells. People are simply desaturating (losing O2 in their blood), and that’s what eventually leads to organ failures that kill them, not any form of ARDS or pneumonia.

All the damage to the lungs you see in CT scans are from the release of oxidative iron from the hemes, this overwhelms the natural defenses against pulmonary oxidative stress and causes that nice, always-bilateral ground glass opacity in the lungs.

Eventually, if the patient’s immune system doesn’t fight off the virus in time before their blood oxygen saturation drops too low, ventilator or no ventilator, organs start shutting down. No fuel, no work. 

The only way to even try to keep them going is max oxygen, even a hyperbaric chamber if one is available on 100% oxygen at multiple atmospheres of pressure, just to give what’s left of their functioning haemoglobin a chance to carry enough O2 to the organs and keep them alive.

Yeah we don’t have nearly enough of those chambers, so some fresh red blood cells with normal haemoglobin in the form of a transfusion will have to do.

The core point being, treating patients with the iron ions stripped from their hemoglobin (rendering it abnormally nonfunctional) with ventilator intubation is futile, unless you’re just hoping the patient’s immune system will work its magic in time. The root of the illness needs to be addressed.

Ideally, this form of treatment needs to happen to:

Patients treated with multiple drug regimen:

Prophylaxis:

1- Hydroxychloroquine 400mg once a week

2- Zinc sulfate 40mg once a day

3- Supplement with Vitamin C & D at daily recommended nutritional dosages

Therapeutic:

1- Hydroxychloroquine 400mg twice on day 1, 200mg twice a day for 4 days following 

2- Azithromycin 500mg day 1, 250mg once a day for 4 days

3- Zinc sulfate 220mg once a day for five days

4- Supplemented with Vitamin C & D daily at high volumes (intravenous or orally)

5- Oxygenation to raise spO2 when dangerous levels of desaturation are reached

MacKenzie&Greeff