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source: https://www.technocracy.news/dr-michael-yeadon-not-one-of-those-things-is-supported-by-the-science/

Author: Michael Yeadon, Ph.D., a life science researcher and former vice-president and chief scientist of allergy and respiratory research at Pfizer

“Viruses are really tiny, and their business is to get as quickly as they can inside your cells. So, they bind to a receptor on the surface and inject themselves into your cell. So, they’re inside. Antibodies are big molecules and they’re generally outside your cells.

So just think about that for a moment. Antibodies and viruses are in separate compartments. The virus is inside the cell, the antibodies outside the cell. I’m not saying antibodies have no role, but they’re really not very important. This has been proven. There are some people in whom a natural experiment has occurred.

They have a defect and they actually don’t make antibodies, but they’re able to fight off COVID-19, the virus SARS-CoV-2, quite well. The way they do that is, they have T-cell immunity, cellular immunity. [T-cells] are cells that are trained to detect virus-infected cells and to kill those cells. That’s how you defend yourself against a virus.

So, all of these mentions of antibody levels, it’s just bunk. It is not a good measure of whether or not you’re immune. It does give evidence that you’ve been infected, but their persistence is not important as to whether you’ve got immunity …

We’ve known this for decades. We’ve known about T-cells for decades. They were clearly in my undergraduate textbooks. And we’ve known about their importance in defending you against respiratory viruses since probably the 1970s, certainly the 1980s. So, don’t believe anything where people suggest to you that their role is uncertain. We’ve known for a very long time that they are absolutely central.”

source: https://www.technocracy.news/dr-michael-yeadon-not-one-of-those-things-is-supported-by-the-science/ Author: Michael Yeadon, Ph.D., a life science researcher and former vice-president and chief scientist of allergy and respiratory research at Pfizer >“Viruses are really tiny, and their business is to get as quickly as they can inside your cells. So, they bind to a receptor on the surface and inject themselves into your cell. So, they’re inside. Antibodies are big molecules and they’re generally outside your cells. > So just think about that for a moment. Antibodies and viruses are in separate compartments. The virus is inside the cell, the antibodies outside the cell. I’m not saying antibodies have no role, but they’re really not very important. This has been proven. There are some people in whom a natural experiment has occurred. > They have a defect and they actually don’t make antibodies, but they’re able to fight off COVID-19, the virus SARS-CoV-2, quite well. The way they do that is, they have T-cell immunity, cellular immunity. [T-cells] are cells that are trained to detect virus-infected cells and to kill those cells. That’s how you defend yourself against a virus. > So, all of these mentions of antibody levels, it’s just bunk. It is not a good measure of whether or not you’re immune. It does give evidence that you’ve been infected, but their persistence is not important as to whether you’ve got immunity … > We’ve known this for decades. We’ve known about T-cells for decades. They were clearly in my undergraduate textbooks. And we’ve known about their importance in defending you against respiratory viruses since probably the 1970s, certainly the 1980s. So, don’t believe anything where people suggest to you that their role is uncertain. We’ve known for a very long time that they are absolutely central.”

(post is archived)

[–] 0 pt

They kinda took a left turn at the conclusion. I'm gonna have to reread that.

The Salk one is exactly what I've been trying to tell people. It's great someone proved it.

Exposure to this pseudovirus resulted in damage to the lungs and arteries of an animal model—proving that the spike protein alone was enough to cause disease. Tissue samples showed inflammation in endothelial cells lining the pulmonary artery walls.

It all pretty much lines up with what I know, other than I don't see how overwhelming ACE2 is beneficial to the host.

The antibody to which they are referring is the CR3022 protein. This attaches to the spike, preventing cell adhesion. Zinc ionophores seemingly also block adhesion.

Once the spike is attached, should it not get an antibody, the T cells take over the fight.

From what I can tell, this is a twofer. Metabolic problems leading to lethargy and weight gain along with higher risk of endocarditis... weakening people. As well as screwing the fertility.

It's like what the US Military was trying to do with Lyme; make an illness that didn't kill, but was a series of co infections that meant to prevent any soldiering.