COVID-19 Is a Vascular Disease: Coronavirus’ Spike Protein Attacks Vascular System on a Cellular Level

md_a

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COVID-19 Is a Vascular Disease: Coronavirus’ Spike Protein Attacks Vascular System on a Cellular Level​

TOPICS:Cell BiologyCOVID-19Infectious DiseasesMolecular BiologyPopularSalk Institute
By SALK INSTITUTE MAY 2, 2021

SARS-CoV-2 Spike Protein Vascular Endothelial Cells
Representative images of vascular endothelial control cells (left) and cells treated with the SARS-CoV-2 Spike protein (right) show that the spike protein causes increased mitochondrial fragmentation in vascular cells. Credit: Salk Institute
Salk researchers and collaborators show how the protein damages cells, confirming COVID-19 as a primarily vascular disease.
Scientists have known for a while that SARS-CoV-2’s distinctive “spike” proteins help the virus infect its host by latching on to healthy cells. Now, a major new study shows that they also play a key role in the disease itself.

The paper, published on April 30, 2021, in Circulation Research, also shows conclusively that COVID-19 is a vascular disease, demonstrating exactly how the SARS-CoV-2 virus damages and attacks the vascular system on a cellular level. The findings help explain COVID-19’s wide variety of seemingly unconnected complications, and could open the door for new research into more effective therapies.

“A lot of people think of it as a respiratory disease, but it’s really a vascular disease,” says Assistant Research Professor Uri Manor, who is co-senior author of the study. “That could explain why some people have strokes, and why some people have issues in other parts of the body. The commonality between them is that they all have vascular underpinnings.”
Salk researchers collaborated with scientists at the University of California San Diego on the paper, including co-first author Jiao Zhang and co-senior author John Shyy, among others.
While the findings themselves aren’t entirely a surprise, the paper provides clear confirmation and a detailed explanation of the mechanism through which the protein damages vascular cells for the first time. There’s been a growing consensus that SARS-CoV-2 affects the vascular system, but exactly how it did so was not understood. Similarly, scientists studying other coronaviruses have long suspected that the spike protein contributed to damaging vascular endothelial cells, but this is the first time the process has been documented.

In the new study, the researchers created a “pseudovirus” that was surrounded by SARS-CoV-2 classic crown of spike proteins, but did not contain any actual virus. 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.

The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.
Previous studies have shown a similar effect when cells were exposed to the SARS-CoV-2 virus, but this is the first study to show that the damage occurs when cells are exposed to the spike protein on its own.

“If you remove the replicating capabilities of the virus, it still has a major damaging effect on the vascular cells, simply by virtue of its ability to bind to this ACE2 receptor, the S protein receptor, now famous thanks to COVID,” Manor explains. “Further studies with mutant spike proteins will also provide new insight towards the infectivity and severity of mutant SARS CoV-2 viruses.”
The researchers next hope to take a closer look at the mechanism by which the disrupted ACE2 protein damages mitochondria and causes them to change shape.

Reference: “SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2” by Yuyang Lei, Jiao Zhang, Cara R. Schiavon, Ming He, Lili Chen, Hui Shen, Yichi Zhang, Qian Yin, Yoshitake Cho, Leonardo Andrade, Gerald S. Shadel, Mark Hepokoski, Ting Lei, Hongliang Wang, Jin Zhang, Jason X.-J. Yuan, Atul Malhotra, Uri Manor, Shengpeng Wang, Zu-Yi Yuan and John Y-J. Shyy, 31 March 2021, Circulation Research.
DOI: 10.1161/CIRCRESAHA.121.318902

Other authors on the study are Yuyang Lei and Zu-Yi Yuan of Jiaotong University in Xi’an, China; Cara R. Schiavon, Leonardo Andrade, and Gerald S. Shadel of Salk; Ming He, Hui Shen, Yichi Zhang, Yoshitake Cho, Mark Hepokoski, Jason X.-J. Yuan, Atul Malhotra, Jin Zhang of the University of California San Diego; Lili Chen, Qian Yin, Ting Lei, Hongliang Wang and Shengpeng Wang of Xi’an Jiatong University Health Science Center in Xi’an, China.
The research was supported by the National Institutes of Health, the National Natural Science Foundation of China, the Shaanxi Natural Science Fund, the National Key Research and Development Program, the First Affiliated Hospital of Xi’an Jiaotong University; and Xi’an Jiaotong University.

 
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md_a

md_a

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Focus on the induction of antibodies by vaccines to define immunity has led to a dangerous disregard for the basic facts of health. The present testing of a vaccine containing the RNA that specifies the most destructive spike protein of the corona virus, the part that inactivates our protective ACE2 enzyme, is being done in a culture that avoids consideration of the meaning of our massive endogenous system of RNA-responsive reverse transcriptases and retroelements. The consequences of incorporating the spike protein of the virus into our genetic repertoire are hard to imagine. The mindless activation of our huge epigenetic system of retroelements, with no knowable benefits, should be stopped. – Ray Peat

The spike protein causes inflammation by inactivating the enzyme (ACE2) that inactivates angiotensin, so the spike protein essentially turns on our inflammatory system, the angiotensin system, and the RNA allows our own cells to manufacture spike protein, so we are being prepared to manufacture the activator of our own inflammatory system which is basically the only thing that causes people to die from Covid, if they die from it, mostly none of that diagnosis or determination of the cause of death, none of that has been done in a traditional scientific manner but to the extent that virus is harmful to week people, then is causing our body to produce the agent that kills people, and they ignore the fact that we have reverse transcriptase that can turn RNA to DNA and integrated it into our genes so that we can pass on the ability to destroy our defenses against inflammation. - Ray Peat

For years, corona viruses have been known to bind to the angiotensin converting enzyme 2 (ACE2), and that enzyme has been known to have protective effects, destroying angiotensin, and losartan, an angiotensin receptor blocker, has been known to be protective against corona viruses. Angiotensin increases intracellular calcium, and losartan lowers intracellular calcium. In reaction to the new corona virus, a few groups responded quickly, treating successfully with antiinflammatory things—losartan, cinanserin (a serotonin antagonist), aspirin, and azithromycin or erythromycin, which lower intracellular calcium. Aspirin’s effects overlap those of losartan, and it downregulates the angiotensin receptor, ATR1 (Mitra, et al., 2012). - Ray Peat

The problem is that our bodies can copy foreign RNA and DNA and incorporate the copies into our chromosomes. If they are genes for viral proteins, it’s possible that during a future stress, those foreign genes could be expressed throughout our body, creating overwhelming amounts of those toxic proteins. The copies could be inserted into sperm cells and eggs as well as body cells, forming part of future generations. No sane person would consider doing it, if they understood how our cells respond to alien nucleic acids.- Ray Peat
 

Nemo

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Good discussion of this study by Haidut starting at 13:13:


View: https://www.youtube.com/watch?v=8nLw0X2Ee_M


Like Ray, he points out it's also a serotonergic disease.

Thanks for posting with the great Ray quotes, md_a.

I keep thinking about what a military contractor friend told me about the Pfizer vax being developed at Ft. Detrick alongside the bioweapon. Frank Olson was a biological warfare scientist at Ft. Detrick before the ClA dropped him out of a 13th-story window.

They had him killed because they feared he would spill the beans about the CIA's ARTICHOKE interrogation program and the use of biological weapons by the United States in the Korean War.

I don't believe this crowd wouldn't know the effects of this "vax."
 
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AlaskaJono

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Yeah, where all y'all at?

I read this article via https://www.salk.edu/news-release/the-novel-coronavirus-spike-protein-plays-additional-key-role-in-illness/
in July, and finally decided to post something. I searched and already it was posted. Thanks.

But more to the point, if the spike protein in the "sars cov 2" is so dangerous, then why give it in the billions in a "vaccine"? And why the genetic aspect to turn your body into a Spike protein factory via the mrna or dna aspects? So, WTF? Seems like a no brainer "stupidest idea ever" blue ribbon winner! I sent this to a friend who is a nurse and he rightly wrote back,"I wondered what was meant by this the bit in parentheses in this sentence:

Now, a major new study shows that the virus spike proteins (which behave very differently than those safely encoded by vaccines) also play a key role in the disease itself.

This sentence is not in the original post above by md_a, but it is in my webpage which is even dated April 30. ? Same folks, Salk.edu.... hmmmm.

So why would the spike proteins be more "safe" in the clot shots vs the "wild virus" as stated above? Please explain. This is really a 'not good" situation. Maybe I missed something.

Over and out.
 

Tbone107

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Good discussion of this study by Haidut starting at 13:13:


View: https://www.youtube.com/watch?v=8nLw0X2Ee_M


Like Ray, he points out it's also a serotonergic disease.

Thanks for posting with the great Ray quotes, md_a.

I keep thinking about what a military contractor friend told me about the Pfizer vax being developed at Ft. Detrick alongside the bioweapon. Frank Olson was a biological warfare scientist at Ft. Detrick before the ClA dropped him out of a 13th-story window.

They had him killed because they feared he would spill the beans about the CIA's ARTICHOKE interrogation program and the use of biological weapons by the United States in the Korean War.

I don't believe this crowd wouldn't know the effects of this "vax."

Woah. Anymore you can elaborate on this??
 

yerrag

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Manila

COVID-19 Is a Vascular Disease: Coronavirus’ Spike Protein Attacks Vascular System on a Cellular Level​

TOPICS:Cell BiologyCOVID-19Infectious DiseasesMolecular BiologyPopularSalk Institute
By SALK INSTITUTE MAY 2, 2021

SARS-CoV-2 Spike Protein Vascular Endothelial Cells
Representative images of vascular endothelial control cells (left) and cells treated with the SARS-CoV-2 Spike protein (right) show that the spike protein causes increased mitochondrial fragmentation in vascular cells. Credit: Salk Institute
Salk researchers and collaborators show how the protein damages cells, confirming COVID-19 as a primarily vascular disease.
Scientists have known for a while that SARS-CoV-2’s distinctive “spike” proteins help the virus infect its host by latching on to healthy cells. Now, a major new study shows that they also play a key role in the disease itself.

The paper, published on April 30, 2021, in Circulation Research, also shows conclusively that COVID-19 is a vascular disease, demonstrating exactly how the SARS-CoV-2 virus damages and attacks the vascular system on a cellular level. The findings help explain COVID-19’s wide variety of seemingly unconnected complications, and could open the door for new research into more effective therapies.

“A lot of people think of it as a respiratory disease, but it’s really a vascular disease,” says Assistant Research Professor Uri Manor, who is co-senior author of the study. “That could explain why some people have strokes, and why some people have issues in other parts of the body. The commonality between them is that they all have vascular underpinnings.”
Salk researchers collaborated with scientists at the University of California San Diego on the paper, including co-first author Jiao Zhang and co-senior author John Shyy, among others.
While the findings themselves aren’t entirely a surprise, the paper provides clear confirmation and a detailed explanation of the mechanism through which the protein damages vascular cells for the first time. There’s been a growing consensus that SARS-CoV-2 affects the vascular system, but exactly how it did so was not understood. Similarly, scientists studying other coronaviruses have long suspected that the spike protein contributed to damaging vascular endothelial cells, but this is the first time the process has been documented.

In the new study, the researchers created a “pseudovirus” that was surrounded by SARS-CoV-2 classic crown of spike proteins, but did not contain any actual virus. 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.

The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.
Previous studies have shown a similar effect when cells were exposed to the SARS-CoV-2 virus, but this is the first study to show that the damage occurs when cells are exposed to the spike protein on its own.

“If you remove the replicating capabilities of the virus, it still has a major damaging effect on the vascular cells, simply by virtue of its ability to bind to this ACE2 receptor, the S protein receptor, now famous thanks to COVID,” Manor explains. “Further studies with mutant spike proteins will also provide new insight towards the infectivity and severity of mutant SARS CoV-2 viruses.”
The researchers next hope to take a closer look at the mechanism by which the disrupted ACE2 protein damages mitochondria and causes them to change shape.

Reference: “SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2” by Yuyang Lei, Jiao Zhang, Cara R. Schiavon, Ming He, Lili Chen, Hui Shen, Yichi Zhang, Qian Yin, Yoshitake Cho, Leonardo Andrade, Gerald S. Shadel, Mark Hepokoski, Ting Lei, Hongliang Wang, Jin Zhang, Jason X.-J. Yuan, Atul Malhotra, Uri Manor, Shengpeng Wang, Zu-Yi Yuan and John Y-J. Shyy, 31 March 2021, Circulation Research.
DOI: 10.1161/CIRCRESAHA.121.318902

Other authors on the study are Yuyang Lei and Zu-Yi Yuan of Jiaotong University in Xi’an, China; Cara R. Schiavon, Leonardo Andrade, and Gerald S. Shadel of Salk; Ming He, Hui Shen, Yichi Zhang, Yoshitake Cho, Mark Hepokoski, Jason X.-J. Yuan, Atul Malhotra, Jin Zhang of the University of California San Diego; Lili Chen, Qian Yin, Ting Lei, Hongliang Wang and Shengpeng Wang of Xi’an Jiatong University Health Science Center in Xi’an, China.
The research was supported by the National Institutes of Health, the National Natural Science Foundation of China, the Shaanxi Natural Science Fund, the National Key Research and Development Program, the First Affiliated Hospital of Xi’an Jiaotong University; and Xi’an Jiaotong University.

Thanks.

I've been suspecting that virus/pathogen doesn't only affect the respiratory system and this strengthens my suspicion.

A friend died last year 2 weeks after a trip to Japan. This was just before the crisis came into full gear, February of last year. He started with gut discomfort, and after a week he checked into the hospital. It got worse as it affected both the liver and his nervous system. Before he died, he was in the ICU and he was shaking uncontrollably. But cause of death was unknown, as that was before the COVID saga began.

But why is it expressed predominantly in the respiratory system? Is it because it is the chokepoint, as this is where oxygen is obtained, and also the rapid response system for acid-base balance?

Or is it simply because symptoms are more easily observed when it is respiratory in nature?

My friend had a case of hepatitis before, so he probably also had liver issues that disposed him to being affected by the pathogen. Probably the liver would have easily detoxed the spike proteins if it were healthy. But instead the spike proteins destroyed the capillaries feeding the liver as the liver got backed up with toxins. How it affected his nervous system is anybody's guess, but I suspect drugs such as Cipro could have been used, which would destroy neurons and in his state this would have an outsize side effect on his nervous system.

I've been using a system of checking my breath rate and my urine and saliva pH to give me an indication of my internal balance. If the internal balance is out of whack, I could see it with this system. It is something I developed from ideas from the Biomedx website, but I've not validated this as I'm the only sample.

I was thinking of getting an informal study made in this forum to validate it, but I don't get to do it because I feel I would not get a good sample size given that people are generally not interested given the lack of responses to polls. The only poll that generated huge interest was political, and it was about whether Trump would win in 2016.
 
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