In recent scientific articles, it has been discovered how the spike protein not only is a respiratory disease but also damages blood vessels cells directly, and is connected with higher risk of trombosis. So, does the Spike Protein produced by the covid-19 vaccine also bring the same risks and damage?

How many spike proteins the immune systems produces after being instructed by the vaccine, and how do they behave afterwards ?

Thank you

EDIT: adding some references -1) https://www.salk.edu/news-release/the-novel-coronavirus-spike-protein-plays-additional-key-role-in-illness/ -2) https://scitechdaily.com/covid-19-is-a-vascular-disease-coronavirus-spike-protein-attacks-vascular-system-on-a-cellular-level/ -3) here it says how the "creation" of the spike protein happens-> Can spike protein induced cell fusion be triggered by the mRNA vaccine?

EDIT2: Someone in the comments pointed out how articles 1 and 2 reference the same paper, and one paper doesn't constitute discovery. But how the spike protein which are "created" after the vaccine, behave? Are they the same as the one from Covid-19? Are they harmful? if not, why ?

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    $\begingroup$ Both of those news releases reference the same paper. One paper does not a discovery make. Do you have any references to any other published papers showing the same thing? $\endgroup$
    – MattDMo
    May 13 at 13:21
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    $\begingroup$ Where did you read that spike proteins are "created" by the vaccine? Vaccines induce the production of antibodies that bind to viral structures, not the structures perse $\endgroup$
    – MikeKatz45
    May 13 at 13:54
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    $\begingroup$ here: biology.stackexchange.com/questions/98449/… "they only lead to the production of the spike protein in the cell." $\endgroup$
    – Cris
    May 13 at 14:26
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    $\begingroup$ @MikeKatz45 your comment is true of most vaccines but several of the new covid vaccines cause the body to produce antigens, to which the immune system then creates antibodies. $\endgroup$
    – timeskull
    May 13 at 14:56
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    $\begingroup$ Ah very well I see now, so we are not sure if the spike has the trombogenic effect even if its modified to not fuse as the linked question says $\endgroup$
    – MikeKatz45
    May 13 at 15:11

The spike proteins expressed by cells that take up mRNA or ChAdOx vaccines are modified so they cannot induce membrane fusion. However, the research article you refer to indicates that circulating spike protein damages endothelial cells simply by binding ACE2, which suggests vaccine derived spike protein could still cause this kind of damage if it enters the bloodstream somehow:

we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.

Spike protein is necessarily attached to a membrane, so for it to damage cells by binding ACE2, bits of membrane containing the spike would need to be exported from the cells. The SARS-CoV-2 genes that allow it to do this in a real infection are not present in the vaccines, of course. The only other route I know of by which S protein could theoretically enter the blood is in exosomes. This article analyzed circulating exosomes from COVID patients and did not detect any viral proteins:

We did not identify viral proteins via the purification of exosomes; thus, we can conclude that viral particles were not purified together with exosomes

Research creating hybrid S-protein that can make spike-coated exosomes indicates the natural spike protein does not get into exosomes:

the S protein could not be detected in the sample from pSwt-transfected cells. In contrast, the SGTM protein could be detected in the pelleted supernatant of pSGTM-transfected cells.

I was not able to find any studies looking for spike protein in exosomes of vaccinated people, but it should be less likely than for the actual virus.

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    $\begingroup$ Thank you, so the vaccine derived spike protein also does damage after inoculating the vaccine? "how many" spike proteins are going to be present in the bloodstream after injection compared to a real infection? What do you mean "if it enters the bloodstream somehow" (since the vaccine is actually injected into the bloodstream) ? could you explain in more detail this part ? $\endgroup$
    – Cris
    May 13 at 16:50
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    $\begingroup$ @Cris, "it" in "if it enters the bloodstream somehow" refers to the subject in the clause, which is "vaccine derived spike protein" and not "vaccine". $\endgroup$
    – mgkrebbs
    May 13 at 17:02
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    $\begingroup$ as mgkrebbs says, when the vaccine is injected into the bloodstream it is mRNA, which cannot bind to ACE2. The vaccine enters a cell and causes the cell to produce spike protein. The spike protein can bind ACE2, in theory, but it is stuck to the cell and cannot reach. There does not appear to be any way for the spike protein from a vaccine to reach ACE2, so it should not be able to cause damage in the way described by your article. $\endgroup$
    – timeskull
    May 13 at 18:33
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    $\begingroup$ I don't really know. You should probably ask another question for that. Here is a question related to yours, reading it will give you some background information: biology.stackexchange.com/questions/96886/… $\endgroup$
    – timeskull
    May 14 at 14:54
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    $\begingroup$ That's a good question. My impression is the immune system would kill the cells displaying spike through phagocytosis, so the membranes would be recycled and the proteins digested. But I don't know enough about immunology to say for sure. $\endgroup$
    – timeskull
    May 20 at 14:45

Funny how only the Chinese financially sponsored this research you're talking about, despite the fact that the paper has some American co-authors. Anyway, it's the dose that makes the poison. This research may been published in good faith, but its findings have been used by anti-vaxxers out of context.

Downregulation of some ACE2 receptors, which is what the paper claims (in its title), isn't that big of a deal unless it happens at large scale. The study itself says that

vaccination-generated antibody and/or exogenous antibody against S protein not only protects the host from SARS-CoV-2 infectivity but also inhibits S protein-imposed endothelial injury.

In other words, they concede the condition is probably self-limiting in the immunocompetent.

Following [Moderna] mRNA vaccination (which has the highest dose of mRNA among the approved mRNA vaccines), levels of spike protein in the blood have generally too low to detect except by "ultrasensitive single-molecule array (Simoa) assays" and more importantly (with rare exceptions) anti-bodies cleared the spikes from blood in a few days, following the 1st dose, and from everyone in the test group a couple of days after the 2nd dose.

S1 antigen was detected as early as day 1 postvaccination, and peak levels were detected on average 5 days after the first injection.

enter image description here

The mean spike peak level was 62 pg/mL ± 13 pg/mL. After the second vaccine dose, no S1 or spike was detectable, and both antigens remained undetectable through day 56. For one individual (participant 8), spike was detected at day 29, 1 day after the second injection and was undetectable 2 days later.

Alas the latter paper lacks a comparison basis with what's detected following actual infections with SARS-CoV-2. Anyway, in correspondence to the press the lead author of this latter study concluded that

“We found that within a few days of the antigen appearing, the individuals developed antibodies that removed the antigen from the bloodstream,” he added. “Our conclusion was that the vaccine is working as intended.”

In other words, it's not a real clinical concern in most people. I'm not like totally dissing these findings, as they might be related to the myocarditis side effect of mRNA vaccines, but the fact that the latter most often happened after the 2nd dose suggests it's not the spike directly that's involved in that one.

By the way, "damages some [heart] cells" is true of bare mRNA (vaccine) released into the bloodstream as well, in animal models and in sufficient dose, at least in terms of detected inflammatory response. (For what's that worth, a co-author of this latter study is "the inventor [of] an intranasal influenza vectored SARS-CoV-2", i.e. no injection needed.)


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