Friday, June 11, 2021

Spike Protein Blues


Remember that study published by scientists from the Salk institute that found that the spike protein alone, in the absence of the rest of the virus, can cause damage to endothelial cells? Here is the citation and the link to the press release for your reference:

SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2
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 hang, Jason X.-J. Yuan, Atul Malhotra, Uri Manor, Shengpeng Wang, Zu-Yi Yuan, John Y-J. Shyy Originally published31 Mar 2021 Research. 2021;128:1323–1326

Now another study finds that the spike protein, detached from the rest of the virus, elicits cell signalling in human cells, which "may promote pulmonary vacular remodeling and PAH [pulmonary arterial hypertension] as well as other cardiovascular complications":

Yuichiro J. Suzuki1,* and Sergiy G. Gychka SARS-CoV-2 Spike Protein Elicits Cell Signaling in Human Host Cells: Implications for Possible Consequences of COVID-19 Vaccines. Vaccines 2021, 9(1), 36;

1Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20007, USA

2Department of Pathological Anatomy N2, Bogomolets National Medical University, 01601 Kiev, Ukraine

Here is an instructive excerpt from this research study:

3. SARS-CoV-2 Spike Protein Elicits Cell Signaling in Human Cells
It was found that the treatment of cultured primary human pulmonary artery smooth muscle cells (SMCs) or human pulmonary artery endothelial cells with the recombinant SARS-CoV-2 spike protein S1 subunit is sufficient to promote cell signaling without the rest of the viral components [21]. Furthermore, our analysis of the postmortem lung tissues of patients who died of COVID-19 has determined that these patients exhibited pulmonary vascular wall thickening, a hallmark of pulmonary arterial hypertension (PAH) [21]. Based on these results, we proposed that the SARS-CoV-2 spike protein (without the rest of the viral components) triggers cell signaling events that may promote pulmonary vascular remodeling and PAH as well as possibly other cardiovascular complications [21,22].

I suspect that the hundreds of instances of myocarditis and pericarditis being investigated now by the FDA are the tip of the iceberg. See the FDA presentation here: 

One study provides an explanation of how this might occur in their description of the circulation of the spike protein:

Circulating SARS-CoV-2 Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients

Alana F. Ogata†1,2,3, Chi-An Cheng†1,2,3, MichaĆ«l Desjardins†3,4,5, Yasmeen Senussi1, Amy C. Sherman3,4, Megan Powell4, Lewis Novack4, Salena Von4, Xiaofang Li6, Lindsey R. Baden*3,4,6, David R. Walt*1,2,3. Downloaded from by guest on 25 May 2021


SARS-CoV-2 proteins were measured in longitudinal plasma samples collected from 13 participants who received two doses of mRNA-1273 vaccine. 11 of 13 participants showed detectable levels of SARS-CoV-2 protein as early as day one after first vaccine injection. Clearance of detectable SARS-CoV-2 protein correlated with production of IgG and IgA.

From paper page 1

Here, we provide evidence that circulating SARS-CoV-2 proteins are present in the plasma of participants vaccinated with the mRNA-1273 vaccine. We report antigen and serological data of the mRNA-1273 vaccine in 13 healthcare workers at the Brigham and Women’s Hospital. Ultrasensitive single-molecule array (Simoa) assays were used for the detection of SARS-CoV-2 antigens spike (S1-S2 unit), S1, and nucleocapsid and antibodies IgG, IgA, and IgM against SARS-CoV-2 spike, S1, receptor binding domain (RBD), and nucleocapsid, as previously described6,7. The ultralow detection limits of the Simoa assays enable detection of antigen and antibody production in the early stages post vaccination and quantification of changes in levels over the course of both vaccine injections.

From paper conclusion

evidence of systemic detection of spike and S1 protein production from the mRNA-1273 vaccine is significant and has not yet been described in any vaccine study, likely due to limitations in assay sensitivity and timing assessment. The clinical relevance of this finding is unknown and should be further explored. These data show that S1 antigen production after the initial vaccination can be detected by day one and is present beyond the site of injection and the associated regional lymph nodes.

I wonder if that explains the leaky capillary syndrome as well.  I strongly suspect that the instances of leaky capillary syndrome are not restricted to the AstraZeneca vaccine. See Reuters coverage of this syndrome now documented by the European Medical Authority here: Pushkala Aripaka Ludwig Burger EU adds another rare blood condition as side effect of AstraZeneca shot.

The risk - reward ratio for young people for receiving the vaccine is looking increasingly problematic and I also harbor a terrifying fear that the vaccination campaign may be based on a profound misunderstanding of the spike protein and the appropriateness of the traditional vaccination logic with a genetically engineered virus whose component pieces are highly pathogenic.

I hope I'm wrong and I know that some of you will say, "Look to the efficacy of the vaccine in preventing symptomatic cases!" 

To that I will respond that I hope this is true (meaning that vaccinated people will be safer in the end) but my concern is that you don't get a disease syndrome anew if you already are harboring it.

I will continue to follow the empirical evidence. I expect we will have a clearer understanding of the risk-reward ratio since all the symptoms caused by the vaccine are also caused by the virus by the end of this winter with the P1 and Delta variants circulating and gaining momentum.


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