If Colleges Are Going to Require COVID-19 Vaccines, They'd Better Be Liable for Side Effects

Technically this pathway is referred to by FDA as “priority review”: https://www.fda.gov/patients/fast-track-breakthrough-therapy-accelerated-approval-priority-review/priority-review

Pfizer has stated in their quarterly earnings report that they’re filing in May: https://www.cnbc.com/2021/05/04/pfizer-pfe-earnings-q1-2021.html

I just received a email from wellbeing.com to get the death sentence vaccine.

I ain’t getting it.

Moderna is already moving to essentially end their last trial early, so I expect the Biden admin will give full authorization before the fall and somehow it will be interpreted that colleges and businesses can do that without liability after that.

She will likely be both uninsurable and unemployable.

It seems that the recombinant RNA and DNA gene therapy approaches may have a few hurdles. You might have missed these facts in your quest for truth, In September 2020, another paper was published SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19, that outlined a problem with SARS-CoV-2:

Our findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients.

Specifically, they noted:

SARS-CoV-2 and its Spike protein directly stimulated platelets to facilitate the release of coagulation factors, the secretion of inflammatory factors, and the formation of leukocyte–platelet aggregates.

= = = = = = =

Of more concern was the fantastic work of Margo et al, available as early as October 2020, in a paper entitled Severe COVID-19: A multifaceted viral vasculopathy syndrome.

They demonstrated brilliantly that in small blood vessels the spike protein, all by itself, can induce clotting by docking in various tissues.

[V]iral spike protein without viral RNA localized to ACE2+ endothelial cells in microvessels that were most abundant in the subcutaneous fat and brain.

{the original article has some nice USA Today type graphics here}

= = = = =

Another paper by Nuovo et al, entitled Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein, which also featured Dr Magro, was available online from 24 December 2020.

It concluded that:

ACE2+ endothelial damage is a central part of SARS-CoV2 pathology and may be induced by the spike protein alone ... including neurological damage in test animals.

= = = = = = = =

{One of my old favorites:}

The journey doesn’t end there. SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: Implications for microclot formation in COVID-19:

Here we suggest that, in part, the presence of spike protein in circulation may contribute to the hypercoagulation in COVID-19 positive patients and may cause substantial impairment of fibrinolysis. Such lytic impairment may result in the persistent large microclots we have noted here and previously in plasma samples of COVID-19 patients. This observation may have important clinical relevance in the treatment of hypercoagulability in COVID-19 patients.

= = = = = = =

Another one: The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood-brain barrier:

[in vitro] [e]vidence provided suggests that the SARS-CoV-2 spike proteins trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function. Together, these results are the first to show the direct impact that the SARS-CoV-2 spike protein could have on brain endothelial cells; thereby offering a plausible explanation for the neurological consequences seen in COVID-19 patients.

Not only can the spike protein cause clots all by itself, that may well be resistant to being broken up, it also looks like it also may alter the blood-brain barrier, causing neurological damage.

As if mocking the intelligence of those that still believe in science this, just published — SARS-CoV-2 spike protein alone may cause lung damage:

“These findings show that the genetically modified mouse together with just a segment of the spike protein can be used to study SARS-CoV-2 lung injury,” said Solopov. “We can use this tool to develop a better understanding of how the spike protein causes lung symptoms—even without the intact virus—in order to develop new targets and therapeutics for COVID-19, 2APtR

Not mine, and I don’t know who to credit:

In September 2020, another paper was published SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19, that outlined a problem with SARS-CoV-2:

Our findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients.

Specifically, they noted:

SARS-CoV-2 and its Spike protein directly stimulated platelets to facilitate the release of coagulation factors, the secretion of inflammatory factors, and the formation of leukocyte–platelet aggregates.

= = = = = = =

Of more concern was the fantastic work of Margo et al, available as early as October 2020, in a paper entitled Severe COVID-19: A multifaceted viral vasculopathy syndrome.

They demonstrated brilliantly that in small blood vessels the spike protein, all by itself, can induce clotting by docking in various tissues.

[V]iral spike protein without viral RNA localized to ACE2+ endothelial cells in microvessels that were most abundant in the subcutaneous fat and brain.

{the original article has some nice USA Today type graphics here}

= = = = =

Another paper by Nuovo et al, entitled Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein, which also featured Dr Magro, was available online from 24 December 2020.

It concluded that:

ACE2+ endothelial damage is a central part of SARS-CoV2 pathology and may be induced by the spike protein alone ... including neurological damage in test animals.

= = = = = = = =

{One of my old favorites:}

The journey doesn’t end there. SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: Implications for microclot formation in COVID-19:

Here we suggest that, in part, the presence of spike protein in circulation may contribute to the hypercoagulation in COVID-19 positive patients and may cause substantial impairment of fibrinolysis. Such lytic impairment may result in the persistent large microclots we have noted here and previously in plasma samples of COVID-19 patients. This observation may have important clinical relevance in the treatment of hypercoagulability in COVID-19 patients.

= = = = = = =

Another one: The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood-brain barrier:

[in vitro] [e]vidence provided suggests that the SARS-CoV-2 spike proteins trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function. Together, these results are the first to show the direct impact that the SARS-CoV-2 spike protein could have on brain endothelial cells; thereby offering a plausible explanation for the neurological consequences seen in COVID-19 patients.

Not only can the spike protein cause clots all by itself, that may well be resistant to being broken up, it also looks like it also may alter the blood-brain barrier, causing neurological damage.

As if mocking the intelligence of those that still believe in science this, just published — SARS-CoV-2 spike protein alone may cause lung damage:

“These findings show that the genetically modified mouse together with just a segment of the spike protein can be used to study SARS-CoV-2 lung injury,” said Solopov. “We can use this tool to develop a better understanding of how the spike protein causes lung symptoms—even without the intact virus—in order to develop new targets and therapeutics for COVID-19.