Other research suggests the SARS-CoV-2 spike protein can have a serious impact on your mitochondrial function, which is imperative for good health, innate immunity and disease prevention of all kinds.
When the spike protein interacts with the ACE2 receptor, it can disrupt mitochondrial signaling, thereby inducing the production of reactive oxygen species and oxidative stress. If the damage is serious enough, uncontrolled cell death can occur, which in turn leaks mitochondrial DNA (mtDNA) into your bloodstream.13
Aside from being detected in cases involving acute tissue injury, heart attack and sepsis, freely circulating mtDNA has also been shown to contribute to a number of chronic diseases, including systemic inflammatory response syndrome or SIRS, heart disease, liver failure, HIV infection, rheumatoid arthritis and certain cancers.14 As explained in “COVID-19: A Mitochondrial Perspective”:15
“Apart from its role in energy production, mitochondria are crucial for … innate immunity, reactive oxygen species (ROS) generation, and apoptosis; all of these are important in COVID-19 pathogenesis. Dysfunctional mitochondria predispose to oxidative stress and loss of cellular function and vitality. In addition, mitochondrial damage leads to … inappropriate and persistent inflammation.
SARS coronavirus 2 (SARS-CoV-2) … enters cell by attaching to angiotensin converting enzyme 2 (ACE2) receptors on cell surface … Following infection, there is internalization and downregulation of ACE2 receptors.
At vascular endothelium, ACE2 performs conversion of angiotensin II to angiotensin (1–7). Thus, a low ACE2 activity subsequent to SARS-CoV-2 infection leads to imbalance in renin-angiotensin system with relative excess of angiotensin II.
Angiotensin II through binding to its type 1 receptors exerts pro-inflammatory, vasoconstrictive, and prothrombotic effects, while angiotensin (1–7) has opposing effects … In addition, angiotensin II increases cytoplasmic and mitochondrial ROS generation leading to oxidative stress.
Increased oxidative stress may lead to endothelial dysfunction and aggravate systemic and local inflammation, thus contributing to acute lung injury, cytokine storm, and thrombosis seen in severe COVID-19 illness …
A recent algorithm showed that majority of SARS-CoV-2 genomic and structural RNAs are targeted for mitochondrial matrix. Thus it appears that SARS-CoV-2 hijacks mitochondrial machinery for its own benefit, including DMV biogenesis. Manipulation of mitochondria by virus may lead to mitochondrial dysfunction and increased oxidative stress ultimately leading to loss of mitochondrial integrity and cell death …
Mitochondrial fission enables removal of the damaged portion of a mitochondrion to be cleared by mitophagy (a special form of autophagy). Metabolomic studies suggest that SARS-CoV-2 inhibits mitophagy. Thus, there is accumulation of damaged and dysfunctional mitochondria. This not only leads to impaired MAVS [mitochondrial antiviral signaling] response but also aggravates inflammation and cell death.”
The author, Pankaj Prasun, points out that the virus’ impact on mitochondria helps explain why COVID-19 is so much deadlier for older people, the obese, and those with diabetes, high blood pressure and heart disease.
All of these risk factors have something in common: They’re all associated with mitochondrial dysfunction. If your mitochondria are already dysfunctional, the SARS-CoV-2 virus can more easily knock out more mitochondria, resulting in severe illness and death.
The Spike Protein Is a Bioweapon
In my interview with Seneff and Mikovits (see earlier hyperlink), they both stressed that the key danger — both in COVID-19 and with the vaccines — is the spike protein itself. However, while the spike protein found in the virus is bad, the spike protein your body produces in response to the vaccine is far worse. Why?
When the spike protein interacts with the ACE2 receptor, it can disrupt mitochondrial signaling, thereby inducing the production of reactive oxygen species and oxidative stress. If the damage is serious enough, uncontrolled cell death can occur, which in turn leaks mitochondrial DNA (mtDNA) into your bloodstream.13
Aside from being detected in cases involving acute tissue injury, heart attack and sepsis, freely circulating mtDNA has also been shown to contribute to a number of chronic diseases, including systemic inflammatory response syndrome or SIRS, heart disease, liver failure, HIV infection, rheumatoid arthritis and certain cancers.14 As explained in “COVID-19: A Mitochondrial Perspective”:15
“Apart from its role in energy production, mitochondria are crucial for … innate immunity, reactive oxygen species (ROS) generation, and apoptosis; all of these are important in COVID-19 pathogenesis. Dysfunctional mitochondria predispose to oxidative stress and loss of cellular function and vitality. In addition, mitochondrial damage leads to … inappropriate and persistent inflammation.
SARS coronavirus 2 (SARS-CoV-2) … enters cell by attaching to angiotensin converting enzyme 2 (ACE2) receptors on cell surface … Following infection, there is internalization and downregulation of ACE2 receptors.
At vascular endothelium, ACE2 performs conversion of angiotensin II to angiotensin (1–7). Thus, a low ACE2 activity subsequent to SARS-CoV-2 infection leads to imbalance in renin-angiotensin system with relative excess of angiotensin II.
Angiotensin II through binding to its type 1 receptors exerts pro-inflammatory, vasoconstrictive, and prothrombotic effects, while angiotensin (1–7) has opposing effects … In addition, angiotensin II increases cytoplasmic and mitochondrial ROS generation leading to oxidative stress.
Increased oxidative stress may lead to endothelial dysfunction and aggravate systemic and local inflammation, thus contributing to acute lung injury, cytokine storm, and thrombosis seen in severe COVID-19 illness …
A recent algorithm showed that majority of SARS-CoV-2 genomic and structural RNAs are targeted for mitochondrial matrix. Thus it appears that SARS-CoV-2 hijacks mitochondrial machinery for its own benefit, including DMV biogenesis. Manipulation of mitochondria by virus may lead to mitochondrial dysfunction and increased oxidative stress ultimately leading to loss of mitochondrial integrity and cell death …
Mitochondrial fission enables removal of the damaged portion of a mitochondrion to be cleared by mitophagy (a special form of autophagy). Metabolomic studies suggest that SARS-CoV-2 inhibits mitophagy. Thus, there is accumulation of damaged and dysfunctional mitochondria. This not only leads to impaired MAVS [mitochondrial antiviral signaling] response but also aggravates inflammation and cell death.”
The author, Pankaj Prasun, points out that the virus’ impact on mitochondria helps explain why COVID-19 is so much deadlier for older people, the obese, and those with diabetes, high blood pressure and heart disease.
All of these risk factors have something in common: They’re all associated with mitochondrial dysfunction. If your mitochondria are already dysfunctional, the SARS-CoV-2 virus can more easily knock out more mitochondria, resulting in severe illness and death.
The Spike Protein Is a Bioweapon
In my interview with Seneff and Mikovits (see earlier hyperlink), they both stressed that the key danger — both in COVID-19 and with the vaccines — is the spike protein itself. However, while the spike protein found in the virus is bad, the spike protein your body produces in response to the vaccine is far worse. Why?
Because the synthetic mRNA in the vaccine has been programmed to instruct your cells to produce an unnatural, genetically engineered spike protein. Specific alterations make it far more toxic than that found on the virus itself. Mikovits goes so far as to call the spike protein a bioweapon, as it is a disease-causing agent that demolishes innate immunity and exhausts your natural killer (NK) cells’ ability to determine which cells are infected and which aren’t.
In short, when you get the COVID-19 vaccine, you are being injected with an agent that instructs your body to produce the bioweapon in its own cells. This is about as diabolical as it gets.
In her paper, “Worse Than The Disease: Reviewing Some Possible Unintended Consequences of mRNA Vaccines Against COVID-19,” published in the International Journal of Vaccine Theory, Practice and Research in collaboration with Dr. Greg Nigh,16 Seneff explains why the unnatural spike protein is so problematic.
In summary, normally, the spike protein on a virus will collapse on itself and fall into the cell once it attaches to the ACE2 receptor. The vaccine-induced spike protein does not do this. Instead it stays open and remains attached to the ACE2 receptor, thereby disabling it and causing a host of problems that lead to heart, lung and immune impairment.
What’s more, because the RNA code has been enriched with extra guanines (Gs) and cytosines (Cs), and configured as if it’s a human messenger RNA molecule ready to make protein by adding a polyA tail, the spike protein’s RNA sequence in the vaccine looks as if it is part bacteria,17 part human18 and part viral at the same time.
There’s also evidence suggesting the SARS-CoV-2 spike protein may be a prion, which is yet another piece of really bad news, particularly as it pertains to vaccine-induced spike protein. Prions are membrane proteins and when they misfold, they form crystals in the cytoplasm resulting in prion disease.
Since the mRNA in the vaccines has been modified to spew out very high amounts of spike protein (far greater than that of the actual virus), the risk of excessive buildup in the cytoplasm is high. And, since the spike protein doesn’t enter into the membrane of the cell, there’s a high risk that it can become problematic if indeed it works like a prion.
Remember, the aforementioned research cited by Bridle found the spike protein accumulates in the spleen, among other places. Parkinson’s disease is a prion disease that has been traced back to prions originating in the spleen, that then travel up to the brain via the vagus nerve. In the same way, it’s quite possible COVID-19 vaccines may promote Parkinson’s and other human prion diseases such as Alzheimer’s.
In short, when you get the COVID-19 vaccine, you are being injected with an agent that instructs your body to produce the bioweapon in its own cells. This is about as diabolical as it gets.
In her paper, “Worse Than The Disease: Reviewing Some Possible Unintended Consequences of mRNA Vaccines Against COVID-19,” published in the International Journal of Vaccine Theory, Practice and Research in collaboration with Dr. Greg Nigh,16 Seneff explains why the unnatural spike protein is so problematic.
In summary, normally, the spike protein on a virus will collapse on itself and fall into the cell once it attaches to the ACE2 receptor. The vaccine-induced spike protein does not do this. Instead it stays open and remains attached to the ACE2 receptor, thereby disabling it and causing a host of problems that lead to heart, lung and immune impairment.
What’s more, because the RNA code has been enriched with extra guanines (Gs) and cytosines (Cs), and configured as if it’s a human messenger RNA molecule ready to make protein by adding a polyA tail, the spike protein’s RNA sequence in the vaccine looks as if it is part bacteria,17 part human18 and part viral at the same time.
There’s also evidence suggesting the SARS-CoV-2 spike protein may be a prion, which is yet another piece of really bad news, particularly as it pertains to vaccine-induced spike protein. Prions are membrane proteins and when they misfold, they form crystals in the cytoplasm resulting in prion disease.
Since the mRNA in the vaccines has been modified to spew out very high amounts of spike protein (far greater than that of the actual virus), the risk of excessive buildup in the cytoplasm is high. And, since the spike protein doesn’t enter into the membrane of the cell, there’s a high risk that it can become problematic if indeed it works like a prion.
Remember, the aforementioned research cited by Bridle found the spike protein accumulates in the spleen, among other places. Parkinson’s disease is a prion disease that has been traced back to prions originating in the spleen, that then travel up to the brain via the vagus nerve. In the same way, it’s quite possible COVID-19 vaccines may promote Parkinson’s and other human prion diseases such as Alzheimer’s.
Wodarg_Yeadon_EMA_Petition_Pfizer_Trial_FINAL_01DEC2020_signed_with.pdf
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Wodarg_Yeadon_EMA_Petition_Pfizer_Trial_FINAL_01DEC2020_signed_with_Exhibits_geschwarzt.pdf