SARS-CoV-2 Spike Protein May Damage Mitochondrial Function
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.
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