ACE(2) of Death: The Spike Protein/ACE2 Immune Complex, Autoimmunity and ACE2 Depletion
Vitamin D may only be masking the inexorable destruction of ACE2 in the body.
Mechanisms of virus-induced autoimmunity. (A) Molecular mimicry model: (1) Viruses carry epitopes structurally similar to self-epitopes. (2) Presentation of viral epitopes by antigen presenting cells (APCs) activate autoreactive T cells that bind to both, self and non-self-antigens, and induce tissue damage. (B) Bystander activation model: (1) Non-specific and over reactive antiviral immune responses lead to the liberation of self-antigens and release of inflammatory cytokines from the damaged tissue. (2) Self-antigen is taken up and presented by APCs. (3) Autoreactive T cells activated by APCs, leading to tissue destruction. (C) Epitope spreading model: (1) Persistent viral infection. (2) Continued tissue damage and release of new self-antigens. (3) Self-antigens are taken up and presented by APCs. (4) Nonspecific activation of more autoreactive T cells leading to autoimmunity.
There is a moment in the movie Aliens (1986) when the members of the crew initially do not think anything concerning is happening. Then, slowly, it dawns on them that an entire swarm of aliens are imminently going to attack them. That is how I felt when I had the realization this evening I am about to divulge.
I have not been able to get the ACE2 receptor issue out of my mind. The fact that this receptor is so ubiquitous and so tied to mechanisms of death – both quick and slow – it gives me immense pause regarding research into creating a weapon which could annihilate a species. And, regarding “slow,” what exactly is “slow?” To us humans the slowest slow is but a microblip of time. For Homo Sapiens to disappear “slowly” on a human scale would be instantaneous on a universal scale. I cannot shake the sinking feeling that this is “slowly” happening.
Back to the movie. We may just now be sensing those monsters outside the walls – but in our abode. Building on all of my previous work, I now propose that Long COVID and the excess deaths we are observing are due to the Spike Protein’s immune complex formation with ACE2. Remember, ACE2 can also be SOLUBLE. It can circulate, unbound to cell membranes. It can form complexes with the Spike Protein which can then generate an autoimmune response to ACE2, destroying it and rendering it non-functioning.
There is evidence of this.
(A) Distribution of patients with IgG autoantibodies against ACE2 (n = 17) in relation to the severity of SARS‐CoV‐2 infection. (B) Titers of IgG autoantibodies against ACE2 I in relation to the severity of SARS‐CoV‐2 infection.
The prevalence of IgG anti‐SARS‐CoV‐2 antibodies (against nucleocapsid protein and S2 subunit, but not against receptor‐binding domain) was higher in the subset with ACE2 autoantibodies. Further research is required to understand the potential spectrum and duration of effects of IgG autoantibodies against ACE2 in patients after SARS‐CoV‐2 infection, particularly concerning long COVID‐19.
In summary, this study shows that IgG autoantibodies against ACE2 can be present in individuals who underwent SARS‐CoV‐2 infection. These antibodies appear rare, although we show that they can also occur in mild COVID‐19 and asymptomatic individuals. Further research is required to understand the potential spectrum and duration of effects of IgG autoantibodies against ACE2 in patients after SARS‐CoV‐2 infection, particularly in relation to long COVID‐19.
IgG autoantibodies against ACE2 in SARS‐CoV‐2 infected patients
This is the theory on how it happens:
The overall autoimmune theory is that the combination of the virus and the soluble ACE2 receptor becomes antigenic, which may cause the formation of antibodies against not only the virus, but also parts of the ACE and ACE2 receptor. This pattern of lung injury also occurs in Pulmonary Hypertension secondary to Scleroderma with elevated levels of anti ACE2 antibodies.27 The higher the levels of the soluble receptors in serum, the more likely it is that the body would respond in this way, that is, with an immune response. This could explain the severity of the inflammatory response in cardiac disease and hypertension causing high mortality globally.
COVID-19–A theory of autoimmunity to ACE-2
To investigate further, I decided to only look at papers written before the pandemic on the effects of ACE2 deficiency. And, as I suspected, we find the very essence of Long COVID.
IMPAIRED COGNITIVE FUNCTION
In conclusion, this study showed that ACE2 deficiency in the mouse resulted in impaired cognitive function, and we propose that the mechanisms of the cognitive decline may be associated at least in part with increased oxidative stress as well as a decreased level of BDNF in the hippocampus in ACE2KO mice. Our study could contribute to further understanding of the roles of the ACE2/Ang-(1–7)/Mas axis in cognitive function, and encourage us to examine the more-detailed mechanisms of this protective arm of RAS in preventing cognitive decline, especially in lifestyle-related diseases such as hypertension and diabetes.
Deficiency of angiotensin-converting enzyme 2 causes deterioration of cognitive function
We found that endothelial function was impaired in adult ACE2 KO mice. Moreover, we found that cerebrovascular dysfunction during aging was augmented in old ACE2 KO mice. Because a superoxide scavenger restored endothelial responses to acetylcholine, our data suggest that oxidative stress plays a primary role in dysfunction caused by ACE2 deficiency.
IMPACT OF ACE2 DEFICIENCY AND OXIDATIVE STRESS ON CEREBROVASCULAR FUNCTION WITH AGING
IMPAIRED PHYSICAL PERFORMANCE
ACE2 deficiency leads to an increase in AT1 gene expression in skeletal muscle. ACE expression in soleus was increased in all exercised groups. ACE2 deficiency affects physical performance and impairs cardiac and skeletal muscle adaptations to exercise.
Effects of ACE2 deficiency on physical performance and physiological adaptations of cardiac and skeletal muscle to exercise
PAH is a fatal lung disease that is associated with increased blood pressure in the pulmonary arteries. Decreased expression of ACE2 and enzymatic activity has been observed in animal models of PAH and pulmonary hypertensive patients, along with a substantial increase in circulating Ang II levels.
Angiotensin-Converting Enzyme 2/Angiotensin-(1-7)/Mas Receptor Axis
The Protective Arm of the Renin Angiotensin System (RAS), 2015
The list goes on and on...
Ultimately, what concerns me the most? With repeated exposures to the Spike Protein, in any form, this autoimmune response becomes permanent or so prevalent as to functionally, if not actually, eradicate ACE2. Additionally, it could also be that the therapeutics we are using are Band-Aids, temporary reserves sent in to fight a battle destined to be lost by the ever diminishing resource of ACE2. You can only keep the waves back for so long.
Hence, vitamin D deficiency can exacerbate COVID-19, via its effects on ACE2. In this review we focus on influence of age, gender, and ethnicity on vitamin D-ACE2 interaction and susceptibility to COVID-19.
Vitamin D and COVID-19: Role of ACE2, age, gender, and ethnicity
Of all my hypotheses I wish to disprove, this is the one I most wish to. We need to investigate Spike Protein levels and Anti-ACE2 Antibody levels in large segments of the population to determine whether or not, and to what degree, this may be occurring.
May God protect and bless us all in this fight for truth, discovery and, ultimately, healing.
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