New paper shows how spike protein induced autoimmunity derails the RAAS

Revisiting my video on the RAAS from April 2021 and a new study confirming my original hypothesis

Five years ago almost to the day (April 2021), I posted a YouTube video explaining how the spike protein disrupts the Renin-Angiotensin-Aldosterone System (RAAS) - the key hormone system that regulates blood pressure, electrolytes, and vascular tone. It seemed obvious to me that because ACE-2 is central to the RAAS, and because spike binds ACE-2, flooding the body with genetic instructions for spike protein would inevitably perturb this system and produce downstream symptoms.

In this video, (see below) I lay out the basics of the RAAS and why introducing exogenous spike was always going to cause trouble, mainly through competitive binding.

Recap: How the COVID-19 shots are meant to “work”

The COVID-19 nucleoside modified RNA-LNP injectable products deliver ~0.3–0.5 mL of solution containing billions of LNPs that encapsulate mRNA encoding SARS-CoV-2 spike protein. Upon successful transfection, the mRNA is translated into spike protein in target cells. This induces immune responses directed against antigenic epitopes (antigenic determinants) on the spike protein. Produced spike proteins (in pre-fusion conformation) can still bind ACE-2 receptors, which alone is sufficient to promote ACE-2 down-regulation and internalization and contribute to RAAS imbalance.

In simple terms: If spike is bound to ACE-2 → ACE-2 can’t do its normal job → less Angiotensin-(1–7) is produced via that route (from Angiotensin II (Ang II)) → the protective MAS1 receptor isn’t properly activated → the harmful effects of Ang II on the AT1 receptor go unchecked, driving vasoconstriction, inflammation, oxidative stress, and autonomic dysfunction.

Now let’s look at other potential downstream consequences of this novel mRNA-LNP platform - administered to billions as a “vaccine” - according to what this new study shows.

The new RAAS study

A paper published in Vaccines (MDPI) on April 16, 2026 entitled: Autoimmune Features of Post-COVID-19 Vaccination Syndrome and Their Impacts on the Renin–Angiotensin System¹ confirms much of what I predicted years ago.

The authors propose that Post-Acute COVID-19 Vaccination Syndrome (PACVS) is largely driven by autoimmune dysregulation of the RAAS. In their observational cohort study of 17 SARS-CoV-2–uninfected people² (13 women, 4 men; mean age 44), who were previously healthy and received 1–3 doses of COVID-19 vaccines (mostly mRNA), the researchers documented the following key immunological findings:

• Elevated IL-1β/IL-8 (IL = interleukin) and reduced T regulatory cells (Tregs) (autoimmune signature)

• Frequent G protein-coupled receptor (GPCR) autoantibodies: nearly universal anti-MAS1 (strongly correlated with burning paresthesia) and anti-ACE2 (linked to skin edema/bruising, hypertension, headache)**

• Autoantibodies against several adrenergic and muscarinic receptors (linked to Postural Orthostatic Tachycardia Syndrome (POTS), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), chronic heart failure, and even Chagas cardiomyopathy)

• Elevated Ang-(1–7) in ~67% of cases, despite impaired protective signaling.

Not surprisingly, PACVS shares many features with long COVID (Post-Acute COVID-19 Syndrome (PACS)) (personally I think they’re the same thing), including fatigue, brain fog, dysautonomia, paresthesia and skin issues.

N.B. Suggested reading on causal autoimmunity and brain damage in “long-COVID” and autoimmunity and tolerance.

Why anti-MAS1 is particularly concerning

In a healthy RAAS, Ang-(1–7) binds the MAS1 receptor like a key in a lock, activating a protective ‘brake’ that counters the pro-hypertensive and pro-inflammatory effects of Ang II/AT1 receptor pathway.³

Figure 1: RAAS - role of ACE-II membrane bound. From https://www.youtube.com/watch?v=AsmwQzlYTho

When anti-MAS1 autoantibodies are present - as they were in nearly all study patients - it’s like gum jammed in the lock - Ang-(1–7) can’t bind properly, so the brake system fails leading to vasoconstriction, inflammation, oxidative stress and autonomic dysfunction.

I did a query of these AEs in VAERS data from 2016-2025 and plotted them as absolute counts and according number per 100,000 reports per respective year. Something happened in 2021. Funny that.

Figure 2: VAERS reports of vasoconstriction, vascular inflammation, oxidative stress and autonomic dysfunction. https://vaers.hhs.gov

Anti-idiotypic responses and molecular mimicry

The authors propose that anti-ACE2 autoantibodies arise mainly via anti-idiotypic responses (the anti-idiotype network) or molecular mimicry between spike and ACE2. The former route is well-documented.⁴⁵⁶⁷⁸ There is no known MAS1 peptide homolog in the spike protein, so disruption of the Ang-(1–7)/MAS1 axis occurs through autoantibody-mediated functional blockade.

The authors suggest a more indirect origin for anti-MAS1, including possible epitope spreading⁹ within the idiotypic network and/or structural/functional similarity between the ACE-2 binding site and the MAS1 receptor (they bind very similar peptides - Ang II vs. Ang-(1–7), differing by only one amino acid). Thus, antibodies generated against ACE-2 could cross-react or spread to MAS1. The idea of epitope spreading relies on an expansion of an initial immune response beyond original targeted epitopes whereby additional epitopes on the same or different antigens are recognized.

What’s especially fascinating about this is how the immune system generates antibodies not only against the spike (and ACE2), but also against the anti-spike antibodies themselves! (These are the anti-idiotypic antibodies (Ab2)).

N.B. Anti-idiotypic antibodies form when the immune system perceives the unique antigenic sites (idiotypes) on the original antibodies as foreign.

Figure 2: The Idiotope of the Antibody. https://www.genscript.com/learning-center/what-is-an-anti-id-antibody.html

If you’re familiar with the lost-wax process for bronze casting, you’ll get the idea of anti-idiotypic antibodies quickly. The artist creates a wax sculpture - the positive original (the spike antigen). This is coated in fine plaster that captures every detail, forming a perfect negative mold. After the wax is melted out, molten bronze is poured into the plaster mold, creating a new positive sculpture that is an exact copy of the original wax.¹⁰ In the same way:

• The spike antigen is the original wax sculpture.

• The Ab1 (anti-spike antibody) is the plaster mold - its idiotype (antigen-binding site) is the negative imprint of the spike.

• The Ab2 (anti-idiotypic antibody) is the bronze casting - it mimics the shape of the original spike and can therefore bind ACE-2 just like the spike does.

In other words, the immune system produces antibodies not only against the spike, but also against the anti-spike antibodies themselves because their idiotypes look foreign. These anti-idiotypic antibodies (Ab2) end up structurally resembling the original antigen. It’s wonderfully complex - and it’s the core of Jerne’s idiotypic network theory.¹¹

The authors also note a compensatory rise in Ang-(1–7) via alternative enzymes (ie: neprilysin), but because of the blocked MAS1 receptors, this elevation fails to deliver protection, leaving the system in a dysfunctional, “open” state. So what’s the deal with that?

Why is Ang-(1-7) elevated?

Anti-ACE2 autoantibodies (arising via anti-idiotypic responses or molecular mimicry) block or impair ACE-2’s normal enzymatic activity. This disruption favors a compensatory increase in Ang-(1–7). The authors propose that the elevated levels come from alternative production pathways - enzymes like neprilysin and other endopeptidases that can generate Ang-(1–7) directly from upstream precursors (such as Ang I or Ang-(1–9)), by-passing the damaged ACE-2 route. Could be.

However, with anti-MAS1 autoantibodies jamming the receptor, this extra Ang-(1–7) is largely useless. The protective effects never fully kick in, while the harmful Ang II/AT1R arm continues unchecked. It’s a classic case of the body trying to compensate, but the compensation itself is sabotaged. Ang-(1-7) has actually been suggested as a physiological treatment for both PACVS and PACS.¹²

So what have we learned?

The COVID-19 mRNA and viral-vector injections can trigger autoimmune dysregulation of the RAAS in a subset of individuals, producing persistent vasoconstriction, inflammation, oxidative stress, and autonomic dysfunction.

Beyond these core effects, affected individuals frequently experience a much broader spectrum of related adverse events, including various rashes (urticaria, erythema, maculopapular eruptions), paresthesia, burning sensations, edema, headaches, profound fatigue, brain fog, chest pain, palpitations, and other dermatological and neurological manifestations.

This entire constellation of symptoms was mechanistically predictable, arising from the well-established interaction between the SARS-CoV-2 spike protein and ACE-2, together with the potential for molecular mimicry, anti-idiotypic antibody responses, and epitope spreading.

1. Bellavite P, Di Fede G, Mantovani M, Zanolin E. Autoimmune Features of Post-COVID-19 Vaccination Syndrome and Their Impacts on the Renin–Angiotensin System. Vaccines. 2026; 14(4):354. https://doi.org/10.3390/vaccines14040354

2. None had been previously infected with SARS-2 (all had anti-spike (anti-S) IgG antibodies but negative anti-nucleocapsid (anti-N) IgG, confirming no prior natural infection), but all were injected with COVID-19 shots. They were healthy before injection and received 1–3 doses of modRNA (n=15) or adenoviral vector (n=2) vaccines, and were observed about 20 months post-injection.

3. László Hunyady, Kevin J. Catt, Pleiotropic AT₁ Receptor Signaling Pathways Mediating Physiological and Pathogenic Actions of Angiotensin II, Molecular Endocrinology, Volume 20, Issue 5, 1 May 2006, Pages 953–970, https://doi.org/10.1210/me.2004-0536

Fun fact: Did you know that AT1 receptors are linked to fear memory recall? As in, when you block them, you block fear? Marvar PJ, Goodman J, Fuchs S, Choi DC, Banerjee S, Ressler KJ (June 2014). “Angiotensin type 1 receptor inhibition enhances the extinction of fear memory”. Biological Psychiatry. 75 (11): 864–872. doi:10.1016/j.biopsych.2013.08.024

4. Lai YC, Cheng YW, Chao CH, et al. Antigenic cross-reactivity between SARS-CoV-2 S1-RBD and its receptor ACE2. Front Immunol. 2022;13:868724. doi:10.3389/fimmu.2022.868724

5. Devaux CA, Camoin-Jau L. Molecular mimicry of the viral spike in the SARS-CoV-2 vaccine possibly triggers transient dysregulation of ACE2, leading to vascular and coagulation dysfunction similar to SARS-CoV-2 infection. Viruses. 2023;15(5):1045. doi:10.3390/v15051045

6. Bellavite P, Di Fede G, Mantovani M, Zanolin E. Autoimmune features of post-COVID-19 vaccination syndrome and their impacts on the renin–angiotensin system. Vaccines (Basel). 2026;14(4):354. doi:10.3390/vaccines14040354

7. Nunez-Castilla J, Stebliankin V, Baral P, et al. Potential autoimmunity resulting from molecular mimicry between SARS-CoV-2 spike and human proteins. Front Immunol. 2022;13:943133. doi:10.3389/fimmu.2022.943133

8. Timofeeva AM, Kudinova IA, Gabibov AG, Belogurov AA. SARS-CoV-2 spike protein and molecular mimicry: an immunoinformatic screen for cross-reactive autoantigen candidates. Int J Mol Sci. 2025;26(18):8793. doi:10.3390/ijms26188793

9. Epitope spreading is an immunological phenomenon where the immune response broadens from an initial, dominant epitope to recognize additional subdominant or cryptic epitopes on the same protein (intramolecular spreading) or on different proteins (intermolecular spreading). https://www.creative-biostructure.com/resource-epitope-spreading-overview.htm

10. Here’s one of my sculptures I made in a foundry in Newfoundland way back when. It was meant to be a classical dolphin fountain, but it ended up just being a classical dolphin mounted on the bronze left over from an accident from the pour. Never mind. Everyone was fine.

11. Jerne NK. Towards a network theory of the immune system. Ann Immunol (Paris). 1974;125C(1-2):373-389

12. Aktaş AR (2025) Interaction of SARS-CoV-2 and SARS-CoV-2 vaccines with renin angiotensin aldosterone system, clinical outcomes, and angiotensin (1-7) as a physiological treatment recommendation: hypothesis and theory article. Front. Med. 12:1612442. doi: 10.3389/fmed.2025.1612442