Clinical approach to base spike protein detoxification

The spike protein is responsible for the pathogenicity of the SARS-CoV-2 infection and drives the development of adverse events, injuries, disabilities, and death after vaccination through immunologic and thrombotic mechanisms. The long-lasting spike protein has been found in the brain, heart, liver, kidneys, ovaries, testicles and other vital organs at autopsy in cases of death after vaccination. In the case of vaccine-induced thrombotic injury, the spike protein has been found within the blood clot itself. Thus, there is strong rationale for considering residual SARS-CoV-2 spike protein as a treatment target in post COVID-19 and vaccine injury syndromes. The spike protein participates directly in pathophysiology, incites inflammation, and propels thrombosis.

: Figure 1. Proposed Mechanisms Through Which S1 of Spike Protein Induced Cardiac Mitochondrial Dysfunction, Which Leads to Cardiac Injury in COVID-19 Patients. Spike protein is the glycosylated protein that covers the surface of SARS-CoV-2 and binds to the host ACE2 receptor to mediate the viral cell entry. It is composed of S1 and S2 subunits that are responsible for ACE2 binding and membrane fusion, respectively. S1 possibly binds to ACE2 on the AC16 membrane and is then internalized into the cytosol and localized in organelles, such as mitochondria, which induces the transient increase in fatty acids transport and uptake for biogenetics, Δψm, and permanent mCa2+, and disrupts Δψm later, finally impairing mitochondrial function and promoting ROS production. In turn, ROS further exacerbates mitochondrial function and mitochondrial fragmentation. Moreover, S1 causes downregulation of TOM20; this effect might inhibit the pathways leading to mitochondrial biogenesis. Abbreviations: ACE2 = angiotensin-converting enzyme 2, FAT = fatty acid translocase, PCT1/2 = Carnitine palmitoyltransferase ½, MCD = Malonyl-CoA decarboxylase, ACC = acetyl-CoA carboxylase, AMPK = AMP-activated protein kinase, mCa2+ = mitochondrial calcium, Δψm = mitochondrial membrane potential, ROS = reactive oxygen species. *Figure and legend reprinted from Huynh et al. [14]. The legend title has been slightly adapted. Permission to use this figure has been granted in accordance with the open access Creative Common CC BY 4.0 license.

: Figure 2. Arterial Thrombi From COVID-19 + Patients Contain SARS-CoV-2 Spike Protein But Not Nucleocapsid Protein. Panel 1. Immunostaining positive for SARS-CoV-2 spike protein (SP) (arrows) in representative thrombotic material from COVID-19 + patients, retrieved from cerebral (A) and coronary (C) arteries. Immunohistochemistry for nucleocapsid protein (NP) was negative in the same samples (B-D). Panel 2. Representative immunohistochemical staining positive for SP (E) and NP (F) (arrows) in the lung of a patient affected by COVID-19 (positive control). Representative immunostaining negative for SP (G) and NP (H) in a thrombus retrieved from the middle cerebral artery of a patient not affected by COVID-19 (negative control). Original magnification 20X. Panel 3. Double immunofluorescence of thrombotic material retrieved from COVID-19 and non-COVID-19 patients’ cerebral arteries. In the COVID-19 thrombus, platelets are co-stained with anti-CD61 (red-L,P) and anti-SARS-CoV-2 spike protein (SP) antibodies (green-M,Q), emitting yellow signals in the merged panel (N), while in the control (non-COVID thrombus), only the red CD61 signal is observed (R). *Figure and legend reprinted from De Michele et al. [21]. The legend title has been slightly adapted. Permission to use this figure has been granted in accordance with the open access Creative Common CC BY 4.0 license.

COVID 19 Vaccine Detoxification Protocol

The base spike protein detoxification protocol includes a natural triple-agent oral regimen of nattokinase, bromelain, and curcumin that provides four putative, primary mechanisms of action: 1) proteolytic degradation of spike protein, 2) inhibition of inflammation from spike protein and its fragments in tissues, 3) dissolution of microthrombi, and 4) anticoagulation. Figure 3 below illustrates the base spike detoxification protocol and its mechanisms.

: Base Spike Detoxification (BSD). A: Dissolution of spike protein-induced thrombus. Nattokinase directly degrades fibrinolysis-resistant fibrin (from spike protein), and bromelain upregulates fibrinolysis. B: Inhibition of spike protein via ACE2 receptors. Bromelain and curcumin block the ACE2 receptor, preventing spike protein from binding. C: Proteolytic degradation of spike protein. Nattokinase and bromelain degrade spike proteins, rendering them inactive. D: Attenuation of spike protein-induced inflammation. Bromelain and curcumin downregulate the NF-kB signaling pathway induced by spike protein, leading to the suppression of inflammatory molecules. E: BSD treatment protocol. The full treatment regimen and the addition of other compounds based on clinical indication are illustrated. Abbreviations: TPA = tissue plasminogen activator, PAI-1 = plasminogen activator inhibitor-1, ACE2 = angiotensin converting enzyme-2, NF-kB = nuclear factor kappa B, S1/S2 = spike protein subunits S1/S2, TLR4 = toll-like receptor 4.