Spike Protein Syndrome

Recently has been widely identified what Dr. Thomas Levy calls "Spike Protein Syndrome", a pathology caused by the spread of Spike protein throughout the body, either as a result of COVID-19 disease or as a result of COVID vaccination. Symptoms are mainly autoimmune reactions and may include: heart failure, heart damage, heart attack, myocarditis; pulmonary hypertension, thromboembolism and pulmonary thrombosis, damage to lung tissue, possible pulmonary fibrosis; increased venous and arterial thromboembolic events; diabetes; neurological complications, including encephalopathy, seizures, headaches, and neuromuscular diseases, as well as hypercoagulability and stroke; intestinal dysbiosis, inflammatory bowel disease, and permeable bowel; kidney damage; impairment of male reproductive capacity; skin lesions; general autoimmune diseases, autoimmune hemolytic anemia; liver damage.

Dr. Thomas Levy - known in the United States for his therapeutic applications of Vitamin C in cancer and heart disease - has sounded the alarm in the COVID-19 pandemic, warning of the effects of Spike protein in messenger RNA vaccines and proposing, in the meantime, a non-invasive, inexpensive and personalized approach to healing.[1] Moreover, summarizing the clinical data on chronic forms of COVID, but especially the side effects of COVID vaccines, Dr. Levy launched the concept of "Spike protein syndrome" [2], which he says is manifested: a) in an active COVID-19 infection, b) during long-term COVID syndrome or c) in response to a Spike protein-generating vaccine, such as those based on messenger RNA.

Spike Protein

Starting from the very suggestive description of the physical appearance of the coronavirus, as a sphere of viral proteins surrounded by a kind of spear, Levy explains how the Spike protein works in the body. He associates these "spears", known in medical terminology as "Spike protein", with the spines of a porcupine. Just as the porcupine pierces its prey with its spines, so do the spike proteins penetrate the cell membranes of the human body. After this penetration, the protein-dissolving enzymes are activated, the cell membrane breaks down, the viral sphere enters the cytoplasm through the gap created in the membrane, and the cell's metabolism is "diverted" to produce more and more viral particles. By binding Spike protein to the angiotensin 2 converting enzyme (ACE2) receptors on target cell membranes, dissolution enzymes are released which then allow COVID to enter the cytoplasm, where viral replication can occur. [3]

Due to this phenomenon that occurs through COVID infection, some experts have expressed concern about the spread of Spike protein throughout the body following vaccination. Instead of remaining localized to the injection site to determine the anti-COVID immune response and nothing more, Spike protein has been detected throughout the body of vaccinated individuals. In addition, it appears that some of the circulating Spike proteins only bind ACE2 receptors without entering the cell, thereby inducing an autoimmune response to the entire Spike cell-protein entity.

Thus, an explanation for the problems related to thrombotic tendencies and other symptoms observed in chronic COVID patients and vaccinated individuals is the very presence of the virus Spike protein. Some reports show that Spike protein may continue to be produced after initial binding to ACE2 receptors and entry into some of the target cells. The clinical picture of chronic COVID and post-vaccine toxicity seems very similar and is probably due to the continued presence of Spike protein and its spread throughout the body. [4]

Although located on many different types of cells throughout the body, ACE2 receptors on epithelial cells lining the airways are the first targets of the COVID virus on initial contact when inhaled. [5] In addition, the concentration of these receptors is particularly high in the lung alveolar epithelial cells, which causes the lung tissue to be disproportionately targeted by the virus. [6] This uncontrolled receptor binding and subsequent viral replication within lung cells lead to low blood oxygen levels and Adult Respiratory Distress Syndrome (ARDS). [7] Finally, there is an increase in intracellular oxidation known as the "cytokine storm", which can cause death due to respiratory failure. [8]

It has also been suggested that Spike protein, in large amounts, binds ACE2 receptors without going further into the cell, thus blocking or disabling the normal function of ACE2 in a given tissue. In addition, if the Spike protein binds to a cell wall and "stops" there, it functions as a hapten (antigen) that can initiate an autoimmune (antibody or antibody-like) response to the cell rather than the virus, the particle to which it is usually attached. Depending on the types of cells to which Spike proteins bind, a wide variety of autoimmune diseases can result.

Symptoms of Spike Protein Syndrome

The mechanisms involved are far from fully understood. What is certain is that more and more post-vaccine clinical complications are occurring and need to be addressed as quickly and effectively as possible. Disruption of ACE2 receptor function in so many areas of the body has led to a number of different side effects. Such clinical complications are seen in various organ systems and areas of the body, which may occur in the following three clinical situations: a) in an active COVID-19 infection, b) during long-distance COVID syndrome or c) as a response to a protein spike vaccine. All three are forms of 'Spike protein syndrome', although acute infection always includes all viral particles along with Spike protein during the early stages of the infection.

Thus, the symptoms of the syndrome may include, but are not limited to:

• heart failure, heart damage, heart attack, myocarditis, [9]

• pulmonary hypertension, thromboembolism, and pulmonary thrombosis, damage to lung tissue, possible pulmonary fibrosis, [10]

• increased venous and arterial thromboembolic events, [11]

• diabetes, [12]

• neurological complications, including encephalopathy, seizures, headache, and neuromuscular disease, as well as hypercoagulability and stroke, [13]

• intestinal dysbiosis, inflammatory bowel disease, and permeable bowel, [14]

• kidney damage, [15]

• impairment of male reproductive capacity, [16]

• skin lesions, [17]

• general autoimmune diseases, autoimmune hemolytic anemia, [18]

• liver damage. [19]

The therapeutic solution proposed by Dr. Levy is also interesting. He states that Spike's protein syndrome is treated in the same way as COVID-19. In essence, a clinical protocol to stop the ravages of the persistent presence of Spike protein in the body is similar to that which can effectively treat any form of COVID infection, including active infection, long-term COVID, chronic COVID, and infection. caused by the administration of the COVID vaccine.

References

[1] https://rvr.medfoxpub.com/

[2] Thomas E. Levy, Canceling the Spike Protein, Striking Visual Evidence, http://orthomolecular.org/resources/omns/v17n24.shtml; Thomas E. Levy, Resolving "Long-Haul COVID" and Vaccine Toxicity: Neutralizing the Spike Protein, http://orthomolecular.org/resources/omns/v17n15.shtml

[3] Belouzard S, Millet J, Licitra B, Whittaker G (2012) Mechanisms of coronavirus cell entry mediated by the viral spike protein. Viruses 4:1011-1033. PMID: 22816037; Shang J, Wan Y, Luo C et al. (2020) Cell entry mechanisms of SARS-CoV-2. Proceedings of the National Academy of Sciences of the United States of America 117:11727-11734. PMID: 32376634

[4] Mendelson M, Nel J, Blumberg L et al. (2020) Long-COVID: an evolving problem with an extensive impact. South African Medical Journal 111:10-12. PMID: 33403997; Aucott J, Rebman A (2021) Long-haul COVID: heed the lessons from other infection-triggered illnesses. Lancet 397:967-968. PMID: 33684352; Levy T (2021) Resolving "Long-Haul COVID" and vaccine toxicity: neutralizing the spike protein. Orthomolecular Medicine News Service, June 21, 2021. http://orthomolecular.org/resources/omns/v17n15.shtml; Raveendran A (2021) Long COVID-19: Challenges in the diagnosis and proposed diagnostic criteria. Diabetes & Metabolic Syndrome: Clinical Research & Reviews 15:145-146. PMID: 33341598

[5]Hoffmann M, Kleine-Weber H, Schroeder S et al. (2020) SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 181:271-280. PMID: 32142651

[6] Alifano M, Alifano P, Forgez P, Iannelli A (2020) Renin-angiotensin system at the heart of COVID-19 pandemic. Biochemie 174:30-33. PMID: 32305506

[7] Batah S, Fabro A (2021) Pulmonary pathology of ARDS in COVID-19: a pathological review for clinicians. Respiratory Medicine 176:106239. PMID: 33246294

[8] Perrotta F, Matera M, Cazzola M, Bianco A (2020) Severe respiratory SARS-CoV2 infection: Does ACE2 receptor matter? Respiratory Medicine 168:105996. PMID: 32364961; Saponaro F, Rutigliano G, Sestito S et al. (2020) ACE2 in the era of SARS-CoV-2: controversies and novel perspectives. Frontiers in Molecular Biosciences 7:588618. PMID: 33195436; Hu B, Huang S, Yin L (2021) The cytokine storm and COVID-19. Journal of Medical Virology 93:250-256. PMID: 32592501.

[9] Chen L, Li X, Chen M et al. (2020) The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovascular Research 116:1097-1100. PMID: 32227090; Liu Y, Sawalha A, Lu Q (2021) COVID-19 and autoimmune diseases. Current Opinion in Rheumatology 33:155-162. PMID: 33332890.

[10] McDonald L (2021) Healing after COVID-19: are survivors at risk for pulmonary fibrosis? American Journal of Physiology. Lung Cellular and Molecular Physiology 320:L257-L265. PMID: 33355522; Mishra A, Lal A, Sahu K et al. (2020) An update on pulmonary hypertension in coronavirus disease-19 (COVID-19). Acta Bio-Medica 91:e2020155. PMID: 33525228; Pasqualetto M, Sorbo M, Vitiello M et al. (2020) Pulmonary hypertension in COVID-19 pneumoniae: It is not always as it seems. European Journal of Case Reports in Internal Medicine 7:002160. PMID: 33457379; Potus F, Mai V, Lebret M et al. (2020) Novel insights on the pulmonary vascular consequences of COVID-19. American Journal of Physiology. Lung Cellular and Molecular Physiology 319:L277-L288. PMID: 32551862; Dhawan R, Gopalan D, Howard L et al. (2021) Beyond the clot: perfusion imaging of the pulmonary vasculature after COVID-19. The Lancet. Respiratory Medicine 9:107-116. PMID: 33217366.

[11] Ali M, Spinler S (2021) COVID-19 and thrombosis: from bench to bedside. Trends in Cardiovascular Medicine.

[12] Yang J, Lin S, Ji X, Guo L (2010) Binding of SARA coronavirus to its receptor damages islets and causes acute diabetes. Acta Diabetologica 47:193-199. PMID: 19333547; Lima-Martinez M, Boada C, Madera-Silva M et al. (2021) COVID-19 and diabetes: a bidirectional relationship. Clinica e Investigacion en Arteriosclerosis 33:151-157. PMID: 33303218.

[13] AboTaleb H (2020) Neurological complications in COVID-19 patients and its implications for associated mortality. Current Neurovascular Research 17:522-530. PMID: 32718292; Bobker S, Robbins M (2020) COVID-19 and headache: a primer for trainees. Headache 60:1806-1811. PMID: 32521039; Hassett C, Gedansky A, Migdady I et al. (2020) Neurologic complications of COVID-19. Cleveland Clinic Journal of Medicine 87:729-734. PMID: 32847818; Hess D, Eldahshan W, Rutkowski E (2020) COVID-19-related stroke. Translational Stroke Research 11:322-325. PMID: 32378030.

[14] Perisetti A, Gajendran M, Mann R et al. (2020) COVID-19 extrapulmonary illness-special gastrointestinal and hepatic considerations. Disease-A-Month 66:101064. PMID: 32807535; Zeppa S, Agostini D, Piccoli G et al. (2020) Gut microbiota status in COVID-19: an unrecognized player? Frontiers in Cellular and Infection Microbiology 10:576551 PMID: 33324572.

[15] Han x, Y Q (2021) Kidney involvement in COVID-19 and its treatments. Journal of Medical Virology 93:1387-1395. PMID: 33150973.

[16] Seymen C (2021) The other side of COVID-19 pandemic: effects on male fertility. Journal of Medical Virology 93:1396-1402. PMID: 33200417.

[17] Galli E, Cipriani F, Ricci G, Maiello N (2020) Cutaneous manifestation during COVID-19 pandemic. Pediatric Allergy and Immunology 31 Suppl 26:89-91. PMID: 33236439.

[18] Jacobs J, Eichbaum Q (2021) COVID-19 associated with severe autoimmune hemolytic anemia. Transfusion 61:635-640. PMID: 33274459; Liu Y, Sawalha A, Lu Q (2021) COVID-19 and autoimmune diseases. Current Opinion in Rheumatology 33:155-162. PMID: 33332890.

[19] Roth N, Kim A, Vitkovski T et al. (2021) Post-COVID-19 cholangiopathy: a novel entity. The American Journal of Gastroenterology 116:1077-1082. PMID: 33464757.