1) AN AUTO-VIRUS? TRANSPLANTS AND SARS-CoV-2: TRAUMATIC DAMAGE LEADS TO ALLOIMMUNTY. THE SPIKE PROTEIN MIMICS SELF-PEPTIDE INJECTION
TLR4 and MyD88. These have been discussed at length in my threads dealing with the CYTOTOXIC nature of the SPIKE PROTEIN. There is a parallel
2) scenario which involves these very same proteins and genes. TLR2 or TLR4 deficiency alone or Myd88 deficiency restricted to either donor or host was not sufficient to prevent rejection.
Cell damage or death associated with the transplantation procedure releases a large
3) variety of ‘danger’ molecules that potentiate rejection.
What is interesting is that drugs against HLA antibodies, such as Rituximab and Bortezomib, post transplantation ENHANCE coronavirus disease in mice and COVID-19 in humans. Whilst drugs against alloimmunty, such as
1) AUTOANTIBODIES AGAINST ACE2: THE UNIVERSAL DANGER OF SARS-CoV-2 INFECTION AND REINFECTION. A VERY UNIQUE FORM OF ADE. IT IS SIMPLY DE.
One remarkable finding among severe COVID-19 patients is that 18/66 (27%) patients with severe COVID-19 were found to have IgM autoantibodies
2) recognizing ACE2. This explains the sudden increase of recent widespread severe disease in heretofore mild viruses, such as RSV.
The importance of ACE2 for the immune systems is the following: ACE2 attenuates the formation of aortic plaques in vivo and also limits macrophage
3) expression of several proinflammmatory cytokines in vitro, including TNF-α and IL-6, after an LPS challenge, suggesting that ACE2 can directly blunt the proinflammatory polarization of myeloid cells.
TNF-α and IL-6. By now, these terms are in our daily vocabulary. And they
A very interesting lesson has been learned from observing combat related Traumatic Brain Injury (TBI). A review, coauthored by a researcher in Wuhan, describes how TBI includes both primary and secondary impairments. Iron overload and
2) ferroptosis highly involved in the pathophysiological process of secondary brain injury. Ferroptosis is a form of regulatory cell death, as increased iron accumulation in the brain leads to lipid peroxidation, reactive oxygen species (ROS) production, mitochondrial
3) dysfunction and neuroinflammatory responses, resulting in cellular and neuronal damage.
ACCELERATED AGING AFTER BRAIN INJURY
Traumatic brain injury (TBI) causes long-term structural and functional alterations to the brain. Some of
these changes are thought to be
1) PACS? INCORRECT. LONG COVID IS POST TRAUMATIC INJURY SYNDROME. WE ALREADY HAVE A DEFINITION: PICS (persistent inflammation-immunosuppression and catabolism syndrome).
In a percentage of injured patients, the pro-inflammatory and/or anti-inflammatory responses never resolve,
2) leading to a period of chronic critical illness termed persistent inflammatory-immunosuppressive and catabolic syndrome (PICS). This occurs in patients who have been critically ill for longer than 14 days with significant lymphopenia and chronic inflammation. PICS may persist
3) for months and lead to the risk of developing later MODS and secondary infections with subsequent morbidity and late mortality.
NEVER RETURNING TO PRE TRAUMA FUNCTIONAL STATUS
PICS patients suffer from increased long-term mortality and have increased morbidity associated
1) THE UNIVERSAL CYTOTOXIC NATURE OF THE SPIKE PROTEIN MIMICS THE TISSUE DESTRUCTION AND NECROTIC CELL DEATH INITIATED BY TRAUMATIC INJURIES. IT THEN INDUCES THE BODY'S INJURY RESPONSE, WHICH IS TEXTBOOK COVID.
Among the expanding list of PRRs, TLRs, especially TLR4, have
2) emerged as promiscuous sensors for alarmins following trauma. However, other TLRs and innate immune recognition molecules have also been shown react to alarmins and signal danger responses. It has been shown that TLR4 reactivity is enhanced following trauma and that this
3) increase in TLR4 responsiveness contributes to the development of the two-hit response phenotype in a mouse injury model. This explains the mucormycosis being observed and other opportunistic infections post covid.
This may be the reason why long term murine studies have not
1) AN EXPLANATION FOR THE ISCHEMIA AND STROKES WE ARE OBSERVING MONTHS POST COVID AND POST SPIKE PROTEIN THERAPIES.
The ischemia and strokes we are seeing post COVID and post Spike Protein Therapies may be explained by a post trauma phenomenon. After accident whiplash trauma
2) a 50-year-old taxi driver suffered from headache and episodic visual disturbances. Two months after the accident he suddenly lost consciousness and was admitted to the hospital. A CT scan performed at that time was indicative of basilar thrombosis. The patient died 3 days
3) later. Microscopically, a thrombus adhering to the intima was found in the right vertebral artery. Underneath the thrombus, a minor subintimal hemorrhage was seen. At the same level the media was thickened and the adventitia was partially split from it, while the elastic
1) ANSWERED! RT ASAP! I BELIEVE THE SPIKE PROTEIN MIMICS SEVERE TRAUMA BY ATTACKING THE ACE 2 RECEPTORS IN THE ENDOTHELIUM AND BLOOD BRAIN BARRIER, COMPROMISING THEIR INTEGRITY. THE BODY BELIEVES IT IS BLEEDING TO DEATH, EVERYWHERE. THIS IS THE IMMENSE DANGER OF INJECTING SPIKE
2) PROTEINS, OR HAVING THE BODY CREATE THEM.
THE IMMENSE BINDING AFFINITY TO ACE 2 MIMICS BLUNT FORCE!
In independent, but small, studies of trauma patients, we found that (i) high circulating syndecan-1, a marker of endothelial glycocalyx degradation,15 was associated with
3) inflammation, hypocoagulability, and increased mortality; (ii) the trauma-induced catecholamine surge was closely associated with biomarkers of tissue and endothelial damage, glycocalyx degradation, hypocoagulability including hyperfibrinolysis and independently predicted
1) Evidence SARS-CoV-2 Mimics Trauma. Post-Traumatic Fatal Granulomatosis with Polyangiitis and Disseminated Intravascular Coagulation and Sustained Systemic Inflammatory Response Syndrome Predict Organ Dysfunctions After Trauma. Fatal Fungal Infection Post Trauma.
2) attached looks EXACTLY like COVID pneumonia, doesn't it? It is actually an image taken after thoracic trauma. The physicians were so stunned by the similarity that they published a case report on it.
They found it curious. I find it definitive.
What is also definitive are
3) the findings of post traumatic disseminated intravascular coagulation and sustained systemic inflammatory response syndrome post trauma. Four days post trauma fibroningen levels are very high, and this leads to clotting issues. In fact, this is indicative of the further
PROTEOTOXIC STRESS. MITOCHONDRIAL UNFOLDED PROTEIN RESPONSE. CACHEXIA. A UNIFYING THEORY FOR ALL OBSERVED OVER THE PAST 18 MONTHS.
WE ARE DEALING WITH A BIOWEAPON THAT WAS BEING DEVELOPED TO METABOLICALLY BURN ITS VICTIMS ALIVE .
2) been looking at the wrong Unfolded Protein Response. The Mitochondrial Unfolded Protein Response (mtUPR) which is most important in SARS-CoV-2 infection.
Skeletal muscle cachexia resulting from a chronic imbalance between protein synthesis and breakdown leads to
3) significant long-term morbidity in burn survivors.
The data indicates profound PROTEOTOXIC stress within the mitochondria environment and, most importantly, suggest that this stress is transduced to the nucleus to help combat the accumulation of unfolded proteins within
Prions and immune deificiency emerging simultaneously. Fungi and viral reactivation. The spike, I believe, is also affecting Heat Shock Proteins.
The fundamental problem of autoimmune diseases is the failure of the immune system to
2) downregulate its own potentially dangerous cells, which leads to destruction of tissue expressing the relevant autoantigens. Current immunosuppressive therapies offer relief but fail to restore the basic condition of self-tolerance. They do not induce long-term physiological
3) regulation resulting in medication-free disease remissions. Heat shock proteins (HSPs) have shown to possess the capacity of inducing lasting protective immune responses in models of experimental autoimmune diseases. Especially mycobacterial HSP60 and HSP70 were shown to
1) SARS-CoV-2 (SPIKE) ANTIBODIES MAY CAUSE UNIVERSAL VIRAL ANTIBODY DEPENDENT ENHANCEMENT VIA FcR IMPAIRMENT. THIS ALSO EXPLAINS THE EMERGENCE OF MUCORMYCOSIS.
The immune response to the spike protein antibodies of SARS-CoV-2 may be causing severe FcR receptor dysfunction.
2) These are the receptors that mediate Antibody Dependent Enhancement in disease. A very telling sign is that mice which have FcR's knocked out are susceptible to LETHAL FUNGAL infections while having STRONG IMMUNE RESPONSES to other types of pathogens.
In spite of the
3) deficiency, FcγRIIb−/− mice show highly effective immune responses against several types of pathogens, including bacteria, plasmodia and mycobacteria. The fungal immune responses of FcγRIIb−/− mice have been inadequately tested, despite the high susceptibility to
1) Burkholderia pseudomallei, biowarfare, spike proteins and a recent outbreak.
An interesting idea: There have been three documented cases of Burkholderia pseudomallei in the US recently, yet this bacteria is not endemic to the US nor have the three recent cases traveled
2) outside the US.
If you research Burkholderia pseudomallei you will find that it is often spoken of as a potential bioweapon, given its high (~50%) mortality rate and its ability to mimic a vast array of diseases. In fact, it is known as "the great mimicker."
3) molecular geneticist please examine the spike protein of SARS-CoV-2 and compare it to Burkholderia pseudomallei?
What I find most fascinating is that this bacteria has the same modus operandi as SARS-CoV-2s spike protein. It causes the formation of giant multinucleated cells
1) ARE THE SIDE EFFECTS OF THE SPIKE PROTEIN THERAPIES ACTUALLY VASCULITIS AND NOT THE "IMMUNE SYSTEM WORKING?"
Given the recent and abundant evidence that the S1 subunit of the SARS-CoV-2 spike protein damages blood vessels, is it perhaps more than likely that the spike is
2) being cleaved and the cleaved S1 unit is attacking blood vessels?
If one notes the "side effects" of the spike protein therapies, they are PRECISELY the same as VASCULITIS:
Loss of appetite and weight loss
Joint and muscle pain
3) Abdominal pain and gastrointestinal bleeding
Weakness, fatigue or a general feeling of being unwell
Rash or skin sores
Pain, numbness and tingling in your hands and feet
Severe abdominal pain
Shortness of breath
If the blood vessels in the heart are being attacked by the
1) URGENT! Has the spike protein been created to hijack dendritic cells to cross the blood brain barrier and invade the CNS? Literally commandeering the DCs like a cavalry?
The spike has even HIGHER binding affinity for DC-SIGN than ACE2. DC-SIGN is a recepton on dendritic
2) cells that allows for their manipulation. They INVADE the central nervous system during periods of SEVERE INFLAMMATION.
Besides endothelial cells of the BBB, another endothelial cell type that has been extensively studied in leukocyte migration is the high endothelial venules
3) (HEVs). These specialized postcapillary venules allow exit of blood cells into secondary lymphoid organs. The role of HEVs with respect to leukocyte trafficking into the CNS has not been well studied. HEV differentiation markers, however, have been shown to be expressed in
1) PLATELET FACTOR 4 AUTOANTIBODIES: THE MOST IMPORTANT RISK FACTOR
I believe I have found the most important risk factor for COVID-19. The frequency of preexisting PF4 antibodies is estimated at 1.4% in normal, 4.5% in elderly, 4.8% in pregnant and 8.6% in diabetic subjects!
2) THE DAMAGE DONE BY THE SPIKE PROTEIN TO THE ENDOTHELIUM MIMICS ACUTE CORONARY SYNDROME. THIS ACTIVATES THE IMMUNE RESPONSE TO PF4 AND EXPLAINS WHY HEPARIN MAKES THE CONDITION WORSE!
To explain the preexistence of HIT antibodies, it was proposed that heparin-like molecules
3) (glycosaminoglycans) on injured endothelium bind
with PF4 to form complexes with which the antibodies
react. Neoantigens appeared to cause conformational
change of PF4 to induce the production of heterogenetic antibodies in the Ig subclass in the presence of heparin like