1) HEAT SHOCK PROTEINS AND THE SPIKE

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
4) induce disease inhibitory IL-10-producing regulatory T cells in many different models.

HSPs Are the Most Frequent Cytosolic/Nuclear MHC Class II Natural Ligand Source!

Prion disease is accelerated in mice lacking stress-induced heat shock protein 70 (HSP70)

Also, HSP are
5) involved in the REACTIVATION OF LATENT VIRUSES!

One condition in which HSP expression is increased in vivo is fever. Many viral diseases cause the development of fever in the host and, while hyperthermia has been implicated in the reactivation of viral replication in latent
6) /chronic infection, the possibility that fever could be beneficial during acute viral infections has been often suggested.

pubmed.ncbi.nlm.nih.gov/31320473/

ncbi.nlm.nih.gov/pmc/articles/P…

frontiersin.org/articles/10.33…
UNF*CKING REAL!

Well, well, well. What have we here, Messrs. Baric et Fauci?

SARS-CoV-2 Spike-Heat Shock Protein A5 (GRP78) Recognition may be Related to the Immersed Human Coronaviruses
frontiersin.org/articles/10.33…
I mean, this has to be it.

tandfonline.com/doi/abs/10.108…

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More from @Parsifaler

22 Jul
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 Image
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
Read 6 tweets
22 Jul
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.

The image Image
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 Image
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
Read 7 tweets
21 Jul
1) FIVE ALARM FIRE: TOXINS AND PRIONS

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 .

We have Image
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
Read 6 tweets
21 Jul
1) AN ACT OF WAR: HYPERMETABOLISM MULTIPLE ORGAN FAILURE SYNDROME. ARDS ASSOCIATED WITH COVID-19 IS NOT DUE TO LUNG INFECTION.

The pathophysiology of ARDS was not confined to lungs but is part of a systemic injury-response pattern now known as the hypermetabolism-organ failurr Image
2) syndrome.

THIS IS WHY PATIENTS SUDDENLY DETERIORATE ~ SEVEN DAYS INTO THE DISEASE, IF NOT CLEARED. THE BODY CANNOT KEEP UP WITH THE INDUCED HYPERMETABOLISM. METFORMIN IS USED TO TREAT HYPERMETABOLISM!

This particular syndrome was observed looking at those traumatized in WAR.
3) Does this explain the toxins? It seems the bioweapon is designed to REPLICATE SEVERE TRAUMA! Thereby inducing the hypermetabolism syndrome resulting in ARDS and multiple organ failure.

Is this also the purpose of the SPIKE PROTEIN?

What happens to the body ALSO happens in
Read 4 tweets
18 Jul
1) SARS-CoV-2 INFECTION MIMICS ACUTE SPINAL CORD INJURY VIA SPIKE PROTEIN a7 nAChR ANTAGONISM RESULTING IN HPA AXIS DYSREGULATION AND IMMUNE SYSTEM PARALYSIS

Severe acute spinal cord injury in mice causes massive reduction in a7 nAChR receptors and cholinergic system disruption.
2) The image shows a7 nAChR receptors after acute spinal cord injury in mice compared to (A) control.

The spike antagonistically binds to a7 nAChR recptors, mimicking the cholinergic response to severe spinal cord injury (SCI) - a cascading effect. One of the major impacts of
3) this cascade is to the function of the adrenal gland. In particular, SCI causes hypothalamic-pituitary-adrenal (HPA) dysregulation.

In mice, this dysregulation resulted in devastating immune cell death.

Interestingly, in this situation, “deactivation” of the adrenal glands
Read 9 tweets
15 Jul
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
Read 6 tweets

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