Коронавирус (COVID-19)

Vanlok

deus ex machina
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Spike Proteins Trigger the Clotting Cascade
Many other cells, including lung epithelial cells, enterocytes lining the small intestines, and cardiac pericytes, all express ACE2.

Spike proteins don’t only activate epithelial cells (EC) and promote localized inflammation. They also promote systemic inflammation as ACE2 is almost everywhere inside our major organs and tissues.

Consequently, more pro-inflammatory genes are expressed. More and more immune cells are attracted and sent to the injured or infected tissues (vessels in the lung, heart, gut, etc).

A number of subsequent events collectively contribute to the clotting cascade:

  1. Complement-mediated inflammation of epitheliums (endothelialitis): Spike proteins docking on ACE2 ECs activates the complement pathway and coagulation cascade, resulting in a systemic endothelialitis (lung injury) and procoagulant state (tendency to develop blood clots).
  2. As the complement destroys the endothelium, the procoagulant von Willebrand factor (vWF) and FVIII are released. A significant increase of vWF can form multimers that promote thrombus growth. vWF is secreted mainly from endothelial cells and from a-granules of platelets (megakaryocytes derived). This is comparable to the string in the “beads and string” of a necklace where the beads represent platelets.
  3. Platelet storm: Platelets are a small fragment of the megakaryocytes. The complement anaphylatoxins C3a and C5a activate platelets and increase the production of tissue factor further promoting a clotting forming state.
    ACE2 receptors are present on platelets, and this may contribute to the massive platelet aggregation, which is a characteristic of severe COVID-19 infection.
  4. Activation of neutrophils leads to formation of neutrophil extracellular traps (NETs), a process sometimes referred to as NETosis, which contributes to thrombosis.
  5. EC injury is compounded by toll-like receptor (TLR) activation by viral RNA recognition, with resulting increased reactive oxidative species (ROS) production. The increased ROS further upregulates the expression of vWF.
  6. Spike protein can induce expression and secretion of a series of clotting proteins which cascades into the clotting process, including factor (F)-V, thrombin, and fibrinogen to promote clotting process.
Spike Protein Dysregulates RAAS, Worsening the Clotting State
Due to the spike protein directly interacting with ACE2 expression, COVID-19 patients showed an elevated level of serum angiotensin II indicating a dysregulation of the RAA system (renin angiotensin aldosterone system, or RAAS).

Traditionally, people think angiotensin II is a neurohormone that stimulates the constriction of vascular smooth muscle cells and is responsible for salt and water balance.

However, there have been abundant studies supporting the idea that angiotensin II is capable of initiating and upregulating inflammatory responses, worsening the clotting state.

Epoch Times Photo


In a regulated and self-limited immune response, these mechanisms help to calm down the local injury, with subsequent healing and returning to a resting EC state.

However, for predisposed COVID-19 patients or vaccinated people, the factors strengthening clot formation are way heavier than healing mechanisms, all of which lead to an escalating thrombotic cascade.

Here is a short summary of the first scene of the clot story: spike induced endothelial disruption, massive amounts of vWF released, a subsequent platelet storm, hypoxia induced upregulation and activation of vWF, fibrous network from neutrophil extracellular traps (NETs), as well as increased angiotensin II level, all adding up to initiate thrombogenesis.

This is how the clotting mechanism comes to be. Furthermore, the upcoming second scene takes another pivotal part in the whole story.

A COVID vaccine instructs the cells to produce large quantities of spike proteins. Normal biochemical and physiological processes are “hijacked” in order to make an abnormal amount of these spike proteins.

These abnormal amounts of spike protein have more surprising direct effects on clots.

Spike Proteins Directly Disrupt the Clot Dissolving Mechanism
In a normal healthy person, the body will, in the presence of a blood clot, break it down by a process of fibrinolysis. This is a natural healing and balancing mechanism to prevent an abundance of blood clots.

During this process, Tissue Plasminogen activator (TPA, coming from the endothelium) helps plasminogen change into plasmin and then generate d-dimer (a small protein fragment left when a blood clot dissolves).

It has been discovered that fibrinogen in blood can clot into an abnormal “amyloid” form of fibrin that (like other β-rich amyloids and prions) is relatively resistant to proteolysis (fibrinolysis).

This is strongly manifested in the platelet-poor plasma (PPP) of individuals with long COVID. The extensive fibrin amyloid microclots can persist.

In an outstanding study by Grobbelaar published in Bioscience Reports in August 2021, the biomarker S1 (or the intruding part of the spike protein) alone can induce fibrin resistance to fibrinolysis, leading to unopposed microclot formation.

When spike protein S1 was added to healthy PPP, it resulted in structural changes to β and γ fibrin(ogen), complement 3, and prothrombin. These proteins were substantially resistant to trypsinization in the presence of spike protein S1.

Hence, the results suggest that the presence of spike protein in circulation may contribute to the hyper clotting status, and may cause substantial impairment of the clot dissolving process.

Such lytic impairment may result in the persistent large microclots that people have reported and which have been found in plasma samples of COVID-19 patients.

These microclots block up capillaries, and thus to limit the passage of red blood cells, and hence oxygen exchange, which can actually underpin the majority of these symptoms.

Spike Proteins Form Amyloid-Like Substance
Furthermore, to everyone’s surprise again, spike proteins are identified to present seven amyloidogenic sequences and are able to form amyloid-like substances.

In other words, these spike proteins are similar to those beta-amyloid or tau or alpha-synuclein like substances which may cause neuronal loss in Alzheimer’s or Parkinson’s disease patients.

Their structure makes it easy to form tighter string-like bonded structures with longitudinal twisting as well as cross binding, forming a fibrous-like structure visible under the microscope.

Researchers have found that plasma samples from long COVID patients still contain large anomalous (amyloid) deposits (microclots), which are resistant to fibrinolysis (compared to plasma from controls and diabetes), even after trypsinization (cell dissociation after an enzyme breaks down proteins).

After a second trypsinization, the persistent pellet deposits (microclots) were solubilized. Various inflammatory molecules substantially increased in both the supernatant and trapped in the solubilized pellet deposits of COVID-19, versus that of the control samples.

Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits.

Significant abnormal amyloid microclot formation that are resistant to fibrinolysis, increased α2AP, and the surge of acute phase inflammatory molecules may therefore be central contributors in both COVID-19 infection and as well as COVID vaccine-related syndrome.

Spike Protein Inhibits Another Anti-Clot Mechanism
Spike protein is just one surprise after another.

It’s been reported that the spike protein can competitively inhibit the bindings of antithrombin and heparin cofactor II to heparin, causing abnormal increase in thrombin (clotting) activity.

SARS-CoV-2 spike proteins at a similar concentration (~10 μg/mL) as the viral load in critically ill patients can directly cause blood coagulation and thrombosis in the zebrafish model.

To summarize, these unexpected negative effects of spike protein on the dissolving process of blood clots, plus its amyloid nature, all may be the key contributory factors to the abnormal, lengthy fibrous clots observed in COVID-related conditions.

Spike Protein Is the Smoking Gun
There is clinical evidence that the SARS-CoV-2 spike protein has been detected in clots retrieved from COVID-19 patients with acute ischemic stroke and myocardial infarction.

Recent research conducted by cardiologists from the University of Colorado sheds light on the crucial role of spike protein in the pathology of COVID and COVID vaccine-related injuries.

They analyzed seven COVID-19 patients and six mRNA vaccinated patients with myocardial injury and found nearly identical alterations in gene profiling patterns that would predispose them to clotting state, inflammation, and myocardial dysfunction.

In other words, regardless of whether the myocarditis was caused by the virus or vaccine, the expression of genes responsible for prothrombotic state in response to spike protein, inflammation, and myocardial dysfunction, exhibited similar changes.

Based on gene analysis, COVID-19 and post-mRNA vaccine injury have a common molecular mechanism.

The altered genes pattern includes down-regulation in ACE2, ACE2/ACE ratio, AGTR1, and ITGA5, and up-regulation in ACE and F3 (tissue factor).

What is more alarming and not reported before is that microvascular thrombosis has been found in post-vaccinated patients, indicating that spike protein itself is able to trigger blood clots in susceptible patients.
 

Björn

Does Your Mother Know?
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добро бе, што е факинг ова?

кликнете да прочитате
на кој ли му текнало ова да го напраи и зашто?
 
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Првпат гледам сега и овде на темата што е тоа Коронавирус и Ковид? Без зафрканции некој да објасни гледам сериозно било пред 2 години?
 

Miss.Independent

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Првпат гледам сега и овде на темата што е тоа Коронавирус и Ковид? Без зафрканции некој да објасни гледам сериозно било пред 2 години?
мачкина кашлица
 
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На државно е беспари.
...па дури се фрлаат антиген тестовите им поминал рокот, никој ниту сака да се тестира поради сеуште важечки протокол да биде во изолација 5,7 дена, ако се докаже позитивен со коронавирусот.
 
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На државно е беспари.
Ми треба 24 часа пред операција. А за операцијата не се знае точен датум. Не верувам дека ќе може државно за еден ден да закажам, тестирам и добијам резултати.
 
Член од
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Ми треба 24 часа пред операција. А за операцијата не се знае точен датум. Не верувам дека ќе може државно за еден ден да закажам, тестирам и добијам резултати.
...антигенските тестови се единечни, земи го и чувај го до пред операција, а како така кога сите имаат опертивци ги имаат пред да оперираат да ги проверат пациентите?
 
Член од
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...антигенските тестови се единечни, земи го и чувај го до пред операција, а како така кога сите имаат опертивци ги имаат пред да оперираат да ги проверат пациентите?
Ми беше назначено PCR тест ден пред операцијата, инаку се работи за артроскопија на скочниот зглоб за кој зборев баш со тебе во темата дежурна ординација
 
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Ми треба 24 часа пред операција. А за операцијата не се знае точен датум. Не верувам дека ќе може државно за еден ден да закажам, тестирам и добијам резултати.
Како сакаш, ако се координираш со твојот матичен ќе завршиш работа без проблем. Ако поради некоја причина не сакаш/можеш тогаш мислам дека по 1000 денари се тестовите горе-доле секаде. Никоб Лаб долго време имаа најефтини тестови но не знам како стојат сега со цените, освен за операција или некоја дијагностикака како спирометрија никој не се тестира за ковид повеќе.

Инаку колку што знам за операција треба ковид тест не постар од 72 часа те 3 дена. Не сум сретнал до сега да му треба на некој 24 часовен.
 
Член од
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Како сакаш, ако се координираш со твојот матичен ќе завршиш работа без проблем. Ако поради некоја причина не сакаш/можеш тогаш мислам дека по 1000 денари се тестовите горе-доле секаде. Никоб Лаб долго време имаа најефтини тестови но не знам како стојат сега со цените, освен за операција или некоја дијагностикака како спирометрија никој не се тестира за ковид повеќе.

Инаку колку што знам за операција треба ковид тест не постар од 72 часа те 3 дена. Не сум сретнал до сега да му треба на некој 24 часовен.
Така нагласи докторот 24 часа иначе и јас би сакал на државно. Точно никоб лаб се 1000 денари и се најефтини. Ѕвонев по сите. Генеа 1300 другиве по 2000.
 

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