If
@Drain Todger becomes the Jonas Salk of the China Virus, I will rightfully throw myself in front of the Train that took our lord and savior Terry Davis. A long with, I will do what Trumps Chosen do best, and rewrite history to make it look like that I wasn't one of the skeptics. Lemme just find that pesky delete button, that the newest addition to the slow in the mind circus
@coma.baby.jpg tried finding yesterday...
COVID-19’s pathology is extremely complex. Let me start from the beginning.
So, what the hell is it?
COVID-19 is caused by a virus that the International Committee on the Taxonomy of Viruses has named SARS-CoV-2. SARS-CoV-2 is a close genetic relative of SARS-CoV, the virus that causes SARS. It’s about 79% genetically similar to SARS-CoV. As a betacoronavirus, it belongs to the same family of viruses as OC43, HKU1, SARS-CoV, and MERS-CoV, but it is closest to SARS-CoV in its pathophysiology and its method of attack.
All viruses generally work the same way, with some variations. The cells of eukaryotic organisms have receptors on their surface that act as a kind of molecular semaphore system, signaling cells to behave a certain way, converting amino acids, proteins, and peptides, and so on. For instance, cocaine works by binding to the dopamine transporter, tricking it into leaving without its cargo so more dopamine stays behind in the synapse, and beta blockers bind to beta receptors so adrenaline bounces off of them and does nothing, and so on. Viruses have proteins on their exterior that bind to these receptors, fusing the virus to the cell and permitting it to enter the cell in a process called endocytosis. Once inside, the virus breaks down and releases its genetic payload inside the cell, which, in turn, transcribes into instructions for the cell to make more virus. It is exactly like a guy busting into a waffle factory, pointing a gun at the foreman and demanding he make pancakes instead. The cell releases the finished virions, they go on to infect other cells, and so on.
SARS-CoV and SARS-CoV-2 both use a receptor called ACE2, or Angiotensin Converting Enzyme 2, to infect the human body. There are a couple very important things to know about ACE2.
One, ACE2 is part of the RAAS, the renin-angiotensin-aldosterone system. This is a critical part of the human endocrine system that regulates blood pressure and electrolytes. Two, ACE2 receptors are basically everywhere in the body, because, well, look at what their role is. Blood vessels are everywhere.
Here’s how it works.
Angiotensinogen is secreted from the liver. If you have low blood pressure or hyponatremia (low sodium), your kidneys go “Hey, raise blood pressure and sodium retention!” and they release Renin which converts Angiotensinogen to Angiotensin I. Angiotensin I is inert and does nothing. It must be converted into Angiotensin II by Angiotensin Converting Enzyme to activate it. Angiotensin II is subsequently converted to Angiotensin 1-7 by ACE2 catalyzing the hydrolysis of the former into the latter.
It’s a classic feedback control mechanism. ACE raises blood pressure by making Ang II. ACE2 lowers blood pressure by dialing that back and changing Ang II into Ang 1-7.
Now, this is where SARS-CoV-2 comes along and throws a monkey wrench into the whole thing. The virus binds to the ACE2 receptor, right? But it doesn’t just use the receptor and leave it intact. It actually destroys the ACE2 receptor. The receptor itself is collateral damage. The virus doesn’t care. It just wants to enter the cell. It doesn’t give one single fuck that it’s busted down the door in the process.
So, and this is key, ACE2 is down-regulated by the action of SARS-CoV-2 infecting a cell.
What does the down-regulation of ACE2 do?
Nothing good. Angiotensin II, an AT1 receptor agonist, starts building up. An abnormally large amount. This does a number of very undesirable things. For one, it increases aldosterone secretion (hyperaldosteronism). This makes the body lose potassium through the kidneys. It all gets urinated out. It also promotes sodium retention, vasoconstriction, and various kinds of inflammation, oxidative stress, and fibrosis.
www.nature.com
This process releases a cascade of inflammatory cytokines and reactive oxygen species.
Angiotensin II (Ang II) increases adhesion molecules, cytokines and chemokines and exerts a proinflammatory effect on leucocytes, endothelial cells and vascular smooth muscle cells. Acting via the type 1 receptor, Ang II initiates an inflammatory cascade of reduced nicotinamide-adenine...
www.nature.com
www.nature.com
| NF-κB | Nuclear factor-κB |
| IκB | Inhibitor of κB |
| NADPH oxidase | Reduced nicotinamide-adenine dinucleotide phosphate dehydrogenese |
| p47(phox) | p47 protein component of NADPH oxidase |
| TNF-α | Tumour necrosis factor-α |
| IL-6 | Interleukin-6 |
| MCP-1 | Monocyte chemoattractant protein-1 |
| ICAM-1 | Intercellular adhesion molecule-1 |
| VCAM-1 | Vascular cell adhesion molecule-1 |
| ROS | Reactive oxygen species |
| O2• | Superoxide |
| TF | Tissue factor |
| PAI-1 | Plasminogen activator inhibitor-1 |
| AP-1 | Activator protein-1 |
| MMP | Matrix metalloproteinase |
| CRP | C-reactive protein |
| SAA | Serum amyloid A |
It also up-regulates the receptors for the kinin-kallikrein system. Yes. That’s actually a thing in the body. No, it’s not something from some sci-fi. One of the reasons why you hardly ever hear of the kinin-kallikrein system is because scientists don’t really know what it even does, even though they discovered it like a hundred years ago when they injected piss into people. I shit you not.
The system was discovered in 1909 when researchers discovered that injection with
urine (high in kinins) led to
hypotension (low blood pressure).
[3] The researchers
Emil Karl Frey,
Heinrich Kraut and
Eugen Werle discovered
high-molecular weight kininogen in urine around 1930.
[4]
Each one of these things is useful in moderation, but bad in excess. COVID-19 triggers a ridiculous excess of all of these factors. NF-
κB? Inflammation. NADPH oxidase? Production of ROS and, therefore, oxidative stress. TNF-
α? Inflammation. IL-6? Inflammation. MCP-1/CCL2? It would attract monocytes to the lungs and cause fibrosis. ICAM-1 and VCAM-1 make leukocytes stick to the interior walls of blood vessels. Tissue Factor/CD142 and PAI-1 promote clotting. MMP promotes remodeling of the extracellular matrix. High CRP is often seen in inflammatory contexts.
SARS-CoV-2 does a bunch of other nasty things, too.
- It can invade not only ACE2 receptors, but also CD147/Basigin receptors.
- It dysregulates the balance of electrolytes in the body.
- It depletes nitric oxide bioavailability.
- It disrupts lipid metabolism.
- It disrupts the urea cycle.
- It disrupts normal iron metabolism.
- It kills T lymphocytes.
- It reduces interferon and blunts the innate immune response.
- It encourages cell-to-cell fusion and the formation of multinucleated giant cells.
- It lures megakaryocytes from the bone marrow into the heart.
The sum total of these effects—and the ways in which they interact—is what creates the syndrome of COVID-19.
What does a COVID-19 patient look like?
This is where things get into mindfuck territory. A COVID-19 patient can look like basically anything. If someone comes into the hospital and they have new-onset seizure, encephalitis, meningitis, stroke, heart attack, pulmonary embolism, kidney failure, pneumonia, testicular pain, or what looks like abdominal pain or gastroenteritis, all of those could be COVID-19. That doesn’t mean COVID-19 is hard to detect. Not at all. It has a very specific profile when they start doing a patient’s labs. This mimicry is only a problem if you aren’t looking for it or you don’t know what it looks like. The mimicry is bad for a number of reasons. They could start treating the patient as a heart attack patient or whatever, and not take appropriate precautions for a respiratory disease, getting the healthcare workers sick. It could also delay the proper interventions. This is why, if COVID-19 is suspected, immediate testing and lab work must be done.
When a COVID-19 patient comes into the ER, this is typically what they have:
- Fever
- Dry Cough
- Shortness of Breath
- Hemoptysis (coughing up small flecks of blood)
- Ground-glass opacities in lungs on CT scan
- Low O2 Saturation (<90%)
- Anosmia (loss of sense of smell)
- Abnormal AST/ALT (abnormal liver enzyme levels)
- Lymphopenia (low lymphocytes)
- Thrombocytopenia (low Platelets)
- Hypokalemia (low blood potassium because of hyperaldosteronism)
- Elevated D-dimer (high breakdown products from blood clots)
- Elevated Ferritin (high free iron in circulation)
- Elevated C-Reactive protein (a sign of severe inflammation)
- Albuminuria (albumin in urine)
- Hematuria (blood in urine)
What follows is a fairly comprehensive list of the actual disorders caused by COVID-19 (don’t panic; some of these are much rarer than others; only critical patients will experience nearly all of these at the same time):
- Pulmonary
- Bilateral Viral Pneumonia
- Pulmonary Edema
- Pulmonary Fibrosis
- Pulmonary Embolism
- ARDS
- Vascular
- Endotheliitis
- Viremia
- Systemic Capillary Leak Syndrome
- Antiphospholipid Syndrome
- Coagulopathy
- Shock
- Kawasaki Disease (in pediatric cases, especially)
- Diffuse Intravascular Coagulation
- Metabolic
- Dyslipidemia
- Urea Cycle Disorder
- Hyperferritinemia
- Hepatic
- Renal
- Hypokalemia
- Acute Kidney Injury
- Neurological
- Encephalitis/Meningitis
- Mental Issues/Impaired Consciousness
- Skeletal Muscle Injury
- Cerebrovascular Disease
- Guillain-Barre Syndrome
- Dysautonomia
- Anosmia
- Dysgeusia
- Seizure
- Stroke
- Cardiac
- Myocarditis
- Pericarditis
- Heart Attack
- Arrhythmia
- Gastrointestinal
- GI Inflammation/Injury
- Diarrhea
- Nausea/Vomiting
- Abdominal Pain
- Reproductive
- Skin & Eyes
- Acro-ischemia
- Conjunctivitis
- Rash
- Transient Livedo Reticularis
- Systemic
- Bacterial Co-infections
- Cytokine Release Syndrome
- Multiple Organ Failure
When confronted with an intimidating-looking list like this, the typical reaction is to assume that it’s a hoax and that there’s no way a highly contagious respiratory disease could cause any of these things, but I assure you, any of these complications can occur due to COVID-19.
The typical course of COVID-19 is somewhat straightforward. The incubation period is about 2 to 27 days, with 5 days being the median. This is followed by about 5 to 7 days of what looks and feels like a rough flu, which is technically the best time to be treated with aggressive antiviral therapy (as in, if someone suspects they have it at this phase, they should go to the hospital immediately and get antivirals, not assume that it’s some other, less severe respiratory disease and they can tough it out). After that, there is a brief latent period where it seems like the flu-like symptoms are gone, and then, this is followed by about 9 to 12 days of severe systemic inflammation that ends in either recovery or death. It takes about 19 to 24 days from the point of infection before someone usually recovers from COVID-19 or dies of it. Some patients experience symptoms for periods as long as three months or more. There is a significant lag period. People who were just infected yesterday won’t be healthy and virus-free until September.
The early phase of the virus can be treated with antivirals, but the late, inflammatory phase is mainly treated with steroids, because that’s not the virus. That’s your own body, tricked by the virus into attacking itself. This is essentially the hallmark of SARS-like pathology. Immune under-reaction allows the virus to replicate and damage cells with impunity at first, and immune over-reaction brings on waves of devastating inflammation.
SARS-CoV-2 can enter the body through the respiratory system, through the eyes, through the olfactory nerve, or from being ingested and binding to the GI tract. Once inside, it has some specific targets it likes to attack, particularly the endothelial lining of blood vessels, brain stem, lungs, heart, liver, kidneys, GI tract, and testicles. It gets into the lining of blood vessels and triggers extreme vascular permeability and clotting, causing the bloodstream to fill with blood clots and the blood itself to turn thick and goopy. The capillaries of the lungs start leaking plasma into the alveoli. Viremia passes the virus into each of the vital organs, and it triggers hyper-inflammation inside each one it reaches while also starving them of oxygen. In a typical critical COVID-19 patient who ends up in the ICU on a ventilator, death does not occur because of pneumonia. In fact, the pneumonia tends to be somewhat manageable. Rather, the coagulopathy goes out of control and a blood clot completely cuts off oxygen to one of the vital organs. That means the cause of death is usually heart attack, stroke, PE, diffuse intravascular coagulation, and so on.
Sequelae of COVID-19 are very similar to SARS. Chronic fatigue syndrome, chronic pain, lung fibrosis, and mental issues like brain fog, difficulty concentrating, depression, and so on. This is not the flu. COVID-19 causes
permanent lung and brain damage. Many patients lose as much as 30% of their lung capacity and cannot resume normal activities after recovering. There’s no telling what would happen if they were to get reinfected, or how many millions of people will end up on disability after recovering from COVID-19.
Why is SARS-CoV-2 so much more contagious than SARS-CoV?
COVID-19 is extremely contagious. It is readily aerosolized and can travel 15 feet from someone’s mouth or nose, easily. The reason why SARS-CoV-2 has spread so far and SARS-CoV fizzled out is because SARS-CoV-2 has many, many times the ACE2 binding affinity of SARS-CoV. The key genetic differences pertain to the Spike protein of the virus.
SARS-CoV-2’s Spike has furin cleavage sites that the spike of SARS-CoV lacked. This makes the spikes remarkably similar to HIV gp120 proteins and extremely infectious to human cells. Furin is ubiquitous in the human body.
www.nature.com
Did this thing come out of a laboratory?
Yes, it did. RaTG13, its supposed ancestor, does not exist. It’s a made-up gene sequence, fabricated by the CCP to give SARS-CoV-2 the appearance of having mutated from a wild virus. SARS-CoV-2 has an extremely high binding affinity for human ACE2, but not animal ACE2. There are no intermediate animal hosts for this virus. It is a GOF pathogen, modified by human hands to make a disgusting bioweapon that causes panic and mass casualties to tie up medical resources and hamstring emergency response. Any scientist who says there is no way to prove SARS-CoV-2 came out of a laboratory is a liar.
www.pharmatimes.com
theconversation.com
archive.vn
slate.com
www.thenewbieguide.se
