Halal David Andrew Jamison Jr. / Drain Todger / Train Dodger / *THASF* / The Halo and Sonic Fan / Reveille / GNO-SYS / Spartan043 / b00msl4ng / Allan X - Smug Autist, Tried to Solve COVID-19 by Tarding Out on Google, Erotic Brony Fanfiction Author, Still Living With His Parents at Age 30, Self-Doxing Halal Speedrunner, Crashed His Tardmobile Into the Clown Library



I was intentionally dumbing it down.

Now I'm really going to break down SARS-CoV-2 and COVID-19.

This is SARS-CoV-2:

View attachment 26762

The little diagram in the lower-left shows the virus and its structural proteins. Above it is the genome of the virus with its Open Reading Frames and all the bits of code for the various accessory proteins and viroporins.

View attachment 26763

The SARS-CoV-2 virion consists of a shell enclosing a Nucleocapsid (N) protein that shields the virus's RNA genome. Embedded in the virus's membrane are the Spike (S), Envelope (E), and Membrane (M) proteins.

The goal of this virion, like all viruses, is to fuse with a cell, deposit its genetic material into the cell, and hijack its organelles to manufacture more of the virus.

SARS-CoV-2 Spike is a viral fusion glycoprotein with a huge ectodomain consisting of a trimeric head of three S1 subunits and a tiny endodomain embedded in the virus itself. It looks like the world's nastiest turkey drumstick.

View attachment 26764
View attachment 26765

SARS-CoV-2 Spike happens to prefer to fuse to an enzyme known as ACE2, which is a part of the Renin-Angiotensin-Aldosterone system, or RAAS. The way it does this is by the Spike protein undergoing various processing steps, such as palmitic acid attachment, cleavage by furin proteases, and/or cleavage by TMPRSS2, a membrane-bound protease. When the RBD of Spike's S1 subunit fuses with ACE2, TMPRSS2 comes along and cleaves it. That is, an endogenous human protease actually assists the virus and its proteins by cutting and activating them. This signals to Spike that it is within range of its target; the cell membrane. The three S1 subunits fall away, exposing the S2, which unfurls, digs into the cell membrane, and then folds back onto itself, pulling the cell and virus together and fusing them. The viral nucleocapsid containing the genome of SARS-CoV-2 enters the cell.

From there, things get nasty. Coronaviruses actually form DMVs, or double-membrane vesicles, to act as little virus factories. Not to mention, SARS-CoV-2 and other coronaviruses have E and 3a proteins that behave as calcium ion channels, drawing calcium into the cell. This supercharges the intracellular Ca2+ pathways and speeds up cellular metabolism, which increases viral replication at the expense of stressing out the cell. It also selectively encourages and inhibits autophagy, preventing the cell from digesting the virus's DMVs.

Now, why is this a big deal? Well, as it turns out, ACE2, or Angiotensin Converting Enzyme 2, is mostly expressed by vascular endothelial cells. This requires some explanation.

All proteins in the body are produced the same exact way. Some genetic material in the cell nucleus gets reeled out and the ends tagged, RNA polymerase transcribes it from DNA into an mRNA copy, the mRNA leaves the nucleus and encounters ribosomes, the ribosomes read the mRNA and assemble a polypeptide chain using the three-letter codons as a template for tRNAs to deposit their amino acids, and then, the finished protein wiggles free of the ribosome after it hits the stop codon at the end, folding in on itself to become a protein, before moving to the Golgi apparatus for further processing. Proteins work like LEGO bricks, or kinda like Tetris; their behavior is dictated by how they fit together, bind, and interact. Some proteins leave cells and enter the extracellular space to do stuff there, some stay inside the cell to do things inside the cell, and some migrate to the surface of a cell and act as membrane-bound proteins.

ACE2 is one such membrane-bound protein. Its purpose is to catalyze the conversion of Angiotensin II into Angiotensin 1-7, but it also acts to degrade des-arg9-bradykinin.

The action of ACE2 is actually a form of feedback control system. The purpose of the RAAS is to regulate the tonicity (and therefore, volume) of blood by deciding how much sodium and potassium to retain and how much to excrete. It forms a signaling axis between the brain, liver, kidneys, and vascular system that works a little something like this:

If the RAAS isn't working correctly, the body cannot properly manage blood volume and pressure (i.e. osmoregulation). It is an absolutely crucial system.

COVID-19 has largely been mischaracterized by the media as a respiratory disease. It really isn't. SARS-CoV-2 is a vascular virus. In fact, SARS-CoV-2 virions seek out vascular endothelial cells and pericytes to infect, pretty much above and beyond anything else.

Our blood vessels are made up of multiple layers, like so:

View attachment 26766

There's the tunica externa, the outermost layer, the tunica media with the external lamella and smooth muscle, and the tunica intima with the internal lamella, basement membrane, and the vascular endothelium and its glycocalyx. The innermost layer of blood vessels is the one-cell-thick endothelium, which is made up of an interlocking grid of endothelial cells. The endothelium, being the part that interfaces directly with the blood, is studded with various proteins that form signal pathways that regulate vascular tone, blood volume, immune responses, the extravasation of immune cells, et cetera.

It is this layer of ECs that SARS-CoV-2 preferentially infects. This is why it appears to be a "multi-organ" disease; in severe cases, it actually infects the vascular endothelium everywhere, in every organ with blood vessels (which is all of them), leading to sepsis and multiple organ failure.

SARS-CoV-2's attack on blood vessels is so profound, it induces endothelial dysfunction, viremia, and sepsis rather directly. Endothelial cells start sloughing off, exposing the underlying basement membrane. This leads to EC activation and the release of von Willebrand factor, which promotes clotting. The body responds to all of this the same way as if the blood vessels had actually been mechanically cut, by promoting coagulation to counter it. The process actually releases vascular endothelial growth factor and promotes angiogenesis; people with severe COVID-19 tend to have whole new tiny blood vessels try branching off of the ones injured by the virus, a process known as intussusceptive angiogenesis.

In the really severe cases of COVID-19, by now, the patient has severe pulmonary edema, fluid leaking into the air spaces of their lungs, pneumonia and ARDS, and coagulopathy everywhere. I spoke with a nurse along my commute, once. He described a patient who needed both of her legs to be amputated from the knees down because of COVID-19-induced blood clots.

SARS-CoV-2 actually has tropism for far more than vascular ECs, however.

It also attacks...
  • The blood-brain barrier, permeabilizing it.
  • Brain astrocytes and the cardiorespiratory center of the medulla. It can enter the brain by the transcribial route, leading to injury to the olfactory nerve (hence the loss of smell), the parahippocampal gyrus (whoops, loss of memory/brain fog), and the orbitofrontal area (whoops, there go your inhibitions and spatial reasoning). So, when people told me that I was talking shit when I said COVID-19 was neurotropic, they were categorically fucking wrong. Unfortunately.
  • The liver and bile ducts, leading to altered liver enzyme levels.
  • Renal tubules and podocytes, promoting kidney failure.
  • The epithelium of the GI tract (the anal swabs weren't actually a bad idea; the virus is 100% shed in stool and may be transmissible by the oral-fecal route).
  • Pancreatic islet cells. Hello, new-onset diabetes!
  • The seminiferous ducts of the testis.
  • T lymphocytes, directly, by binding to their LFA-1 integrins just like HIV.
  • And much, much more!
The vasoactive peptide known as bradykinin is a part of the little-known kinin-kallikrein system. It plays a role in the condition known as hereditary angioedema, where unregulated bradykinin levels cause, well, angioedema.

Normally, ACE2 acts to reduce blood pressure by converting Angiotensin II, an AT1/2R agonist, into its opposite, Angiotensin 1-7, a MASr agonist.

Ang II and Ang 1-7 have exactly opposite effects. Ang II is proinflammatory and vasoconstrictive, increasing blood pressure, while Ang 1-7 is anti-inflammatory and vasodilatory, decreasing blood pressure.

View attachment 26767

Spike's interaction with ACE2 can potentially affect des-arg9-bradykinin (DABK) levels, since ACE2 also degrades this form of bradykinin. If DABK increases, this would lead to the activation of bradykinin B1 receptors, increasing the concentration of cytosolic Ca2+ ions. That is, calcium.

Intracellular calcium levels play a direct role in oxidative stress. Calcium ions act something like a throttle, turning cellular metabolic processes up and down as needed. If there are too many intracellular calcium ions, it will literally make the mitochondria go berserk like a runaway diesel engine, killing the cell.


These stress processes also promote the release of inflammatory transcription factors, like NF-kB and AP-1 and the like. Inflammation is when cells detect damage and say "oh my god, help me!" and throw out a smoke signal in the form of inflammatory cytokines (little tiny protein beacons) to draw in immune cells to deal with the threat. Those cytokines are produced by transcription factors/pathways like NF-kB which specifically promote the activation of the genes inside cell nuclei to make mRNA that codes for cytokines.

Inflammatory transcription factors being triggered in a cell = "Make smoke signals and draw in neutrophils and macrophages right the fuck now!"

Too much Ca2+ pathway activation and intracellular ROS can actually set off these inflammatory transcription pathways by oxidative phosphorylation of their upstream triggers. ROS means danger, it means the cell is being stressed to death and consuming shitloads of oxygen in the process. Oxygen is kind of like a toxin, in itself. The body handles it with kid gloves every step of the way; here bind to iron, okay, now go here and act as an electron acceptor. It's absolutely necessary for life, but it's also quite destructive, as every pile of rusted iron can attest to.

Vitamin D actually helps counteract this rather directly; it activates Calcium ATPase and pumps excess calcium out of cells. Guess which country is 40% Vitamin D deficient, rising to 60% in Hispanics and 80% in African-Americans? That's right. America.

As a matter of fact, African-Americans have higher rates of endothelial dysfunction than basically anyone else, making them prone to hypertension and heart disease and harming their life expectancy.


Excessive intracellular calcium pathway activity also promotes vascular NADPH oxidase activity, which leads to the release of superoxide ROS into the extracellular space.

Superoxide radicals are also referred to as "kindling radicals", because they act as the precursor to basically all other types of reactive oxygen species. Superoxide also has another nasty little trick. It can interact with vascular nitric oxide to form peroxynitrite.

Healthy blood vessels constantly release nitric oxide (NO) to act as a signaling molecule, because it diffuses rapidly through cell membranes and modulates their activity. Normally, the plasma membrane of cells acts to keep the good stuff like organelles and proteins and genetic material inside and the bad stuff outside. It also acts to demarcate the perimeter of the cell and allow it to serve its function in the body, of course. For human cells and bacteria, for instance, these membranes are made up of a phospholipid bilayer that self-organizes into a wall because of hydrophilic/hydrophobic interactions. NO can zip right through this membrane and send a signal to the interior of a cell.

NO is normally synthesized by endothelial nitric oxide synthase (eNOS), an enzyme that catalyzes its production using tetrahydrobiopterin and L-arginine from the urea cycle as substrates. NO also happens to be antiviral against SARS-like viruses, directly inhibiting the palmitoylation of the Spike. Peroxynitrite, on the other hand, does not do jack shit to stop SARS-CoV-2 from fusing to cells and replicating in them.

When superoxide reacts with nitric oxide (NO) to form peroxynitrite (ONOO-), this ONOO- reacts with the tetrahydrobiopterin cofactor of endothelial nitric oxide synthase, destroying it. This leads to eNOS becoming "uncoupled", having lost one of its necessary cofactors.

The product of the activity of uncoupled eNOS is, horrifyingly enough, more superoxide. Which reacts with any available nitric oxide to produce more peroxynitrite. Which destroys the tetrahydrobiopterin cofactors of more eNOS enzymes. This proceeds in a vicious cycle until all the NO is gone.

This is proven to happen in COVID-19 patients. They have highly elevated nitrotyrosine (nitrated tyrosine, a biomarker of peroxynitrite) and very low nitric oxide levels.

This is where things get a little tragicomic. These cells spewing ROS and cytokines inevitably summon neutrophils. Neutrophils attack pathogens by, uhh, blasting them with hydrogen peroxide and hypochlorous acid. That is, more ROS. Normally, this is a good thing. If bacteria invade a cut in someone's finger, the standard response by the body is to send neutrophils to engulf the bacteria and dissolve their lipid membranes with peroxide and hypochlorous acid.

Just one problem. Human cell walls are made of exactly the same stuff as bacterial cell walls. Normally, cells protect themselves from this carnage by using antioxidant enzymes like glutathione peroxidase, catalase, etc. A great deal of antioxidant pathway activity in the body is governed by Nrf2, a.k.a. Nuclear factor erythroid 2-related factor 2, one of the master antioxidant regulators.

SARS-CoV-2's proteins directly suppress the Nrf2 pathway, increasing cellular susceptibility to oxidative damage.

When neutrophils see all this, they go absolutely crazy, undergoing a process called neutrophil extracellular trap formation. That is, the neutrophils literally start vomiting their own guts everywhere, consisting of histones, nuclear DNA, and pro-oxidant destructive enzymes. They don't care that they're literally spewing out the contents of their cell nuclei; neutrophils are suicide bombers. They are terminally differentiated and always ready to die. They fling their caustic organs at bacteria happily.

The accumulation of neutrophil extracellular traps is known as NETosis, and COVID-19 patients also, technically, suffer from NETosis in their blood vessels, which is a sure sign of sepsis setting in.


These NETs promote even more clotting, and they also contain destructive enzymes that are constantly spewing hypochlorous acid.

This hypochlorous acid is produced in such large amounts, it starts stripping iron out of heme, leaving RBCs incapable of carrying as much oxygen, and unliganded iron floating around in the extracellular space.

Bare iron ions are reactive, the same exact way that iron sitting on a table is reactive and will readily form rust if exposed to air and moisture. Normally, the body stores iron in proteins, like heme iron and ferritin. Bare iron in the body is also referred to as "unliganded iron", because it's not bound to anything.

When you have iron, superoxide, and hydrogen peroxide all in the same place, you get a very nasty pair of chemical reactions called the Haber-Weiss and Fenton reactions:

View attachment 26768

The oxidation states in the iron catalyst flip back and forth. Ferric ions in the +3 oxidation state exposed to Superoxide undergo a redox reaction, making ferrous ions in the +2 oxidation state. Fe2+ and hydrogen peroxide make Fe3+ and hydroxyl radicals in the Fenton reaction.

Hydroxyl radicals are extremely nasty and cannot be detoxified by any enzymes in the body. That is to say, there aren't any enzymes that exist to break these things down. Their half-life in the body is very, very brief. The reaction between hydroxyl radicals and things in their environment is so rapid, whatever they bump into is oxidized in nanoseconds.


When hydroxyl radicals encounter cell membranes, they rip electrons out of them, oxidizing them immediately. This leads to lipid peroxidation and the buildup of lipid hydroperoxides. These lipid hydroperoxides are recognized by the body as foreign objects, which results in autoantibody formation against oxidized lipids, just like systemic lupus erythematosus, a.k.a. fucking lupus. Hydroxyl radicals are actually generated on purpose in industrial settings using hydrogen peroxide and iron catalyst to bleach wastewater streams and destroy biological material in them.

This is what is happening to the cells of a COVID-19 patient. They literally start bleaching out.

This leads to two different forms of cell death, known as ferroptosis and parthanatos.

Ferroptosis is when iron-induced lipid peroxidation kills a cell deader than a doornail.


Parthanatos is when oxidative stress (among other things) leads to PARP-1 overactivation and kills a cell deader than a doornail.


There are a bunch of ways to treat this problem of extreme lipid peroxidation and autoimmune cascade.
  • Prevent excess intracellular calcium influx with Vitamin D or calcium channel blockers.
  • Raise NO levels with dietary nitrate intake, nose breathing, et cetera, for the antiviral and superoxide-scavenging effects.
  • Inhibit the effect of bradykinin with methylene blue.
  • Chelate the excess iron out with deferoxamine.
  • Inhibit the Fenton reaction directly with certain antioxidant substances proven to break up Fenton reactions (i.e. famotidine)
  • Inhibit ROS production by hypoxanthine with allopurinol.
  • Inhibit ROS production by NADPH oxidase with NADPH oxidase inhibitors like apocynin or APX-115.
  • Just pump craploads of glycine and NAC into people to try and bump up their glutathione levels.
These interventions are best employed very early, before the above cascades and irreversible damage set in.

What are doctors doing to treat COVID-19?

First, they put people on ventilators, which pump their lungs up with O2, which causes their oxygen-starved cells to revert from anaerobic to aerobic metabolism, which leads to hypoxanthine and succinate breakdown, which leads to a burst of superoxide release, which promotes the exact ROS cascade I just described (this is called ischemia-reperfusion injury, or, if caused by a ventilator, VILI). It's a catch-22; their cells need oxygen for them to live, of course.

They also give them corticosteroids to try and reduce the inflammation. However, all the ROS attacks glucocorticoid receptors (GR) which results in steroid insensitivity and inflammatory rebound.

So now, the patient has even more ROS in their lungs and even more inflammation.

Hello, jerky lung!

View attachment 26769

Now, why shouldn't you take a COVID-19 vaccine to stop this? Numerous reasons why.

First of all, the vast majority of vaccine doses in the US are the Pfizer and Moderna vaccines. These vaccines are based on mRNA tech that was funded to the tune of hundreds of millions of dollars by DARPA and BARDA for purposes that they haven't elaborated much upon, likely as part of some secret Pentagon biodefense program.

These vaccines use mRNA transfection tech that has never been used on people before. Basically, they use human cells as bioreactors. Gene goes in, protein comes out. This concept is extremely novel and has never undergone long-term testing in humans. In Moderna's case, it's their first-ever commercial product. If you got the Moderna vaccine, you got a company's first-ever product, which went through minimal, highly accelerated testing with a very questionable methodology, and which is excused from legal liability by purchase agreements that specifically indemnify the manufacturer. Good luck!

To make matters worse:
  • The vaccines are not sterilizing and do not prevent transmission.
  • The PEGylated lipid nanoparticles are extremely potent allergens.
  • The pseudouridylated mRNA persists in the body, does not break down quickly, and may inhibit toll-like receptors, reducing immune surveillance of infections and tumor cells.
  • SARS-CoV-2 Spike is an extremely toxic molecule that is capable of aggregating amyloid fibrils, penetrating the blood-brain barrier, inducing inflammation, inhibiting DNA repair, binding to integrins on lymphocytes, and all sorts of other nasty things.
  • Cells that express Spike are targeted by the immune system for elimination, so if the vaccine circulates around the body, it actually paints a bullseye on whatever it transfects, leading to autoimmune attack. This may actually cause heart scarring from myocarditis if the vaccine enters the bloodstream.
Basically, it's reasonable to conclude that this "vaccine" was developed for the purpose of deliberate depopulation and democide. It's basically a slow-kill poison, aging people by amyloidosis, chronic inflammation, and autoimmunity. Why would they do this? Simple. To keep old folk from collecting social security, to deal with overpopulation, and to demolish the world's governments and institutions to pave the way for the NWO.

I cannot even begin to tell you how much all of this smells like glownigger shit. It would blow your fucking mind.
  • All of these foreign DTRA-funded biolabs are connected to the Nunn-Lugar CTR.
  • They move viruses around from facility to facility under a diplomatic cover, using diplomatic vehicles.
  • The money is laundered through NGOs like EcoHealth Alliance, Metabiota, and Labyrinth Global Health.
  • USAID is a CIA slush fund, so the CIA are directly involved in funding them as well.
  • Andrew Huff, the former VP of EcoHealth Alliance, admitted that Peter Daszak, the president of EcoHealth, told him he was working for the CIA. Peter Daszak also helped pen the Lancet lab leak letter exonerating the Wuhan Institute of Virology. He told Ralph Baric not to sign this letter, fearing the conflict of interest it might reveal.
  • Peter Daszak also acted as a Facebook fact-checker and a WHO investigator on the ground in Wuhan, where he investigated himself and found himself not guilty.
  • Anthony Fauci took part in the coverup due to the NIH's culpability in all of this.
  • Ralph Baric took delivery of a Coronavirus mRNA vaccine candidate "jointly owned by Moderna and NIH" a whole month before Moderna claim they even received the sequence for SARS-CoV-2 upon which they based their vaccine Spike sequence. He was also responsible for validating Gilead's Remdesivir, which is very expensive, very toxic to the liver, and doesn't even work.
  • Nathan Wolfe, the head of Metabiota, the NGO funded by Hunter Biden's firm Rosemont Seneca, was a member of EcoHealth Alliance's editorial board, a member of DARPA's now-defunct DSRC, and a direct associate of the child sex trafficker Ghislaine Maxwell.
  • SARS-CoV-2 Spike actually contains a sequence the reverse complement of which is a sequence found in a Moderna patented cell line, which is smoking gun evidence that Moderna were actually involved in the virus's creation.
COVID-19 was not an accident. It was racketeering, fraud, and treason, and there are people who absolutely must be prosecuted and then motherfucking hang for this.
mother fucker, I aint reading all that shit.

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I, too, have an incredible cock-thirst. I wish I was Celestia in this, lapping and sucking at Twilight's big salty futa dick
This is incredibly funny and I totally see david as someone who would say this. What a read that was, and just when I thought I had to be getting done with the OP, David flies in with more weapon's grade autism. Dude is absolutely filthy.


This is incredibly funny and I totally see david as someone who would say this. What a read that was, and just when I thought I had to be getting done with the OP, David flies in with more weapon's grade autism. Dude is absolutely filthy.
who is celestia?