For a long time, they indeed used CGI images of the virus. When I google Coronavirus under microscrope I find a few images:
Anything can be faked tho, I mean, I'm not saying Covid is fake but still.
@
Drain Todger thanks for digging deep. I had a nasty feeling *they* are all connected....
They're small. Very small. Like 120nm across. That's only a couple times the width of a transistor gate from the late 90s.
@borsabil
@Lichen Bark
SARS-CoV-2 pathogenesis, based on everything I've seen, goes something like this. SARS-CoV-2 Spike fuses the virus to a cell and it releases its genome into a cell, but the Spike binding to ACE2 also down-regulates ACE2's function, causing bradykinin to over-accumulate. Bradykinin increases cAMP, cGMP, COX, and intracellular Ca2+ signaling. The virus's own proteins, E and 3a, behave as viroporins, introducing even more calcium into the cell. Through various processes, vis a vis increased intracellular calcium consumption, the endoplasmic reticulum is made to dump its calcium stores. This greatly increased intracellular calcium signaling is further enhanced by increased GRP78 activity, which also encourages mitochondrial membrane permeabilization. The virus's own proteins also suppress the Nrf2 antioxidant pathway. The infected cells start pumping out tons of superoxide radicals. Superoxide forms peroxynitrite with nitric oxide, which is proven by how COVID-19 patients have elevated serum nitrotyrosine, a nitrosative stress marker indicative of the presence of peroxynitrite. Peroxynitrite destroys the BH4 cofactor needed by NOS to make nitric oxide, causing NOS to become uncoupled and pump out more superoxide instead, further increasing the depletion of nitric oxide and formation of peroxynitrite in a feedback loop. The virus loves this, since nitric oxide is actually antiviral against SARS-CoV-2's Spike, preventing the palmitoylation of the Spike and reducing its binding efficiency; this is why people with endothelial dysfunction (diabetes, obesity, hypertension, old age, African-American race) suffer more severe COVID-19 illness; they have lower nitric oxide levels by default due to redox equilibrium differences. All this superoxide forms hydrogen peroxide from superoxide dismutase enzymes. Then, myeloperoxidase enzymes take hydrogen peroxide and chlorine ions in the body and make hypochlorous acid, which is way more reactive than sodium hypochlorite bleach.
The excess of hypochlorous acid bleaches iron out of heme, reducing the oxygen-carrying capacity of blood. This is why ventilators do nothing. In fact, not only do ventilators do nothing, they are potentially hitting an oxidative stress bomb and blowing it up by supplying enzymes like xanthine oxidase (which are over-activated in hypoxia and ischemia) with the oxygen they need to make even more reactive oxygen species.
The free iron, hydrogen peroxide, and superoxide combine to make deadly hydroxyl radicals that attack various lipids, DNA, et cetera. Phospholipids, PUFAs, cardiolipin, and so on. This results in aggressive lipid peroxidation and the formation of OSEs, or oxidation-specific epitopes. The oxidized fats are recognized by the immune system as foreign objects and attacked with autoantibodies. They also trigger receptors that detect DAMPs, which activates more transcription factors that pump out more inflammatory cytokines, which summons even more immune cells to blast the area with even more reactive oxygen species, oxidizing even more lipids, and producing even more damage. This occurs in a feedback loop until the patient dies in the ICU of neutrophilia, coagulopathy, and acute sepsis.
The cure for this is not Ivermectin, HCQ, Kaletra, or Remdesivir. In fact, antivirals do not work very well at all on COVID-19 if someone has hyperinflammation symptoms, which is the point where most of these patients are being enrolled in these sham clinical trials for antivirals that demonstrate absolutely nothing about their prophylactic effects. The reason for this is because the viral load of COVID-19 peaks right when someone becomes symptomatic and tapers off to almost nothing by the time hyperinflammation sets in, which means that the ideal window of time for antiviral therapy (pre-exposure, or immediately post-exposure) has been missed.
The cure for this ROS-driven inflammation is an aggressive, proactive regimen of potent antioxidants that scavenge superoxide, peroxynitrite, hydrogen peroxide, hypochlorous acid, and hydroxyl radicals or inhibit their production. This, in turn, raises nitric oxide levels and prevents stripping of heme iron.
There are dietary supplements people could be taking right now to improve this state of affairs:
- Vitamin A
- Vitamin C
- Vitamin D
- Vitamin E
- NAC
- Selenium
- Zinc
- Dietary Nitrate
- Curcumin
- Quercetin
- Resveratrol
There are also plenty of drugs with antioxidant effects.
- Melatonin (scavenges peroxynitrite)
- Fluvoxamine (scavenges ROS)
- Indomethacin (prevents iron-driven oxidation of arachidonic acid into isoprostanes)
- Budesonide (not just an inhaled steroid; actually scavenges superoxide and peroxynitrite)
- Apocynin & Paeonol (dimerized into diapocynin by myeloperoxidase; potent inhibitor of NF-kB and ROS-producing enzymes in neutrophils)
- Famotidine (scavenges hydroxyl radicals)
- Cimetidine (scavenges hydroxyl radicals)
- Ranitidine (scavenges hydroxyl radicals)
How long have I been saying people should be given antioxidants for this disease? A year? More? Scientists very early on noticed that neutrophil-driven lung damage was a key feature of ARDS and that defanging neutrophils with antioxidants may help with that. There were people on ResearchGate back in March of 2020 who were like "wait a minute, let's use antioxidants".
Instead, they shove a tube down people's throats and hit an oxidative stress bomb with even more oxygen. Because Fauci said so.
They're straight-up killing people.
