Wuhan Coronavirus: Megathread - Got too big

[Quixotic Man]

I have no idea if this is real or fake, which in itself is kind of scary.

View attachment 2438307

I don't know. To me that reads as someone being nervous for going in front of the camera, and for some reason they went with the first take.

 

[SneedEyeMitch]

I don't know. To me that reads as someone being nervous for going in front of the camera, and for some reason they went with the first take.

It can be seen as that, she'll literally shaking and sounded like she broke into tears/laughter before cut off.

 

[A Proud Black Woman]

Does anyone have a screen shot of an idiot posing with their vaccination card with the lot number and date visible?

Thanks, I need it to play Minecraft.

 

[King Dead]

Deaths are catching up, hospital and ICU admissions are also spiking. Keep in mind that more than 90% of elderly in Israel are fully vaccinated.

Spoiler

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I did a comparison of the case/death graphs because I was curious:


Now, the usual disclaimers apply (I am not a statistician or medical professional, these graphs are a rolling 7-day average, data may not be fully accurate), but it looks to me that this wave is indeed less deadly than previous, which is what you'd come to expect. The timing is weird though since we're still months away from fall and winter when the previous spikes occurred, which does make me a bit concerned that the shots are indeed fucking with people's natural immunity. Time will tell, I suppose.

 

[Black Yoshi]

CDC BTFO

 

[JosephStalin]

 

[Drain Todger]

These people are criminals. They planned all of this.

 

[FarmerKhourtney]

I’ve seen that chicken pox comparison on our local news several times recently. TBH it does sound scary but then didn’t they already say it was more contagious than the flu etc ten times as contagious yada yada I wish they’d just give it to us straight

 

[The golden neckbeard]

I have no idea if this is real or fake, which in itself is kind of scary.

View attachment 2438307

stage fright

suffered from major anxiety is my teenage years. That is exactly 100% what that is.

aka: PTSD shivers...Its authentic but probably emotionally attached to something she saw recently or in the past.

Probably not related to what she has seen. If you are not a social person this happens when you are thrust front and center

My dad used to chain me to the waterheater in a dark closet for hours on end when i was a kid and beat the shit out of me when he was drunk and lost money gambling. Took me 20 years to get over that shit. Lots of couch therapy. But i would get like this in high school or around people for awhile when i had to give a presentation or whatever

 

[LowLowHighLow]

Sweden had not suffered a single Covid death for months until July when they started to spike up. Sweden is maybe the only country on the planet that actually stuck to the pandemic response plan that was considered best practice prior to 2020, protect the vulnerable as best you can, allow for some restrictions on public gatherings, but otherwise encourage herd immunity, and guess what? It worked. Covid was done with, but of course being full of gullible white people they also got on board the vaccine train and in June vaccination rates started to ramp up and now they're starting to see Covid cases and some death occur again.

I assume that the charts relate to Sweden? If so: where did you get these numbers from?
https://ourworldindata.org/covid-deaths is telling a completely different story.

This doesn‘t show that the vaccine is doing some crazy shit (at least not yet) - if anything, then that it works in reducing deaths.

However what the data may indicate, is, that covid overall was (and hopefully is) getting less deadly - the "wave" in April 21 was nearly as huge as the wave in January 21, but the death count spike in April was only a 1/6th of the one in winter.

 

[tehpope]

The Coachella and Stagecoach music festivals will require fans to show proof of vaccination in order to attend, festival organizers have announced.

Coachella, Stagecoach festivals to require fans to show proof of vaccination in order to attend

The Coachella and Stagecoach music festivals will require fans to show proof of vaccination in order to attend, festival organizers announced Thursday.

abc7.com

"We have come to the conclusion that, as a market leader, it was up to us to take a real stand on vaccination status," said Jay Marciano, chairman and CEO of AEG Presents.

"Just a few weeks ago, we were optimistic about where our business, and country, were heading. The Delta variant, combined with vaccine hesitancy, is pushing us in the wrong direction again. We realize that some people might look at this as a dramatic step, but it's the right one. We also are aware that there might be some initial pushback, but I'm confident and hopeful that, at the end of the day, we will be on the right side of history and doing what's best for artists, fans, and live event workers,'' he added.

I wanna see how attendance fares now from 2019 to 2022.

 

[knobslobbin]

 

[tehpope]

https://twitter.com/disclosetv/status/1425792790387204099

 

[Drain Todger]

COVID-19's hyperinflammation is characterized by the presence of overactivated neutrophils, monocyte-derived alveolar macrophages, and CD4+/CD8+ T cells.

Neutrophils and COVID-19: The road so far

The SARS-Cov2 infection triggers a multisystem inflammatory disorder, knowing as COVID-19, a pandemic disease. This disease is characterized by acute respiratory distress syndrome, cytokine-driven hyperinflammation, and leukocytes count changes. The innate immune response has been linked to COVID-19 immunopathogenesis (e.g., dysfunctional IFN response and myeloid inflammation). In this regard, neutrophils have been highlighted as essential effector cells in the development of COVID-19. This review summarized the significant finds about neutrophils and its effector mechanisms (e.g., neutrophils enzymes and cytokines, neutrophil extracellular traps) in COVID-19 so far.
Keywords: Inflammation, Chemokines, NETs, SARS-CoV2

It is also characterized by an excessive release of hypochlorous acid by myeloperoxidase enzymes via NETosis:

A Multiple-Hit Hypothesis Involving Reactive Oxygen Species and Myeloperoxidase Explains Clinical Deterioration and Fatality in COVID-19

Multi-system involvement and rapid clinical deterioration are hallmarks of coronavirus disease 2019 (COVID-19) related mortality. The unique clinical phenomena in severe COVID-19 can be perplexing, and they include disproportionately severe hypoxemia ...

www.ncbi.nlm.nih.gov

Multi-system involvement and rapid clinical deterioration are hallmarks of coronavirus disease 2019 (COVID-19) related mortality. The unique clinical phenomena in severe COVID-19 can be perplexing, and they include disproportionately severe hypoxemia relative to lung alveolar-parenchymal pathology and rapid clinical deterioration, with poor response to O2 supplementation, despite preserved lung mechanics. Factors such as microvascular injury, thromboembolism, pulmonary hypertension, and alteration in hemoglobin structure and function could play important roles. Overwhelming immune response associated with “cytokine storms” could activate reactive oxygen species (ROS), which may result in consumption of nitric oxide (NO), a critical vasodilation regulator. In other inflammatory infections, activated neutrophils are known to release myeloperoxidase (MPO) in a natural immune response, which contributes to production of hypochlorous acid (HOCl). However, during overwhelming inflammation, HOCl competes with O2 at heme binding sites, decreasing O2 saturation. Moreover, HOCl contributes to several oxidative reactions, including hemoglobin-heme iron oxidation, heme destruction, and subsequent release of free iron, which mediates toxic tissue injury through additional generation of ROS and NO consumption. Connecting these reactions in a multi-hit model can explain generalized tissue damage, vasoconstriction, severe hypoxia, and precipitous clinical deterioration in critically ill COVID-19 patients. Understanding these mechanisms is critical to develop therapeutic strategies to combat COVID-19.

Now, read that abstract again:

However, during overwhelming inflammation, HOCl competes with O2 at heme binding sites, decreasing O2 saturation.

Hypochlorous acid is so reactive, it crowds out oxygen and prevents hemoglobin from accepting it. Sound familiar? What disease do you know of where they intubate people and they still can't get oxygen into their red blood cells?

There is already a substance that could, in all likelihood, treat or prevent the hyper-inflammation of COVID-19. It's called Apocynin, or Acetovanillone. It is one of the main constituents of the Picrorhiza Kurroa root which is found in Ayurvedic medicine, where the ground-up root is known as Kutki powder. However, we also have chemically-isolated, pure Apocynin, as well, which is vastly more potent.

DEFINE_ME

Ischemia and reperfusion (IR) of isolated sheep lungs caused polymorphonuclear leukocyte (PMN) sequestration, pulmonary hypertension secondary to thromboxane (TX), edema, and increased vascular permeability.
1
PMN depletion attenuated this injury, suggesting that PMN-derived O2 radicals were involved.
2
Apocynin (Apo) is a methoxy-substituted catechol that requires activation by myeloperoxidase to inhibit the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and thus prevents O2− production from activated PMN leukocytes. To determine the effect of Apo in IR injury, we subjected 20 sheep lungs to 30 min of ischemia and 180 min of reperfusion with blood. We injected 3 mM, 0.3 mM, 0.03 mM Apo, or diluent (n = 5 each) into the pulmonary artery early in ischemia and the reservoir before reperfusion. Peak pulmonary artery pressure, peak perfusate TXB2 concentration, and the reflection coefficient for albumin were measured (Table 1) . The ability of Apo to inhibit in vitro O2− production from zymosan-activated sheep PMN leukocytes was also assessed (n = 3).

It has also been compounded with paeonol to create APPA, which is being investigated as a drug for osteoarthritis:

APPA (apocynin and paeonol) modulates pathological aspects of human neutrophil function, without supressing antimicrobial ability, and inhibits TNFα expression and signalling - Inflammopharmacology

Neutrophils are key players in the pathophysiological process underlying inflammatory conditions not only by release of tissue-damaging cytotoxic enzymes, reactive oxygen species (ROS) but also by secretion of important immunomodulatory chemokines and cytokines. Here, we report the effects of...

link.springer.com

Neutrophils are key players in the pathophysiological process underlying inflammatory conditions not only by release of tissue-damaging cytotoxic enzymes, reactive oxygen species (ROS) but also by secretion of important immunomodulatory chemokines and cytokines. Here, we report the effects of the novel agent APPA, undergoing formal clinical development for treatment of osteoarthritis, and its constituent components, apocynin (AP) and paeonol (PA) on a number of neutrophil functions, including effects on TNFα- expression and signalling. Neutrophils were treated with APPA (10–1000 µg/mL) prior to the measurement of cell functions, including ROS production, chemotaxis, apoptosis and surface receptor expression. Expression levels of several key genes and proteins were measured after incubation with APPA and the chromatin re-modelling agent, R848. APPA did not significantly affect phagocytosis, bacterial killing or expression of surface receptors, while chemotactic migration was affected only at the highest concentrations. However, APPA down-regulated neutrophil degranulation and ROS levels, and decreased the formation of neutrophil extracellular traps. APPA also decreased cytokine-stimulated gene expression, inhibiting both TNFα- and GM-CSF-induced cell signalling. APPA was as effective as infliximab in down-regulating chemokine and IL-6 expression following incubation with R848. Whilst APPA does not interfere with neutrophil host defence against infections, it does inhibit neutrophil degranulation, and cytokine-driven signalling pathways (e.g. autocrine signalling and NF-κB activation), processes that are associated with inflammation. These observations may explain the mechanisms by which APPA exerts anti-inflammatory effects and suggests a potential therapeutic role in inflammatory diseases in which neutrophils and TNFα signalling are important in pathology, such as rheumatoid arthritis.

COVID-19 activates many of the same inflammatory pathways as arthritis, except instead of being in the joints, it's in the lining of blood vessels and small capillaries in the lungs:

COVID-19 revisiting inflammatory pathways of arthritis - Nature Reviews Rheumatology

This Perspective article explores similarities in the inflammatory processes underlying coronavirus disease 2019 (COVID-19) and rheumatoid arthritis, including the role of pro-inflammatory cytokines and the potential of anti-cytokine therapies to treat COVID-19, as well as the effect of the...

www.nature.com

Coronavirus disease 2019 (COVID-19) is an infectious disease, caused by severe acute respiratory syndrome coronavirus 2, which predominantly affects the lungs and, under certain circumstances, leads to an excessive or uncontrolled immune activation and cytokine response in alveolar structures. The pattern of pro-inflammatory cytokines induced in COVID-19 has similarities to those targeted in the treatment of rheumatoid arthritis. Several clinical studies are underway that test the effects of inhibiting IL-6, IL-1β or TNF or targeting cytokine signalling via Janus kinase inhibition in the treatment of COVID-19. Despite these similarities, COVID-19 and other zoonotic coronavirus-mediated diseases do not induce clinical arthritis, suggesting that a local inflammatory niche develops in alveolar structures and drives the disease process. COVID-19 constitutes a challenge for patients with inflammatory arthritis for several reasons, in particular, the safety of immune interventions during the pandemic. Preliminary data, however, do not suggest that patients with inflammatory arthritis are at increased risk of COVID-19.

Apocynin can defang neutrophils by having a potent antioxidant effect, reducing ROS formation, NETosis and release of myeloperoxidase enzymes into the extracellular space, et cetera. It also reduces the production of certain key inflammatory cytokines that have been noted to be elevated in COVID-19.

COVID-19 hyperinflammation can and should be treated with antioxidants, including plant-derived antioxidants. Look at what the current critical care protocol is:

MATH+ Protocol - FLCCC | Front Line COVID-19 Critical Care Alliance

The MATH+ Hospital Treatment Protocol for Covid-19 is a physiologic-based combination treatment regimen created by leaders in critical care medicine.

covid19criticalcare.com

https://covid19criticalcare.com/wp-content/uploads/2021/01/FLCCC-Alliance-MATHplus-Protocol-ENGLISH.pdf

METHYLPREDNISOLONE, ASCORBIC ACID, THIAMINE, HEPARIN, IVERMECTIN, Fluvoxamine, Cyproheptadine, Anti-Androgen Therapy, Vitamin D, Atorvastatin, Melatonin, Zinc, Famotidine, Therapeutic Plasma Exchange

Ascorbic Acid is, of course, Vitamin C. They're promoting high-dose Vitamin C, Vitamin D, Melatonin, and Famotidine, and those are all antioxidants. Vitamin C shields lipids from oxidation by donating electrons to radicals. Vitamin D activates calcium pumps to decalcify cells and drive down ROS production, among many other things. Melatonin scavenges peroxynitrite. Famotidine and the other related H2 blockers, Cimetidine and Ranitidine, are scavengers of hydroxyl radicals and have a potent antioxidant effect separate from their use as H2-blocking antacid drugs.

They're basically admitting that antioxidants have a central place in COVID-19 critical care, as adjunct therapies alongside steroids, antivirals, blood thinners, NSAIDs, etc.

 

[ToroidalBoat]

Why don't they make the "vaccine" a real vaccine with inert virus particles that gives immunity?

Why this RNA BS that makes the "vaccine" fairly ineffective?

Assuming the former can be, I guess they do the latter instead to keep the scam going endlessly.

 

[The Nothingness]

View attachment 2439471

https://twitter.com/disclosetv/status/1425792790387204099

Still pushing the bat narrative.

 

[Drain Todger]

Neutrophils kill invading pathogens by making hydrogen peroxide and bleach to try and destroy the cell walls of bacteria (that is, dunking them in a caustic mix of chemicals until they pop like a balloon). Human cell walls aren’t much different from bacterial cell walls. They’re made of the same stuff. Our cells have defensive antioxidant enzymes like glutathione peroxidase to break down excess ROS. These antioxidant enzymes becoming overwhelmed with oxidative stress are hallmarks of endothelial dysfunction, obesity, diabetes, atherosclerosis, and so on.

https://www.ahajournals.org/doi/10.1161/01.HYP.0000142232.29764.a7

SARS-CoV-2’s proteins induce Nrf2 down-regulation, directly compromising the antioxidant enzyme defenses of our cells:

SARS-CoV2-mediated suppression of NRF2-signaling reveals potent antiviral and anti-inflammatory activity of 4-octyl-itaconate and dimethyl fumarate - Nature Communications

Viral infections usually cause disease through direct cytopathogenic effects and excessive inflammatory responses. Here, Olagnier et al. show that two NRF2 agonists, 4-OI and DMF, possess broad IFN-independent antiviral activity and decrease host inflammatory response to SARS-CoV-2 infection.

www.nature.com

Nrf2 is a master regulator of cellular antioxidant defenses:

Role of Nrf2 in Oxidative Stress and Toxicity

Radicals start stripping electrons from lipids, PUFAs, and so on, forming lipid hydroperoxides, which, on their own, are highly pro-inflammatory and promote autoimmunity.

DEFINE_ME

The body recognizes oxidized fats as foreign objects and makes antibodies against them. Many severely ill COVID-19 patients involve elevated levels of autoantibodies against oxidatively-modified lipids.

Antiphospholipid antibodies in COVID-19: a meta-analysis and systematic review | RMD Open

This is something you see in autoimmune diseases like Lupus.

If there were more widespread acceptance of antioxidants being used to treat COVID-19, thousands of lives could have been saved. Instead, what do we get?

FDA changes in usage of NAC & it’s impact on Baseline+ – Protea Nutrition

proteanutrition.com

Pre-FBI raid, doctor said patients would be supercharged vs COVID-19 with vitamin C treatment

Dr. Charles Mok one week ago explained to FOX 2 how his Vitamin C infusions were supposedly helping COVID-19 patients.

www.fox2detroit.com

The authorities are cracking down on antioxidant use in COVID-19. They unironically want people to die.

 

[mandatorylurk]

The push to scare people by using the kids is going to fail when you keep lying this badly.

 

[wildhoney]

Neutrophils kill invading pathogens by making hydrogen peroxide and bleach to try and destroy the cell walls of bacteria (that is, dunking them in a caustic mix of chemicals until they pop like a balloon). Human cell walls aren’t much different from bacterial cell walls. They’re made of the same stuff. Our cells have defensive antioxidant enzymes like glutathione peroxidase to break down excess ROS. These antioxidant enzymes becoming overwhelmed with oxidative stress are hallmarks of endothelial dysfunction, obesity, diabetes, atherosclerosis, and so on.

https://www.ahajournals.org/doi/10.1161/01.HYP.0000142232.29764.a7

View attachment 2439623

SARS-CoV-2’s proteins induce Nrf2 down-regulation, directly compromising the antioxidant enzyme defenses of our cells:

SARS-CoV2-mediated suppression of NRF2-signaling reveals potent antiviral and anti-inflammatory activity of 4-octyl-itaconate and dimethyl fumarate - Nature Communications

Viral infections usually cause disease through direct cytopathogenic effects and excessive inflammatory responses. Here, Olagnier et al. show that two NRF2 agonists, 4-OI and DMF, possess broad IFN-independent antiviral activity and decrease host inflammatory response to SARS-CoV-2 infection.

www.nature.com

Nrf2 is a master regulator of cellular antioxidant defenses:

Role of Nrf2 in Oxidative Stress and Toxicity

Radicals start stripping electrons from lipids, PUFAs, and so on, forming lipid hydroperoxides, which, on their own, are highly pro-inflammatory and promote autoimmunity.

DEFINE_ME

The body recognizes oxidized fats as foreign objects and makes antibodies against them. Many severely ill COVID-19 patients involve elevated levels of autoantibodies against oxidatively-modified lipids.

Antiphospholipid antibodies in COVID-19: a meta-analysis and systematic review | RMD Open

This is something you see in autoimmune diseases like Lupus.

If there were more widespread acceptance of antioxidants being used to treat COVID-19, thousands of lives could have been saved. Instead, what do we get?

FDA changes in usage of NAC & it’s impact on Baseline+ – Protea Nutrition

proteanutrition.com

Pre-FBI raid, doctor said patients would be supercharged vs COVID-19 with vitamin C treatment

Dr. Charles Mok one week ago explained to FOX 2 how his Vitamin C infusions were supposedly helping COVID-19 patients.

www.fox2detroit.com

The authorities are cracking down on antioxidant use in COVID-19. They unironically want people to die.

So interesting....would it be that there is more $$$ in making these complex vaccines as opposed to something as 'simple' as vitamin tablets or certain fruit and veggies?

 

[Never Scored]

View attachment 2439725

The push to scare people by using the kids is going to fail when you keep lying this badly.

A CNN story about Florida had a similar correction. I don't think it's an accident at this point.