Wuhan Coronavirus: Megathread - Got too big

[PittyKitty]

Italian Doctor, Pioneer of Successful Plasma Technique Against Covid, ‘Suicides’

So a week ago, the president of Madagascar, a place where artemisia is being produced against parasites and malaria, and used effectively against Covid, had an assassination attempt made on him and some of his colleagues. Now, just this week, an Italian lung specialist supposedly killed himself at home by hanging. He, too, had a role to play against Covid: he had pioneered a successful plasma therapy drawn from recovered Covid patients.

 

[Hollywood Hitler]

The best part is the media wont be able to call muslims super spreaders, which they will be, because;
1. a ton run corner shops in majority black neighborhoods
2. they still go to the mosque and big family get-togethers

Maybe Islam really is the answer.

Not convert to Islam, but Christians should use their methods. All church donation's should go towards truck rentals.

I give it till the end of next year at most before we all start being hunted down like wild animals. They're going to lock everything down one more time by fall through winter and shift the reasoning behind it on the "evil anti-vaxxers" as one final push to get the public to agree on throwing all dissenters into concentration camps if not outright slaughterhouses.

Finally! Always wanted to use justifiable lethal force.

View attachment 2394591

A male nurse, ha!

 

[Vince McMahon]

Great, putting bar codes on themselves, there is no better way to affirm you are a product.

Something something mark of the beast.

 

[Drain Todger]

I want to preface this by saying the BIORXIV stuff is all in preprint, and not peer reviewed yet, but I still find this troubling. I have avoided the topic, but it seems to keep reappearing. It's getting harder to ignore the neurological implications of COVID, and the worse thing about it is that this neurological side of things has the longest fuse, the longest delay time to figuring out what's going on. I have a feeling it's going to take years to figure it all out. I have to ask myself do I throw all of this info away? The MSM is picking up this stuff and magnifying it, does that mean it's all spin? I think that's the hardest thing, sifting the spin from the actual information.

The macaque study you linked spooked me. Again, it's preprint, but still. They found stuff in the brains that is associated with Parkinson's disease in all covid infected macaques. If you don't know what Parkinson's is think Michael J. Fox, he had Parkinson's disease.

View attachment 2394165

The only positive is that if this is the case, and we are going to have an epidemic of this disease, maybe it will get the attention it deserves and a ton more research. Then you might say what about the vaccine!? But then there's this to consider: https://pubmed.ncbi.nlm.nih.gov/33789211/

View attachment 2394183
They suggest the spike itself could lead to these amyloid clumps forming as well. This doesn't make me sleep better. The lag time on this is so frustrating, it takes years to develop these diseases. @Drain Todger why do you always find the worst news? I have no idea who you are, what your motives truly are (aside from a doomposting affinity), but even so, this is a hard one to just hand wave away.

What can you do? I have to agree on the fitness/nutrition advice. There are quite a few unknows, like just how prevalent this might be, and if you can have a better chance the more fit you are (probably). If this isn't a severe wakeup for anyone who's been neglecting their fitness, diet, etc. I'm not sure what to say. Do all variants of this disease cause the neurological symptoms to the same degree? If the virus gets weaker, as it has been doing in regards to mortality rate, does this apply to it's neurological component. The thing that has me wondering now, is that you have all these vaccinated asymptomatic carries of covid now, walking around with the virus in their bodies, is that a good thing? I would want it out of me as fast as possible, not hiding under the radar. Is the immune system attacking covid as hard as it should in the vaccinated? If it hangs around in you a long time, is that more chance of it opening an "CHAZ automonous zone" in your brain? I hate having so many questions, and very few answers. I need a drink.

In many of the papers I’ve read, even very early on, SARS-CoV-2 has been characterized as neurotropic. In fact, some scientists have speculated that the loss of smell from the virus is actually related to the virus infecting the brain through the transcribial route.

The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients

Following the severe acute respiratory syndrome coronavirus (SARS‐CoV) and Middle East respiratory syndrome coronavirus (MERS‐CoV), another highly pathogenic coronavirus named SARS‐CoV‐2 (previously known as 2019‐nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS‐CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID‐19) with clinical symptoms similar to those reported for SARS‐CoV and MERS‐CoV. The most characteristic symptom of patients with COVID‐19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID‐19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS‐CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse‐connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS‐CoV and SARS‐CoV2, it remains to make clear whether the potential invasion of SARS‐CoV2 is partially responsible for the acute respiratory failure of patients with COVID‐19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS‐CoV‐2‐induced respiratory failure.

Infection Mechanism of SARS-COV-2 and Its Implication on the Nervous System

In late December 2019, multiple atypical pneumonia cases resulted in severe acute respiratory syndrome caused by a pathogen identified as a novel coronavirus SARS-CoV-2. The most common coronavirus disease 2019 (COVID-19) symptoms are pneumonia, fever, dry cough, and fatigue. However, some...

www.frontiersin.org

Growing evidence shows that some coronaviruses first invade peripheral nerve terminals, then are anterograde/retrograde spread throughout the CNS via synapses (19, 24, 38), a well-documented neuroinvasive route for coronaviruses such as HEV67 (24, 39) and OC43-CoV (23). Among the peripheral nerves, the olfactory nerve is considered one of the strongest candidates for SARS-CoV-2 dissemination into CNS because of its close localization to olfactory epithelium (27). The olfactory epithelium cells highly express the ACE-2 receptor and the TMPRSS2, necessary for viral binding, replication, and accumulation (40). Recent studies found that neuropilins also have an essential role in cell infectivity. Interestingly, while neuropilin-1 alone promotes SARS-CoV-2 entry and infection, its coexpression with ACE-2 and TMPRSS2 markedly potentiates this effect (41). Similar to ACE-2 and TMPRSS2, the neuropilins are expressed abundantly in the respiratory and olfactory epithelium, becoming the nasal cavity epithelium, a key infection site for CNS infection (8, 41). A recent study presented evidence of SARS-CoV-2 entrance to CNS by crossing the neural-mucosal interface with subsequent penetration of defined neuroanatomical areas receiving olfactory tract projections, including the primary respiratory and cardiovascular control center in the medulla (42). Here, SARS-CoV-2 RNA and characteristic CoV substructures were detectable in the olfactory epithelium and olfactory mucus cells. A subsequent colocalization study within the olfactory mucosa using neuronal markers revealed a perinuclear S protein immunoreactivity in TuJ1+, NF200+, and OMP+ neural cells (42). In this way, SARS-CoV-2 may penetrate the CNS throughout the olfactory receptor cells that pass the cribriform plate contacting second-order neurons of the spherical glomeruli (32, 43). This passage of the olfactory nerve via the cribriform plate of the ethmoidal bone was termed transcribial route.

Other studies contradict this:

The olfactory nerve is not a likely route to brain infection in COVID-19: a critical review of data from humans and animal models - Acta Neuropathologica

One of the most frequent symptoms of COVID-19 is the loss of smell and taste. Based on the lack of expression of the virus entry proteins in olfactory receptor neurons, it was originally assumed that the new coronavirus (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2) does not...

link.springer.com

One of the most frequent symptoms of COVID-19 is the loss of smell and taste. Based on the lack of expression of the virus entry proteins in olfactory receptor neurons, it was originally assumed that the new coronavirus (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2) does not infect olfactory neurons. Recent studies have reported otherwise, opening the possibility that the virus can directly infect the brain by traveling along the olfactory nerve. Multiple animal models have been employed to assess mechanisms and routes of brain infection of SARS-CoV-2, often with conflicting results. We here review the current evidence for an olfactory route to brain infection and conclude that the case for infection of olfactory neurons is weak, based on animal and human studies. Consistent brain infection after SARS-CoV-2 inoculation in mouse models is only seen when the virus entry proteins are expressed abnormally, and the timeline and progression of rare neuro-invasion in these and in other animal models points to alternative routes to the brain, other than along the olfactory projections. COVID-19 patients can be assured that loss of smell does not necessarily mean that the SARS-CoV-2 virus has gained access to and has infected their brains.

The transcribial route is the same route into the brain used by naegleria fowleri amoeba. Those amoeba get into people's brains by contaminated water entering their nose and coming in contact with the olfactory nerve, rising up through the cribriform plate and into the olfactory bulb, causing a brain infection that is almost invariably lethal.

Naegleriasis - Wikipedia

en.wikipedia.org

Other suggested routes of SARS-CoV-2 entering the brain include infiltration of peripheral nerves from the lungs to the brain, or vice versa, as well as viremia and passage through the blood-brain barrier.

SARS-CoV-2 Dissemination Through Peripheral Nerves Explains Multiple Organ Injury

Coronavirus disease (CoVID-19), caused by recently identified severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2), is characterized by inconsistent clinical presentations. While many infected individuals remain asymptomatic or show mild respiratory symptoms, others develop severe pneumonia or even respiratory distress syndrome. SARS-CoV-2 is reported to be able to infect the lungs, the intestines, blood vessels, the bile ducts, the conjunctiva, macrophages, T lymphocytes, the heart, liver, kidneys, and brain. More than a third of cases displayed neurological involvement, and many severely ill patients developed multiple organ infection and injury. However, less than 1% of patients had a detectable level of SARS-CoV-2 in the blood, raising a question of how the virus spreads throughout the body. We propose that nerve terminals in the orofacial mucosa, eyes, and olfactory neuroepithelium act as entry points for the brain invasion, allowing SARS-CoV-2 to infect the brainstem. By exploiting the subcellular membrane compartments of infected cells, a feature common to all coronaviruses, SARS-CoV-2 is capable to disseminate from the brain to periphery via vesicular axonal transport and passive diffusion through axonal endoplasmic reticula, causing multiple organ injury independently of an underlying respiratory infection. The proposed model clarifies a wide range of clinically observed phenomena in CoVID-19 patients, such as neurological symptoms unassociated with lung pathology, protracted presence of the virus in samples obtained from recovered patients, exaggerated immune response, and multiple organ failure in severe cases with variable course and dynamics of the disease. We believe that this model can provide novel insights into CoVID-19 and its long-term sequelae, and establish a framework for further research.

SARS-CoV-2 Spike has been confirmed to harm blood-brain barrier integrity, increasing its permeability.

The S1 protein of SARS-CoV-2 crosses the blood–brain barrier in mice - Nature Neuroscience

Rhea at al. show that intravenously injected, radiolabeled SARS-CoV-2 spike 1 protein crosses the mouse blood–brain barrier, likely through the mechanism of adsorptive transcytosis and is also taken up by peripheral tissues.

www.nature.com

Following the severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), another highly pathogenic coronavirus named SARS-CoV-2 (previously known as 2019-nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS-CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID-19) with clinical symptoms similar to those reported for SARS-CoV and MERS-CoV. The most characteristic symptom of patients with COVID-19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID-19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS-CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse-connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS-CoV and SARS-CoV2, it remains to make clear whether the potential invasion of SARS-CoV2 is partially responsible for the acute respiratory failure of patients with COVID-19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS-CoV-2-induced respiratory failure.

The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood–brain barrier

As researchers across the globe have focused their attention on understanding SARS-CoV-2, the picture that is emerging is that of a virus that has ser…

www.sciencedirect.com

As researchers across the globe have focused their attention on understanding SARS-CoV-2, the picture that is emerging is that of a virus that has serious effects on the vasculature in multiple organ systems including the cerebral vasculature. Observed effects on the central nervous system include neurological symptoms (headache, nausea, dizziness), fatal microclot formation and in rare cases encephalitis. However, our understanding of how the virus causes these mild to severe neurological symptoms and how the cerebral vasculature is impacted remains unclear. Thus, the results presented in this report explored whether deleterious outcomes from the SARS-CoV-2 viral spike protein on primary human brain microvascular endothelial cells (hBMVECs) could be observed. The spike protein, which plays a key role in receptor recognition, is formed by the S1 subunit containing a receptor binding domain (RBD) and the S2 subunit. First, using postmortem brain tissue, we show that the angiotensin converting enzyme 2 or ACE2 (a known binding target for the SARS-CoV-2 spike protein), is ubiquitously expressed throughout various vessel calibers in the frontal cortex. Moreover, ACE2 expression was upregulated in cases of hypertension and dementia. ACE2 was also detectable in primary hBMVECs maintained under cell culture conditions. Analysis of cell viability revealed that neither the S1, S2 or a truncated form of the S1 containing only the RBD had minimal effects on hBMVEC viability within a 48 h exposure window. Introduction of spike proteins to in vitro models of the blood-brain barrier (BBB) showed significant changes to barrier properties. Key to our findings is the demonstration that S1 promotes loss of barrier integrity in an advanced 3D microfluidic model of the human BBB, a platform that more closely resembles the physiological conditions at this CNS interface. Evidence provided suggests that the SARS-CoV-2 spike proteins trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function. Together, these results are the first to show the direct impact that the SARS-CoV-2 spike protein could have on brain endothelial cells; thereby offering a plausible explanation for the neurological consequences seen in COVID-19 patients.

It is very likely that the virus can force itself through the blood-brain barrier and into the brain if it is circulating in the bloodstream. Viremia in COVID-19 is correlated with more severe disease:

SARS-CoV-2 viremia predicts severe COVID-19 disease outcomes

The SARS-CoV-2 plasma viremia has been linked to severe disease and death in COVID-19 cases in small-scale cohort studies. The current study, published on the pre-print server medRxiv, aimed to study the mechanisms behind this relationship.

www.news-medical.net

There is increasing evidence that COVID-19 manifests pathology beyond the pulmonary tract. As the virus spread across the globe, many people experienced symptoms showing that the disease does not only impact the respiratory tract but also other parts of the body, including the cardiovascular system.

SARS-CoV-2 nucleic acids have been detected in a wide range of body parts like the spleen, heart, liver, and digestive system in both immunocompromised and immunocompetent hosts.

Further, vascular and organ damage have been reported, while viremia has been implicated in transplacental transmission.

Plasma viremia occurs when free viruses, the ones not present within cells, are detected in the plasma of humans infected with SARS-CoV-2. Detecting plasma viremia in infection is optimal for virus detection.

All these show that infection occurs not only in the respiratory tract, and how it moves into the circulatory system is a critical step for the COVID-19 disease process. Knowing how this happens may help in formulating new therapies to combat the coronavirus pandemic.

The key thing to keep in mind is that the primary site of infection of COVID-19 is the lining of blood vessels, and all organs have blood vessels, so all organs can be affected by COVID-19 induced viremia, neutrophilia, endothelial cell activation, micro-clotting, inflammation, oxidative stress, hypoxemia, and so on.

COVID-19 is, in the end, an endothelial disease

Abstract. The vascular endothelium provides the crucial interface between the blood compartment and tissues, and displays a series of remarkable properties that

academic.oup.com

This video is an hour long, but it goes into considerable detail:

Any therapy for treating COVID-19 must be aimed at preventing EC activation and sloughing and restoring endothelial barrier integrity. This, in turn, would reduce clotting and prevent edema.

I don't think people realize just how bad severe oxidative stress in the lining of blood vessels can be, and what the consequences can be like.

Innate sensing of oxidation-specific epitopes in health and disease - Nature Reviews Immunology

Oxidation-specific epitopes (OSEs) function as markers of oxidative damage of membrane lipids. This Review discusses the immune recognition of OSEs, as well as their role in the maintenance of tissue homeostasis and their contribution to the development of inflammatory diseases.

www.nature.com

Ageing, infections and inflammation result in oxidative stress that can irreversibly damage cellular structures. The oxidative damage of lipids in membranes or lipoproteins is one of these deleterious consequences that not only alters lipid function but also leads to the formation of neo-self epitopes — oxidation-specific epitopes (OSEs) — which are present on dying cells and damaged proteins. OSEs represent endogenous damage-associated molecular patterns that are recognized by pattern recognition receptors and the proteins of the innate immune system, and thereby enable the host to sense and remove dangerous biological waste and to maintain homeostasis. If this system is dysfunctional or overwhelmed, the accumulation of OSEs can trigger chronic inflammation and the development of diseases, such as atherosclerosis and age-related macular degeneration. Understanding the molecular components and mechanisms that are involved in this process will help to identify individuals with an increased risk of developing chronic inflammation, and will also help to indicate novel modes of therapeutic intervention.

When fats are oxidatively modified, the body starts recognizing them as foreign objects and forms antibodies against them, promoting inflammation and autoimmunity. Cytokine and chemokine release summons more leukocytes from the innate immune system to deal with what the body perceives as a threat, however, this just makes the oxidative stress worse, since the cells of the innate immune system use reactive oxygen species to attack and destroy pathogens. It goes in a loop. Oxidative stress modifies lipids, lipids feed into receptors that detect damage, those receptors activate transcription factors that produce chemical signaling molecules that summon more immune cells, immune cells start blasting everything in sight with more oxidative stress, more lipids are oxidized, and so on and so forth.

This is feedback. It's exactly like holding a microphone up to an amplifier and hearing it whine, except it's happening in a biological system. What do you do to prevent feedback? You dampen the system. You let energy bleed out faster than it can be put in. Likewise, if it's possible to somehow dampen oxidative stress in these patients (as an adjunct therapy alongside steroids), it might suppress a great deal of unnecessary inflammation.

One thing is clear. Intubation should be avoided as long as possible. I'm almost completely certain that it's killing people, and a high-flow nasal cannula is better. This virus attacks and weakens blood vessels and small capillaries in the lungs, making them leaky. Stretching those tissues with invasive ventilation will just make this worse, possibly leading to micro-hemorrhages.

 

[Heinrich Maneuver]

UK scraps plans for vaccines to be mandatory for uni students attending lectures and halls (archive) despite the government signing 1.6million covid passport contracts. Please boris, just piss away our money. Any britfags had any luck faking one of the vax cards? the NHS covid letter for travel pdf is up online but has a barcode that could get scanned.
Oh yeah the Telegraph ran with the fact our wonderful NHS made secret plans to deny care to the elderly today. When will people realise it was never about nan?

 

[borsabil]

So I guess we're heading towards the end game.

The vaccines provide short term protection against severe illness by stimulating binding and neutralizing antibodies against the spike protein.

The neutralizing antibodies wear off after a few months but the binding antibodies remain (and you'll have them for life).

When exposed to wild virus the binding antibodies have the potential to cause more severe disease than in the unvaccinated (ADE).

The solution is to inject the vaccinated with booster shots in a never ending race to provide neutralizing antibodies against whatever new variants show up in the future.
A constant game of whack a mole, loser gets to drown in their own body fluids.

If you haven't been vaccinated just don't.
If you have been and you're offered a booster in the next few months also don't. Try and get your hands on some Ivermectin, take Vitamin D, lose weight, and pray.

 

[Protistology]

The solution is to inject the vaccinated with booster shots in a never ending race to provide neutralizing antibodies against whatever new variants show up in the future.

Medicine (and everything else) as a subscription service. You'll own nothing and and be happy.

 

[SneedEyeMitch]

I guess maybe there was something to that whole Mark of the Beast after all.

I wouldn't worry about, the Russians give up on their passports when the majority of the pop just stop doing business with anyone trying to enforce that kind of shit. Which is a message to all of us, the elite class only get what they want if you comply to them, or in a more "spiritual tone", the devil doesn't make you do anything, he merely calls your name, you answered.

 

[borsabil]

Iceland has 98% of it's adult population vaccinated.

Iceland says reintroduced COVID-19 restrictions may stick for 15 years

Iceland, one of the first countries in the world to abolish all COVID-19 restrictions for vaccinated tourists, may see recently reimposed safety protocols

english.alarabiya.net

Iceland says reintroduced COVID-19 restrictions may stick for 15 year…

archived 31 Jul 2021 10:29:17 UTC

archive.ph

Iceland says reintroduced COVID-19 restrictions may stick for 15 years​

Thorolfur Gudnason saidthat the COVID-19 epidemic will not end in Iceland until it is abolished all over the world.
He also admitted that the vaccine protection against infection was lower, maintained that the defense against serious illnesses was still estimated at 90 percent.

Now to be fair no one is dying of muh Delta in Iceland. No one has died of Covid in Iceland in months.
So the vaccines are working as intended then. Yes you will catch and transmit the coof but you won't get as sick.
I mean that's what they told us the whole time, we're just sperging coz we don't understand the science.

Here's what the Icelandic government were saying back in April, while they were rolling out the vaccines

Official information about COVID-19 in Iceland

archived 31 Jul 2021 10:25:09 UTC

archive.ph

Official information about COVID-19 in Iceland

Latest COVID-19 updates, advice, facts and trustworthy information on actions taken to contain the outbreak.

www.covid.is

The vaccines for COVID-19 that will be used in Iceland are safe and provide the best possible protection against the disease. The object of the vaccination is to protect individuals from contracting COVID-19 and to achieve herd immunity, which will prevent the spread of the pandemic.

Resist the gas lighting.

The Vaccines weren't sold to the public as preventative therapies, only lunatic conspiracy theorists believed that, they were sold as fucking vaccines.

Like the 'pandemic of the unvaccinated' and the '95% of ICU patients' the 'yeah it won't stop you catching it but it will stop you getting sick' is a cope.

Just wait a little while and we'll start seeing those case fatality rates ramp up as whatever neutralizing antibodies they have left wear off and the ADE kicks in hard.
Copium only takes you so far.

 

[Drain Todger]

Well, it's pretty much confirmed that COVID-19 is causing peroxynitrite formation and possible NOS uncoupling. They've found high serum nitrotyrosine, a sign of peroxynitrite.

Decreased availability of nitric oxide and hydrogen sulfide is a hallmark of COVID-19

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is involved in a global outbreak affecting millions of people who manifest a variety of s…

www.sciencedirect.com

3.6. A case-study of a single COVID-19 patient – association between CRP and gasotransmitters​

C-reactive protein (CRP) levels have been shown to be an early prognosticator in COVID-19 pneumonia and can indicate disease severity, whereas the gasotransmitters NO and H2S are known for their anti-inflammatory properties[17]. We measured nitrotyrosine, CRP as well as NO and H2S levels in a single subject who was initially a control subject, but 9 days later contracted a COVID-19 infection (Fig. 6). The subject’s CRP levels, which were significantly elevated with COVID-19 infection (1.35 mg/dL, normal range 0.3–1.0 mg/dL), were further elevated (1.77 mg/dL) within 3 days of infection, and then returned to the normal range (0.78 mg/dL) following antiviral therapy with remdesivir for 5 days (Fig. 6, middle panel). Total NO and sulfide levels were significantly reduced during COVID-19 infection (280 nM and 0.8523 μM, respectively) in this individual from pre-infection baseline (400 nM and 1.11039 μM, respectively) (Fig. 6, bottom panel). However, both the NO and sulfide levels were elevated following remdesivir antiviral therapy coinciding with decreased COVID-19 symptoms (5 days post-treatment: 200 nM and 1.07555 μM; 14 days post-treatment: 280 nM and 1.44706 μM). The subject’s level of nitrotyrosine, an oxidant marker, was significantly increased with COVID-19 infection and at day-5 post COVID-19 infection (22.52 nm and 133.99 nM respectively) compared to the baseline (2.56 nM) (Fig. 6, top panel), in close alignment with the increasing CRP levels and decreasing NO and H2S levels. Nitrotyrosine level then steeply decreased at day-14 post COVID-19 infection (52.97 nM) with corresponding increase in NO and H2S levels.

Excess peroxynitrite leads to this:

Endothelial nitric oxide synthase uncoupling: Is it a physiological mechanism of endothelium-dependent relaxation in cerebral artery?

See article by Drouin et al.[8](pages 73–81) in this issue.

academic.oup.com

Nitric oxide (NO) is generated from the conversion of L -arginine to L-citrulline by endothelial nitric oxide synthase (eNOS), which requires Ca2+/calmodulin, FAD, FMN, and tetrahydrobiopterin (BH4) as cofactors. Chemical studies in vitro demonstrated that the catalytic mechanisms of NOS involve flavin-mediated electron transport from a flavin-containing reductase domain to a heme-containing oxygenase domain. Here, oxygen is reduced and incorporated into the guanidine group of L-arginine, giving rise to NO and L-citrulline. Calcium/calmodulin binding to NOS increases the rate of reduction of both flavins and the heme iron. Reduction of iron (III) to iron (II) facilitates oxygen binding to the heme group to form a transient ferrous–dioxygen complex. NOS can also produce superoxide under certain conditions. Superoxide is generated from the oxygenase domain by dissociation of the ferrous–dioxygen complex [1,2]. This state is referred to as the “uncoupled state of eNOS” (eNOS uncoupling). BH4 couples L-arginine oxidation to NADPH consumption and prevents dissociation of the ferrous–dioxygen complex. Although in vitro data using purified eNOS demonstrate that modulation of the BH4 concentration may regulate the ratio of superoxide to NO generated by eNOS, it is as yet unclear how the endothelium regulates the production of these radicals in vivo. Although there are some methods to detect and quantify free radicals superoxide as well as NO in chemical systems, their detection in vivo has potential limitations. NO has a variety of functions, but its action as the endothelium-derived relaxing factor (EDRF) is the most important for the maintenance of vascular homeostasis. Recently, it was revealed that under certain pathological circumstances, eNOS becomes dysfunctional and produces superoxide rather than NO [3]. The pathophysiological role of dysfunctional eNOS has attracted attention in vascular disorders, including atherosclerosis, hypertension, and diabetes mellitus [4–6].

Among a number of molecular mechanisms proposed for eNOS uncoupling, evidence indicates that BH4 may be a key molecule in the control of NO and superoxide generation, and consequently the formation of hydrogen peroxide and peroxynitrite by eNOS [7]. Thus, it is conceivable that BH4 may switch eNOS activity from NO to superoxide generation at two levels: decreases in BH4 binding affinity or decreases in cellular BH4 concentration. Further studies of mechanisms involved in control of vascular GTP cyclohydrolase I activity and expression as well as metabolism of BH4 in endothelial cells may provide explanation for the role of BH4 in eNOS uncoupling.

In this issue of Cardiovascular Research, Drouin et al. demonstrate that by using pharmacological inhibitors in pressurized cerebral arteries isolated from young, healthy mice, NO derived from eNOS contributes to vascular tone at rest and that H2O2 derived from eNOS activation plays a physiological role as a significant part of endothelium-dependent dilation induced by acetylcholine (Fig. 1) [8]. These observations are in accord with previous observations [9]. They also assessed fluorescence-associated oxygen free radicals (DCF-DA) and NO (DAF-2) production in these arterial preparations. The critical importance of eNOS-derived superoxide as an EDRF was confirmed by using cerebral arteries from eNOS knockout mice. They conclude that H2O2-dependent dilation in mouse cerebral arteries originating from eNOS activation appears to be due to a physiological eNOS uncoupling state.

This is another feedback loop, by the way. Dr. Martin L. Pall calls it "NO/ONOO- Disease".

The NO/ONOO-Cycle as the Central Cause of Heart Failure

Abstract​

The NO/ONOO-cycle is a primarily local, biochemical vicious cycle mechanism, centered on elevated peroxynitrite and oxidative stress, but also involving 10 additional elements: NF-κB, inflammatory cytokines, iNOS, nitric oxide (NO), superoxide, mitochondrial dysfunction (lowered energy charge, ATP), NMDA activity, intracellular Ca2+, TRP receptors and tetrahydrobiopterin depletion. All 12 of these elements have causal roles in heart failure (HF) and each is linked through a total of 87 studies to specific correlates of HF. Two apparent causal factors of HF, RhoA and endothelin-1, each act as tissue-limited cycle elements. Nineteen stressors that initiate cases of HF, each act to raise multiple cycle elements, potentially initiating the cycle in this way. Different types of HF, left vs. right ventricular HF, with or without arrhythmia, etc., may differ from one another in the regions of the myocardium most impacted by the cycle. None of the elements of the cycle or the mechanisms linking them are original, but they collectively produce the robust nature of the NO/ONOO-cycle which creates a major challenge for treatment of HF or other proposed NO/ONOO-cycle diseases. Elevated peroxynitrite/NO ratio and consequent oxidative stress are essential to both HF and the NO/ONOO-cycle.
Keywords: nitrosative stress, reactive oxygen/nitrogen species, free radicals, inflammatory biochemistry, mitochondrial dysfunction, Ca2+ receptors, peroxynitrite, tetrahydrobiopterin oxidation
Go to:

1. Introduction​

The NO/ONOO-cycle is a primarily local, biochemical vicious cycle, which depending on where it is located in the body, may be the cause of various chronic inflammatory diseases [1–8]. Various diseases have been argued to be possible NO/ONOO-cycle diseases, and, for many of them, the cases made have been relatively superficial. Most of these possible NO/ONOO-cycle diseases are probably located primarily in regions of the central nervous system [2–8]. However, a recent, very detailed case, argues that pulmonary arterial hypertension is a probable NO/ONOO-cycle disease [1], suggesting that other types of cardiovascular diseases may also be candidates for being caused by this mechanism.
The current paper explores the possibility that heart failure (HF) may be a NO/ONOO-cycle disease. It is based on findings that each of the 12 elements of the cycle is elevated in HF and that each of them has causal roles in HF. The cycle is centered on the elevation of peroxynitrite (ONOO-), a potent oxidant, and on consequent oxidative stress, making the possible cycle mechanism of HF relevant to this special issue of the journal. The possible causation of HF by the cycle is also supported by findings that various stressors reported to initiate cases of HF act to raise cycle elements and therefore may be able to initiate the cycle by raising such elements. However, in order to assess the strength of these and other arguments regarding the possible etiology of HF, it is necessary to look at the mechanisms of the NO/ONOO-cycle and the consequent predicted properties of cycle-caused diseases.

See how everything in this cycle eventually promotes Nuclear Factor Kappa B activation? This phenomenon can, in extreme cases, trigger cytokine release and inflammation, causing the release of things like Tumor Necrosis Factor Alpha and Interleukin-6. COVID-19 patients have highly elevated TNF-a and IL-6, so we know that NF-kB overactivation is one culprit, given that it's one of the primary regulators of cytokine release in a cell.

NF-κB - Wikipedia

en.wikipedia.org

These pathways are called "cell survival pathways" because they regulate inflammation and programmed cell death.



These pathways decide, based on a wide array of factors, whether or not a cell can be rescued, or if it must undergo apoptosis and get cleaned up by a macrophage because it is unsalvageable.

Melatonin is a rather potent scavenger of peroxynitrite:

Melatonin is a scavenger of peroxynitrite

Peroxynitrite is a toxic oxidant formed from the reaction of Superoxide and nitric oxide under conditions of inflammation and oxidant stress. Here we …

www.sciencedirect.com

Peroxynitrite is a toxic oxidant formed from the reaction of Superoxide and nitric oxide under conditions of inflammation and oxidant stress. Here we demonstrate that the pineal neurohormone melatonin inhibits peroxynitrite-mediated oxidant processes. Melatonin caused a dose-dependent inhibition of the oxidation of dihydrorhodamine 123 to rhodamine in vitro. Moreover, in cultured J774 macrophages, melatonin inhibited the development of DNA single strand breakage in response to peroxynitrite and reduced the suppression of mitochondrial respiration. Thus, melatonin appears to be a scavenger of peroxynitrite. This action may contribute to the antioxidant and antiinflammatory effects of melatonin in various pathophysiological conditions.

Guess what reduces people's chances of getting COVID-19?

A network medicine approach to investigation and population-based validation of disease manifestations and drug repurposing for COVID-19

This study uses network medicine methodologies along with multiomic observations (including SARS-CoV-2 and human interactome, transcriptome, and proteome) to identify widespread disease manifestations and drug repurposing candidates (including melatonin) for COVID-19, validating these findings...

journals.plos.org

The global coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to unprecedented social and economic consequences. The risk of morbidity and mortality due to COVID-19 increases dramatically in the presence of coexisting medical conditions, while the underlying mechanisms remain unclear. Furthermore, there are no approved therapies for COVID-19. This study aims to identify SARS-CoV-2 pathogenesis, disease manifestations, and COVID-19 therapies using network medicine methodologies along with clinical and multi-omics observations. We incorporate SARS-CoV-2 virus–host protein–protein interactions, transcriptomics, and proteomics into the human interactome. Network proximity measurement revealed underlying pathogenesis for broad COVID-19-associated disease manifestations. Analyses of single-cell RNA sequencing data show that co-expression of ACE2 and TMPRSS2 is elevated in absorptive enterocytes from the inflamed ileal tissues of Crohn disease patients compared to uninflamed tissues, revealing shared pathobiology between COVID-19 and inflammatory bowel disease. Integrative analyses of metabolomics and transcriptomics (bulk and single-cell) data from asthma patients indicate that COVID-19 shares an intermediate inflammatory molecular profile with asthma (including IRAK3 and ADRB2). To prioritize potential treatments, we combined network-based prediction and a propensity score (PS) matching observational study of 26,779 individuals from a COVID-19 registry. We identified that melatonin usage (odds ratio [OR] = 0.72, 95% CI 0.56–0.91) is significantly associated with a 28% reduced likelihood of a positive laboratory test result for SARS-CoV-2 confirmed by reverse transcription–polymerase chain reaction assay. Using a PS matching user active comparator design, we determined that melatonin usage was associated with a reduced likelihood of SARS-CoV-2 positive test result compared to use of angiotensin II receptor blockers (OR = 0.70, 95% CI 0.54–0.92) or angiotensin-converting enzyme inhibitors (OR = 0.69, 95% CI 0.52–0.90). Importantly, melatonin usage (OR = 0.48, 95% CI 0.31–0.75) is associated with a 52% reduced likelihood of a positive laboratory test result for SARS-CoV-2 in African Americans after adjusting for age, sex, race, smoking history, and various disease comorbidities using PS matching. In summary, this study presents an integrative network medicine platform for predicting disease manifestations associated with COVID-19 and identifying melatonin for potential prevention and treatment of COVID-19.

Less peroxynitrite = less BH4 destruction = less NOS uncoupling = more nitric oxide = nitric oxide blocks the virus's spike protein from infecting cells.

The role of NO in COVID-19 and potential therapeutic strategies

4.4. NO as an antiviral effector​

Non-specific antiviral effects of NO have been reported in a variety of viral infections, including HIV, vaccinia virus, enterovirus and coronavirus [[55], [56], [57]]. For example, expression of iNOS was found to significantly increase in mouse heart infected with coxsackievirus B3, a common enterovirus. The viral load increased significantly after NG-monomethyl-l-arginine acetate (L-NMMA) or nitro-l-arginine methyl ester (l-NAME) was used to inhibit iNOS [58]. In addition, it was found that the NO donor S-nitroso-N-acetylpenicillamine (SNAP) significantly inhibited the 3C protease of coxsackievirus by acting on the viral replication process [59]. During the SARS outbreak, researchers found that exogenous NO donors effectively suppressed SARS-CoV-1. The mechanisms will be described as below.

4.4.1. Inhibition of NO on the SARS-CoV-1 replication cycle​

In 2004, a Swedish group studied the inhibitory effect of NO donors on SARS-CoV-1 infection in VeroE6 cells [60]. Cells were treated with SNAP and another non-NO donor compound (as control) at various concentrations (0, 50, 100, 200, 400 μM) at 1 h after infection. The 50% tissue culture infection dose (TCID50) was determined after 24 h. The results showed that SNAP significantly inhibited the replication cycle of SARS-CoV-1 at both RNA and cellular levels in a dose-dependent manner. Besides, iNOS expression was found to accompany decreased offspring viruses by 82% [60]. Two NO-mediated antiviral mechanisms were proposed, which were later experimentally verified: (1) NO affected one or two replication-related cysteine proteases encoded by SARS-CoV-1 ORF1a, which directly inhibited viral RNA replication, and (2) NO decreased the palmitoylation level of S protein and inhibited the membrane fusion of offspring virus S protein binding to host cell receptor ACE261.
Replication of SARS-CoV-1 was mediated by the nonstructural proteins nsp1-nsp16, and the later contain two cysteine proteases, which would be discussed in further details below [62,63]. Cysteine protease cleaves pp1ab replicase polyproteins with varied efficiency. Upon treatment with SNAP, two new high-molecular weight peptides were found. It was suggested that NO changed the original cutting mode of cysteine proteases, thereby affecting production of the non-structural proteins, and terminating the replication process of viral RNA [61,64].
The effect of NO on S protein was also investigated. VeroE6 cells infected with recombinant vaccinia virus carrying S gene (rVV-L-S) were treated with 400 μM SNAP, which was labeled with [3H] palmitic acid. After immune-precipitation of the S protein, it was found that SNAP treatment significantly reduced the number of palmitoylated S protein. The intercellular fusion was significantly decreased due to the low expression of S protein after SNAP-treated rVV-L-S was mixed with CHO-ACE2 cells (a cell model that stably expresses ACE2 on the cell surface). The results showed that the entry efficiency of the pseudotyped virus was significantly lower after SNAP treatment, and the virus infection rate decreased by about 70% [61]. O2 - is also produced during viral infection, which reacts with NO readily to produce peroxynitrite (ONOO-) [65], a viral inhibitor. In order to clarify whether ONOO- contributed to this effect, the ONOO- donor SIN-1 was used to treat cells infected with SARS-CoV-1. ONOO- did not show inhibitory effect on SARS-CoV-1 replication, which ruled out the contribution of peroxynitrite in this case [61].

4.4.2. Potential mechanism of NO in COVID-19​

SARS-CoV-2 and SARS-CoV-1 share a similar infection process: they both rely on the membrane fusion mediated by the viral S protein with the host cell receptor ACE2 to promote the injection of viral genetic material [66]. At present, the 3D atomic map of the SARS-CoV-2 S protein has been successfully constructed by cryogenic electron microscopy. The SARS-CoV-2 S protein is a trimer protein with a large number of glycosylation modifications, and its protein sequence is very similar to the S protein of SARS-CoV-1 [67]: although the S2 region (mediated membrane fusion) is highly homologous (99%), there is a difference in amino acid residues of the S protein receptor region (RBD). This difference has been shown to promote the cell entry mechanism of SARS-CoV-2 [68,69]. In addition, the SARS-CoV-2 genome is divided into six main functional open reading frames, including ORF1ab, spinous (S), envelope (E), membrane glycoprotein (M), nucleocapsid (N) and helper gene [70]. The replicase protein pp1ab, formed by ORF1ab, is cleaved into 16 non-structural proteins (nsp) involved in virus replication by papain-like (PLPro) and 3C-like (3CLPro) proteases encoded by SARS-CoV-2. In addition, the homology between the SARS-CoV-2-encoded 3CLPro and that of SARS-CoV-1 is as high as 96%, and their structures are basically similar [71,72].
Therefore, the inhibition of SARS-CoV-2 by NO may be similar to that of SARS-CoV-1. NO also inhibits viral replication by affecting one or two cysteine proteases encoded by the SARS-CoV-2 ORF1a and reducing the palmitoylation level of the S protein [73]. However, the mechanism of NO in SARS-CoV-2 remains unclear. Researchers have recommended NO together with clinically recommended antiviral drugs as an effective strategy for the treatment of COVID-19 [71,74].

Nitric oxide inhibits the spike. Peroxynitrite does not.

Melatonin is often taken as an OTC sleep aid, it's absolutely harmless, and it's three cents a fucking pill.

https://www.amazon.com/Natures-Bounty-Melatonin-Dissolve-Tablets/dp/B000GG6D9A/ref=sr_1_8?dchild=1&keywords=melatonin&qid=1627728662&rdc=1&sr=8-8

Additionally, there are ways to raise one's nitric oxide levels, like increasing intake of the precursors; dietary nitrate, arginine, citrulline, and so on. Watermelon is very high in citrulline. Turkey, pork, chicken, and pumpkin seeds are high in arginine. Dietary nitrate can be found in leafy greens.

People are dying from COVID-19 because of preventable malnutrition brought on by a diet of empty carbohydrates. Look down a typical snack food aisle in the US, and what do you see? Row after row of boxes filled with processed, pressed, baked, and fried grains dusted with salt and paprika. Empty carbs with no nutritional value whatsoever.

Somehow, the USDA convinced millions of people that their diet should primarily be grains.



You know what grains are full of? Lectins that give you even more oxidative stress.

Lectin-induced oxidative stress in human platelets

Previously we have shown that wheat germ agglutinin (WGA) and, with minor potency, Phaseolus vulgaris agglutinin (PHA), but not lens culinarian agglutinin (LCA), induce platelet aggregation, through the PLCƴ2 activation by the concerted action of src/syk and PI3K/BTK pathways. In this study, we have investigated platelet oxidative stress induced by lectins. Several parameters indicative of oxidative stress, such as reactive oxygen species (ROS), superoxide anion, lipid peroxidation and the efficiency of the aerobic metabolism, have been measured. It was found that ROS, superoxide anion formation and lipid peroxidation are significantly increased upon platelet treatment with WGA and PHA while LCA is ineffective. WGA is always more effective than PHA in all experimental conditions tested. In addition, the involvement of NADPH oxidase 1, syk and PI3K in oxidative stress induced by WGA and PHA has been shown. Concerning the lectins effect on aerobic metabolism, WGA and PHA, but not LCA, act as uncoupling agents, determining an increase of oxygen consumption and a decrease of ATP synthesis, with a consequent decrease of P/O value. These results are confirmed by the impairment of platelets proton gradient formation, evaluated by membrane potential, in platelets treated with WGA and PHA. In conclusion lectins, especially WGA, induce oxidative stress in platelets and decrease energy availability through modifications of membrane structure leading to the inefficiency of the aerobic machinery that steers platelets toward death as suggested by the decreased metabolic activity of platelets and the increased lactic dehydrogenase release.

Lectins and gluten are slowly injuring and killing millions of Americans with chronic inflammation and oxidative stress, and along comes a virus that causes even more inflammation and oxidative stress. The results here are predictable.

In fact, if I were going down a row of bioweapons in freezers and I needed a bioweapon that largely killed old people and fat people who eat Wheat Thins and Doritos and chase it with a Mountain Dew, I would pick COVID-19 without hesitation.

 

[Super-Chevy454]

Italian Doctor, Pioneer of Successful Plasma Technique Against Covid, ‘Suicides’

So a week ago, the president of Madagascar, a place where artemisia is being produced against parasites and malaria, and used effectively against Covid, had an assassination attempt made on him and some of his colleagues. Now, just this week, an Italian lung specialist supposedly killed himself at home by hanging. He, too, had a role to play against Covid: he had pioneered a successful plasma therapy drawn from recovered Covid patients.

I guess he was "Pziferized".

Now to be fair no one is dying of muh Delta in Iceland. No one has died of Covid in Iceland in months.
So the vaccines are working as intended then. Yes you will catch and transmit the coof but you won't get as sick.
I mean that's what they told us the whole time, we're just sperging coz we don't understand the science.

"But...but....we was vaccinated". Let's see if Iceland will follow Franch protestors example or if the suicide rate will rise up.

 

[MadStan]

Fascinating release of information by the CDC on the viral loads being seen in vaccinated and unvaccinated people.

Without booster shots, this virus has the potential easily later this year as immunity wanes to entirely decimate the health system on the United States should the data find the immunity is for naught after 6 months for most people - if.

The sad thing is, no doubt as this starts to happen the Vaccination nuts will go "see, told you the vaccine wouldn't work". which is a nasty twist on the reality - booster shots every 6 months to an already anticipated waning of immunity.

However what is not making a lot of sense is the infection rates given the findings of the spread. It suggests a large part of the population did develop some immunity with or without the vaccine to the earlier strains and what we may be seeing is the horror of what was feared - a strain that would thump a significant more people being allowed to prepare itself for an onslaught later this year.

I'd suggest given the reluctance on the part of many to get the vaccine we are going to have a horrid end of year in sight. I'd bank on a number of businesses demanding vaccinations not for anything more other than to ensure it has employees during this recovery cycle.

I think we are in for a bumpy 4th quarter financially as a country, economically as the supply strains that were planned to be gone by the 4th quarter are instead exasperated,

Biden has made some good calls with economic relief and the vaccinations, but I think this virus is going to prove what I feared and that was it wouldn't matter who was at the top, this virus is going to kill the best laid plans of mice (any mouse, GOP or Democrat).

I think the real purpose of insisting Feds get vaccinated is not to show a sign of force or to force public to accept it, but rather to ensure there is a working government if the worst fears are realized. The 4th quarter of the year could mark a significant turning point economically for the USA greatly tilted to the downside and I think markets are soon going to reflect this reality.

 

[Hippopatumus]

Fascinating release of information by the CDC on the viral loads being seen in vaccinated and unvaccinated people.

Without booster shots, this virus has the potential easily later this year as immunity wanes to entirely decimate the health system on the United States should the data find the immunity is for naught after 6 months for most people - if.

The sad thing is, no doubt as this starts to happen the Vaccination nuts will go "see, told you the vaccine wouldn't work". which is a nasty twist on the reality - booster shots every 6 months to an already anticipated waning of immunity.

However what is not making a lot of sense is the infection rates given the findings of the spread. It suggests a large part of the population did develop some immunity with or without the vaccine to the earlier strains and what we may be seeing is the horror of what was feared - a strain that would thump a significant more people being allowed to prepare itself for an onslaught later this year.

I'd suggest given the reluctance on the part of many to get the vaccine we are going to have a horrid end of year in sight. I'd bank on a number of businesses demanding vaccinations not for anything more other than to ensure it has employees during this recovery cycle.

I think we are in for a bumpy 4th quarter financially as a country, economically as the supply strains that were planned to be gone by the 4th quarter are instead exasperated,

Biden has made some good calls with economic relief and the vaccinations, but I think this virus is going to prove what I feared and that was it wouldn't matter who was at the top, this virus is going to kill the best laid plans of mice (any mouse, GOP or Democrat).

I think the real purpose of insisting Feds get vaccinated is not to show a sign of force or to force public to accept it, but rather to ensure there is a working government if the worst fears are realized. The 4th quarter of the year could mark a significant turning point economically for the USA greatly tilted to the downside and I think markets are soon going to reflect this reality.

Shut up faggot

 

[JoseRaulChupacabra]

Iceland has 98% of it's adult population vaccinated.

View attachment 2395038

We should really create a currency based on the number of infections at this point. Coronachan is just swimming in tendies.

 

[NoSpiceLife]

I guess he was "Pziferized".

Speaking of Pfizered, I seriously think that that is what has happened to Morrison in Australia. He is so angry, which is completely different to what he was before he went to G7. I'm not saying that anyone shouldn't be angry with what is being put forward, and what is happening, everyone absolutely should be; I can't imagine being in his position, to have the death threats hanging over him, for himself and everyone he loves from the elites, and then on top of that, the multitude of threats he'd be getting from every corner of Australia, from both sides, politicians and the public alike.

That anger he is carrying, you can see it, it's not anger at the Australian people, after all he chose the right way to go in the first place, it's the type of anger from someone that has enormous internal conflicts happening. The other heads of countries appear to be able to hide it well, Morrison on the other hand, he's Australian, we're just not that sort of people.

 

[Super-Chevy454]

The guy who talked of the "Pziferleaks" or should we said "Pzifergate" got his Twitter account "limited" or more precisely resctricted. https://www.europereloaded.com/the-leaked-pfizer-contracts-is-an-eye-opener/

Too late for that Twitter, now they're archived copies on Archive.ph and the Wayback Machine.

Ehden (@eh_den) | Twitter

archived 29 Jul 2021 12:33:13 UTC

archive.ph

https://web.archive.org/web/20210728191943/https://twitter.com/eh_den/

An allegedly leaked vaccine supply contract between Pfizer and the government of Albania has sent some shockwaves through social media over the last few days.
It doesn’t contain any really groundbreaking information but, if it’s genuine, it certainly confirms the worst suspicions many of us had about the terms of the vaccine supply agreements.

The document was first published by the Albanian independent media outlet Gogo.al back in January, but came to prominence in the Anglosphere three days ago, when Twitter user Ehden posted a long thread breaking down its contents. His account has since been “limited” (we’ve all been there), but you can read his blog here.
In the interests of open discussion, and without endorsing its authenticity, we present the whole document below. We recommend anyone interested download it, just in case it disappears from the net, as potentially embarrassing documents tend to do.

So, is the document genuine?​

That’s hard to say. It certainly wouldn’t be unprecedented for it to be a “honey trap” leak. A document that makes outlandish claims, which many in the alternate media run with, only for it to be debunked and discredit all those who reported it. It happens. It’s why you should always approach any “leak” with supreme caution.
But one argument for the contract’s authenticity is its lack of any “huge groundbreaking admission” that would be the hallmark of a fake leak.
Since it was posted by Ehden, other “contracts” have leaked, which contain similar language and clauses. But, as these aren’t 100% proven genuine either, it would be wrong to use them to corroborate each other.
Stronger evidence can be found on the website of the Israeli Ministry of Health, where they have a (heavily redacted) copy of their “REAL-WORLD EPIDEMIOLOGICAL EVIDENCE COLLABORATION AGREEMENT” with Pfizer (we downloaded a copy of that too, just in case.)

These two documents do have some strong similarities.​

Under “definitions,” for example, both use the same word-for-word phrasing for the definitions of “product” and “affiliate(s)”. “Intellectual Property” is very similar too, as is a lot of the language under “Term and Termination”.
That is evidence that the document could be real…OR it’s evidence that good sources of Pfizer’s boilerplate legal contracts are available on the internet, as a useful resource for fakers. It cuts both ways.
There’s circumstantial evidence for the document’s authenticity, of course. The fact the Twitter account discussing it was “limited” almost immediately, for example. The fact it has been on the internet for nearly seven months and hasn’t been the subject of a single official denial by either party OR a “fact check” from one of those famous “independent fact-checkers”. These are all points in its favour.
As yet, it’s hard to be certain either way. But let’s say, for the sake of argument, that it’s real. What does it say?
A lot of the talk so far has been about the awful financial terms, but that’s not at all unusual in state contracts with private firms. The government agrees to terrible terms for the taxpayer, whilst accepting a back-hander here or there or a cushy job in the future. It’s the way the world works.

 

[borsabil]

Fascinating release of information by the CDC on the viral loads being seen in vaccinated and unvaccinated people.

Without booster shots, this virus has the potential easily later this year as immunity wanes to entirely decimate the health system on the United States should the data find the immunity is for naught after 6 months for most people - if.

The sad thing is, no doubt as this starts to happen the Vaccination nuts will go "see, told you the vaccine wouldn't work". which is a nasty twist on the reality - booster shots every 6 months to an already anticipated waning of immunity.

However what is not making a lot of sense is the infection rates given the findings of the spread. It suggests a large part of the population did develop some immunity with or without the vaccine to the earlier strains and what we may be seeing is the horror of what was feared - a strain that would thump a significant more people being allowed to prepare itself for an onslaught later this year.

I'd suggest given the reluctance on the part of many to get the vaccine we are going to have a horrid end of year in sight. I'd bank on a number of businesses demanding vaccinations not for anything more other than to ensure it has employees during this recovery cycle.

I think we are in for a bumpy 4th quarter financially as a country, economically as the supply strains that were planned to be gone by the 4th quarter are instead exasperated,

Biden has made some good calls with economic relief and the vaccinations, but I think this virus is going to prove what I feared and that was it wouldn't matter who was at the top, this virus is going to kill the best laid plans of mice (any mouse, GOP or Democrat).

I think the real purpose of insisting Feds get vaccinated is not to show a sign of force or to force public to accept it, but rather to ensure there is a working government if the worst fears are realized. The 4th quarter of the year could mark a significant turning point economically for the USA greatly tilted to the downside and I think markets are soon going to reflect this reality.

It was discussed before the vaccine roll ours that the best course of action was to do nothing.

By the end of 2021 the virus had already burned itself out. The worst of the pandemic was done. Epidemiologists knew exactly what was happening, Covid was following the same path every single respiratory pandemic has followed throughout recorded history. The first wave hits us like a freight train, the second is a bitch but not as bad, but then something amazing happens. A mixture of acquired immunity and the virus responding to evolutionary pressure sees it become just another circulating nuisance. The 19th century Russian flu, the Spanish flu, the Hong Kong flu. the swine flu all followed this path and there was nothing that suggested Covid was going to be anything different.

But instead of leaving well enough alone drug companies motivated by greed, politicians drunk on power and a population terrified by an irresponsible media it was decided to interfere and inject hundreds of millions of people with barely tested not vaccines. We will now pay the price for our hubris and stupidity. We deserve what's coming.

Perhaps you're tight, maybe the virus will mutate into something horrifying because of the skewed environment created by the vaccines. More deadly variants would usually whither on the vine and be out competed by more infectious but less virulent strains. Instead they're being allowed to circulate among the vaccinated. There's a risk of that happening for sure and maybe that's what the government is planning for. More likely is the virus being allowed a free run in the vaccinated due to their fucked immune systems. Nothing we can do now except kick back and wait.

 

[Vince McMahon]

Fascinating release of information by the CDC on the viral loads being seen in vaccinated and unvaccinated people.

Without booster shots, this virus has the potential easily later this year as immunity wanes to entirely decimate the health system on the United States should the data find the immunity is for naught after 6 months for most people - if.

The sad thing is, no doubt as this starts to happen the Vaccination nuts will go "see, told you the vaccine wouldn't work". which is a nasty twist on the reality - booster shots every 6 months to an already anticipated waning of immunity.

However what is not making a lot of sense is the infection rates given the findings of the spread. It suggests a large part of the population did develop some immunity with or without the vaccine to the earlier strains and what we may be seeing is the horror of what was feared - a strain that would thump a significant more people being allowed to prepare itself for an onslaught later this year.

I'd suggest given the reluctance on the part of many to get the vaccine we are going to have a horrid end of year in sight. I'd bank on a number of businesses demanding vaccinations not for anything more other than to ensure it has employees during this recovery cycle.

I think we are in for a bumpy 4th quarter financially as a country, economically as the supply strains that were planned to be gone by the 4th quarter are instead exasperated,

Biden has made some good calls with economic relief and the vaccinations, but I think this virus is going to prove what I feared and that was it wouldn't matter who was at the top, this virus is going to kill the best laid plans of mice (any mouse, GOP or Democrat).

I think the real purpose of insisting Feds get vaccinated is not to show a sign of force or to force public to accept it, but rather to ensure there is a working government if the worst fears are realized. The 4th quarter of the year could mark a significant turning point economically for the USA greatly tilted to the downside and I think markets are soon going to reflect this reality.

Don't choke on that doom porn.

 

[Kiwi Lime Pie]

Great, putting bar codes on themselves, there is no better way to affirm you are a product.

Or property.

Either way, it's the same dehumanizing action that gets bounced and squeaked about by the same people who expect nothing less than 100% vaccination rates across the globe.

 

[borsabil]

https://twitter.com/CDCgov/status/1379483036979490824

CDC on Twitter: "Getting a COVID-19 vaccine is an important tool to h…

archived 31 Jul 2021 12:11:20 UTC

archive.ph

I just can't.

I know they have nothing but contempt for us, but holy mother of God.