Spartacus Speaks

It is the opinion of ICENI, and other independent researchers, that the world's governments are covertly engaged in an act of genocide against their own populations. This will not be tolerated.

Omar Zaid
Omar Zaid

he Spartacus Letter - Rev. 2 (2021-09-28) | Spartacus


My name is Spartacus, and I've had enough.

We have been forced to watch America and the Free World spin into inexorable decline due to a biowarfare attack. We, along with countless others, have been victimized and gaslit by propaganda and psychological warfare operations being conducted by an unelected, unaccountable Elite against the American people and our allies.

Our mental and physical health have suffered immensely over the course of the past year and a half. We have felt the sting of isolation, lockdown, masking, quarantines, and other completely nonsensical acts of healthcare theater that have done absolutely nothing to protect the health or wellbeing of the public from the ongoing COVID-19 pandemic.

Now, we are watching the medical establishment inject literal poison into millions of our fellow Americans without so much as a fight.

We have been told that we will be fired and denied our livelihoods if we refuse to vaccinate. This was the last straw.

We have spent thousands of hours analyzing leaked footage from Wuhan, scientific papers from primary sources, as well as the paper trails left by the medical establishment.

What we have discovered would shock anyone to their core.

First, we will summarize our findings, and then, we will explain them in detail. References will be placed at the end.


  • COVID-19 is a blood and blood vessel disease. SARS-CoV-2 infects the lining of human blood vessels, causing them to leak into the lungs.
  • Current treatment protocols (e.g. invasive ventilation) are actively harmful to patients, accelerating oxidative stress and causing severe VILI (ventilator-induced lung injuries). The continued use of ventilators in the absence of any proven medical benefit constitutes mass murder.
  • Existing countermeasures are inadequate to slow the spread of what is an aerosolized and potentially wastewater-borne virus and constitute a form of medical theater.
  • Various non-vaccine interventions have been suppressed by both the media and the medical establishment in favor of vaccines and expensive patented drugs.
  • The authorities have denied the usefulness of natural immunity against COVID-19, even though natural immunity confers protection against all of the virus's proteins, and not just one.
  • Vaccines will do more harm than good. The antigen that these vaccines are based on, SARS-CoV- 2 Spike, is a toxic protein. SARS-CoV-2 may have ADE, or antibody-dependent enhancement; current antibodies may not neutralize future strains, but instead help them infect immune cells. Also, vaccinating during a pandemic with a leaky vaccine removes the evolutionary pressure for a virus to become less lethal.
  • There is a vast and appalling criminal conspiracy that directly links both Anthony Fauci and Moderna to the Wuhan Institute of Virology.
  • COVID-19 vaccine researchers are directly linked to scientists involved in brain-computer interface ("neural lace") tech, one of whom was indicted for taking grant money from China.
  • Independent researchers have discovered mysterious nanoparticles inside the vaccines that are not supposed to be present.
  • The entire pandemic is being used as an excuse for a vast political and economic transformation of Western society that will enrich the already rich and turn the rest of us into serfs and untouchables.

COVID-19 Pathophysiology

COVID-19 is not a viral pneumonia. It is a viral vascular endotheliitis and attacks the lining of blood vessels, particularly the small pulmonary alveolar capillaries, leading to endothelial cell activation and sloughing, coagulopathy, sepsis, pulmonary edema, and ARDS-like symptoms. This is a disease of the blood and blood vessels. The circulatory system. Any pneumonia that it causes is secondary to that.1-5

In severe cases, this leads to sepsis,6,7 blood clots,8-10 and multiple organ failure,11-13 including hypoxic and inflammatory damage to various vital organs, such as the brain,14-17 heart (COVID-19 was initially thought to cause myocarditis, but this has proven rare),18,19 liver,20-22 pancreas,23-26 kidneys,27-29 and intestines.30-32

Some of the most common laboratory findings in COVID-19 are elevated D-dimer, elevated prothrombin time, elevated C-reactive protein, neutrophilia, lymphopenia, hypocalcemia, hyperferritinemia, and inflammatory cytokines, essentially matching a profile of coagulopathy and immune system hyperactivation/immune cell exhaustion.33-39

COVID-19 can present as almost anything, due to the wide tropism of SARS-CoV-2 for various tissues in the body's vital organs. While its most common initial presentation is respiratory illness and flu-like symptoms, it can present as brain inflammation, gastrointestinal disease, or even heart attack, stroke, or pulmonary embolism.40-47 COVID-19 is more severe in those with specific comorbidities, such as obesity, diabetes, and hypertension.48,49 This is because these conditions involve endothelial dysfunction, which renders the circulatory system more susceptible to infection and injury by this particular virus.50,51

The vast majority of COVID-19 cases are mild and do not cause significant disease.52-55 80% of known cases are mild and 20% are severe or critical.56-58 However, this ratio is only correct for known cases, not all infections. The number of actual infections is much, much higher. Consequently, the mortality and morbidity rate are lower than a CFR may indicate.59-61 However, COVID-19 spreads very quickly (especially in densely-populated areas with greater exposure to respiratory aerosols in public transport), meaning that there are a significant number of severely ill and critically ill patients appearing in a short time frame.62,63

The breakdown of the pathology is as follows:

SARS-CoV-2 Spike binds to ACE2.64,65 Angiotensin Converting Enzyme 2 is an enzyme that is part of the renin-angiotensin-aldosterone system, or RAAS.66,67 The RAAS is a hormone control system that moderates blood pressure and fluid volume (i.e. osmolarity) of the circulatory system by controlling vascular tone and salt retention and excretion.68-72 This protein, ACE2, is ubiquitous in every part of the body that interfaces with the circulatory system, particularly in vascular endothelial cells and pericytes, brain astrocytes, renal tubules and podocytes, pancreatic islet cells, bile duct and intestinal epithelial cells, and the seminiferous ducts of the testis, all of which SARS-CoV-2 can potentially infect, not just the lungs.73-75

SARS-CoV-2 infects a cell as follows: SARS-CoV-2 Spike undergoes a conformational change where the S1 trimers flip up and extend, locking onto ACE2 bound to the surface of a cell. TMPRSS2, or transmembrane protease serine 2, comes along and cuts off the heads of the Spike, exposing the S2 stalk-shaped subunit inside. The remainder of the Spike undergoes a conformational change that causes it to unfold like an extension ladder, embedding itself in the cell membrane. Then, it folds back upon itself, pulling the viral membrane and the cell membrane together. The two membranes fuse, with the virus's proteins migrating out onto the surface of the cell. The SARS-CoV-2 nucleocapsid enters the cell, disgorging its genetic material and beginning the viral replication process, hijacking the cell's own structures to produce more virus.76-78

SARS-CoV-2 Spike proteins embedded in a cell can actually cause human cells to fuse together, forming syncytia/MGCs (multinucleated giant cells).79,80 They also have other pathogenic, harmful effects. SARS- CoV-2's viroporins, such as its Envelope and 3a proteins, act as calcium ion channels, introducing calcium into infected cells, a property that is shared with similar coronaviruses, such as SARS.81-83 The virus suppresses the natural interferon response, resulting in delayed inflammation. SARS-CoV-2 N protein and ORF3a can also directly activate the NLRP3 inflammasome.84-86 Also, it suppresses the Nrf2 antioxidant pathway.87-90 The suppression of ACE2 by binding with Spike is claimed to cause a buildup of bradykinin that would otherwise be broken down by ACE2, but this is also contradicted by studies that show that Spike-ACE2 binding can upregulate ACE2 activity.91-95

This constant calcium influx into the cells is correlated with noticeable hypocalcemia, or low blood calcium, especially in people with Vitamin D deficiencies and pre-existing endothelial dysfunction.96-98 The vasoactive peptide bradykinin upregulates cAMP, cGMP, COX, and Phospholipase C activity.99-107 This, along with the ongoing expression of various SARS-CoV-2 viroporins, collectively results in prostaglandin release and vastly increased intracellular calcium signaling (including dumping of Ca2+ stores from the endoplasmic reticulum), which promotes highly aggressive ROS release and ATP depletion.108-112 NADPH oxidase releases superoxide into the extracellular space.113-115 Superoxide radicals react with nitric oxide to form peroxynitrite.116-119 Peroxynitrite reacts with the tetrahydrobiopterin cofactor needed by endothelial nitric oxide synthase, destroying it and "uncoupling" the enzymes, causing nitric oxide synthase to synthesize more superoxide instead.120-122 This proceeds in a positive feedback loop until nitric oxide bioavailability in the circulatory system is depleted.123,124

Dissolved nitric oxide gas produced constantly by eNOS serves many important functions,125-127 but it is also antiviral against SARS-like coronaviruses, preventing the palmitoylation of the viral Spike protein and making it harder for it to bind to host receptors.128-130 The loss of NO allows the virus to begin replicating with impunity in the body. Those with endothelial dysfunction (i.e. hypertension, diabetes, obesity, old age, African-American race) have redox equilibrium issues to begin with, giving the virus an advantage.131-136

Due to the extreme cytokine release triggered by these processes, the body summons a great deal of neutrophils and monocyte-derived alveolar macrophages to the lungs.137-140 Cells of the innate immune system are the first-line defenders against pathogens. They work by engulfing invaders and trying to attack them with enzymes that produce powerful oxidants, like SOD and MPO.141,142 Superoxide dismutase takes superoxide and makes hydrogen peroxide, and myeloperoxidase takes hydrogen peroxide and chlorine ions and makes hypochlorous acid, which is many, many times more reactive than sodium hypochlorite bleach.143-146

Neutrophils have a nasty trick. They can also eject these enzymes into the extracellular space, where they will continuously spit out peroxide and bleach into the bloodstream. This is called neutrophil extracellular trap formation, or NETosis.147,148 In severe and critical COVID-19, there is actually rather severe NETosis.149-152

COVID-19's pathology is, from this point onward, dominated by extreme oxidative stress and neutrophil respiratory burst. Heme iron is stripped out of heme by hypochlorous acid. No amount of supplemental oxygen can oxygenate blood that chemically refuses to bind O2 due to HOCl outcompeting O2 at its binding sites.153-155 Red blood cells lose the ability to transport oxygen, causing the sufferer to turn blue in the face.156,157 Unliganded iron, hydrogen peroxide, and superoxide in the bloodstream undergo the Haber-Weiss and Fenton reactions, producing extremely reactive hydroxyl radicals that violently strip electrons from surrounding fats and DNA, oxidizing them severely.158-165

Haber-Weiss Reaction:

Fe3+ + - O2− → Fe2+ + O2

Fenton Reaction:

Fe2+ + H2O2 → Fe3+ + OH− + - OH

Hydroxyl radicals are extremely reactive, have a very short half-life in the body, and cannot be detoxified by enzymatic action. They occur naturally in the upper atmosphere, where they destroy pollutants. They are also extremely destructive to biological matter and, in industrial applications, they are often generated on purpose and introduced into wastewater streams to sanitize them through their powerful oxidative effect.166-171

In severe hypoxia, cellular metabolic shifts cause ATP to break down into hypoxanthine, which, upon the reintroduction of oxygen, causes xanthine oxidase to produce tons of highly damaging radicals that attack tissue.172-175 In the mitochondria, succinate buildup due to sepsis-induced hypoxia does the same exact thing; when oxygen is reintroduced, it makes superoxide radicals.176-179 This is called ischemia- reperfusion injury, and it's why the majority of people who go on a ventilator are dying. Make no mistake, intubation will kill people who have COVID-19 by greatly accelerating the oxidative damage caused by the virus's processes.180-183

The end-stage of COVID-19 is severe lipid peroxidation, where fats in the body start to "rust" due to damage by oxidative stress.184,185 This drives autoimmunity. Oxidized lipids appear as foreign objects to the immune system, which recognizes and forms antibodies against OSEs, or oxidation-specific epitopes.186,187 Also, oxidized lipids feed directly into pattern recognition receptors, triggering even more inflammation and summoning even more cells of the innate immune system that release even more destructive enzymes.188,189

This condition is not unknown to medical science. The actual name for all of this is acute sepsis.190-192

We know this is happening in COVID-19 because people who have died of the disease have noticeable ferroptosis signatures in their tissues, as well as various oxidative stress biomarkers such as nitrotyrosine, 4-HNE, and malondialdehyde.193-199

There are many other peculiarities involved in COVID-19, such as increases in gene activity associated with ubiquitination,200,201 endothelial cell activation,200-203 vWF release,204-206 mast cell activation,207,208 and complement system activation.209-212 Overall, the inflammatory profile of COVID-19 is somewhat like a severe autoimmune reaction. It is reminiscent of lupus and rheumatoid arthritis, but centered in the vasculature.213-216

Hyperinflammatory COVID-19 is a severe, SARS-like inflammatory syndrome that can put a sufferer in the ICU. It is not to be trifled with. However, if hyperinflammatory COVID-19 and the associated sepsis can be effectively treated, then the lethality of the virus will be lessened significantly.

COVID-19 Treatments

In those who have critical COVID-19-induced sepsis, hypoxia, coagulopathy, and ARDS, the most common treatments are intubation, injected corticosteroids, and blood thinners. This is not the correct treatment for COVID-19.217-219 When you intubate someone with this condition, you are setting off a free radical bomb by supplying the cells with O2. It's a catch-22, because we need oxygen to make Adenosine Triphosphate (that is, to live), but O2 is also the precursor of all these damaging radicals that lead to lipid peroxidation.220-224

The correct treatment for severe COVID-19 related sepsis is non-invasive ventilation, steroids, and antioxidant infusions. Most of the drugs repurposed for COVID-19 that show any benefit whatsoever in rescuing critically ill COVID-19 patients are antioxidants.225,226 N-acetylcysteine, melatonin, fluvoxamine, budesonide, famotidine, cimetidine, and ranitidine are all antioxidants.227-238 Indomethacin prevents iron-driven oxidation of arachidonic acid to isoprostanes.239There are powerful antioxidants such as apocynin that have not even been tested on COVID-19 patients yet which could defang neutrophils, prevent lipid peroxidation, restore endothelial health, and restore oxygenation to the tissues.240-242

Scientists who know anything about pulmonary neutrophilia, ARDS, and redox biology have known or surmised much of this since March 2020.243 In April 2020, Swiss scientists confirmed that COVID-19 was a vascular endotheliitis.244 By late 2020, experts had already concluded that COVID-19 causes a form of viral sepsis.245,246 They also know that sepsis can be effectively treated with antioxidants.247-249None of this information is particularly new, and yet, for the most part, it has not been acted upon. Doctors continue to use damaging intubation techniques despite high lung compliance and poor oxygenation, killing an untold number of critically ill patients with medical malpractice.250,251

Because of the way they are constructed, Randomized Control Trials will never show any benefit for any antiviral against COVID-19. Not Remdesivir, not Kaletra, not HCQ, and not Ivermectin. The reason for this is simple; for the patients that they have recruited for these studies, such as Oxford's ludicrous RECOVERY study, the intervention is too late to have any positive effect.252,253

The clinical course of COVID-19 is such that by the time most people seek medical attention for hypoxia, their viral load has already tapered off to almost nothing.254If someone is about 10 days post-exposure and has already been symptomatic for five days, there is hardly any virus left in their bodies, only cellular damage and derangement that has initiated a hyperinflammatory response.255

In these trials, they give antivirals to severely ill patients who have no virus in their bodies, only a delayed hyperinflammatory response, and then absurdly claim that antivirals have no utility in treating or preventing COVID-19.256These clinical trials being cited by the media as evidence of the ineffectiveness of antivirals do not recruit people who are pre-symptomatic. They do not test pre- exposure or post-exposure prophylaxis. This is like using a defibrillator to shock only flatline, and then absurdly claiming that defibrillators have no medical utility whatsoever when the patients refuse to rise from the dead. The intervention is too late. These trials for antivirals show systematic, egregious selection bias. They are providing a treatment that is futile to the specific cohort they are enrolling.257-261

India went against the instructions of the WHO and mandated the prophylactic usage of Ivermectin. They have almost completely eradicated COVID-19.262,263 The Indian Bar Association of Mumbai has brought criminal charges against WHO Chief Scientist Dr. Soumya Swaminathan for recommending against the use of Ivermectin.264,265

Ivermectin is not "horse dewormer". Yes, it is sold in veterinary form as a dewormer for animals.266 It has also been available in pill form for humans for decades, as an antiparasitic drug.267

The media and the FDA have disingenuously claimed that because Ivermectin is an antiparasitic drug, it has no utility as an antivirus.268,269 This is incorrect. Ivermectin has utility as an antiviral. It blocks importin, preventing nuclear import, effectively inhibiting viral access to cell nuclei. Many drugs currently on the market have multiple modes of action. Ivermectin is one such drug. It is both antiparasitic and antiviral.270-274

In Bangladesh, Ivermectin costs $1.80 for an entire 5-day course.275 Remdesivir, which is toxic to the liver, costs $3,120 for a 5-day course of the drug.276 Billions of dollars of utterly useless Remdesivir were sold to our governments on the taxpayer's dime, and it ended up being totally useless for treating hyperinflammatory COVID-19. The media has hardly even covered this at all.261

The opposition to the use of generic Ivermectin is not based in science. It is purely financially and politically motivated. An effective non-vaccine intervention would jeopardize the rushed FDA approval of patented vaccines and medicines for which the pharmaceutical industry stands to rake in billions upon billions of dollars in sales on an ongoing basis.277-279

There is mounting evidence that histamine blockers such as diphenhydramine, famotidine, ranitidine, and cimetidine may have utility in treating COVID-19, possibly by direct antiviral effects, or acting to reduce mast cell activation, in addition to modulating redox activity.280-283

Melatonin has been found to have some utility as an adjunct treatment for COVID-19.284,285 So have indomethacin, budesonide, and other immunomodulatory treatments.286-288 Indomethacin was known to be directly antiviral against SARS-CoV.289

COVID-19 Transmission

COVID-19 is airborne. Initially, the WHO carried water for China by claiming that the virus was only droplet-borne. Our own CDC absurdly claimed that it was mostly transmitted by fomite-to-face contact, which, given its rapid spread from Wuhan to the rest of the world, would have been physically impossible.290-293

The ridiculous belief in fomite-to-face being a primary mode of transmission led to the use of surface disinfection protocols that wasted time, energy, productivity, and disinfectant.294

The 6-foot guidelines are absolutely useless. The minimum safe distance to protect oneself from an aerosolized virus is to be 15+ feet away from an infected person, no closer. Realistically, no public transit is safe.295-297

Surgical masks and cloth masks do not protect you from aerosols. The virus is too small and the filter media has too large of gaps to filter it out. They may catch respiratory droplets and keep the virus from being expelled by someone who is sick, but they do not filter a cloud of infectious aerosols if someone were to walk into said cloud.298,299

The minimum level of protection against this virus is quite literally a P100 respirator, a PAPR/CAPR, or a 40mm NATO CBRN respirator, ideally paired with a full-body tyvek or tychem suit, gloves, and booties, with all the holes and gaps taped.300-303

Live SARS-CoV-2 may potentially be detected in sewage outflows, and there may be oral-fecal transmission.304-306 During the SARS outbreak in 2003, in the Amoy Gardens incident, hundreds of people were infected by aerosolized fecal matter rising from floor drains in their apartments.307-309

COVID-19 Vaccine Dangers

The vaccines for COVID-19 are not sterilizing and do not prevent infection or transmission. They are "leaky" vaccines. This means they remove the evolutionary pressure on the virus to become less lethal. It also means that the vaccinated are perfect carriers. In other words, those who are vaccinated are a threat to the unvaccinated, not the other way around.310-313

Natural immunity to COVID-19 from a past infection is far more robust than vaccine-induced immunity. This is because the immune system is exposed to all of the pathogen's proteins, not just one single protein in isolation.314,315

All of the COVID-19 vaccines currently in use have undergone minimal testing, with highly accelerated clinical trials. Though they appear to limit severe illness, the long-term safety profile of these vaccines remains unknown.316,317

Some of these so-called "vaccines" utilize an untested new technology that has never been used in vaccines before. Traditional vaccines use weakened or killed virus to stimulate an immune response. The Moderna and Pfizer-BioNTech vaccines do not. They are purported to consist of an intramuscular shot containing a suspension of lipid nanoparticles filled with messenger RNA.318-321 The way they generate an immune response is by fusing with cells in a vaccine recipient's shoulder, undergoing endocytosis, releasing their mRNA cargo into those cells, and then utilizing the ribosomes in those cells to synthesize modified SARS-CoV-2 Spike proteins in vivo.322,323

These modified Spike proteins then migrate to the surface of the cell, where they are anchored in place by a transmembrane domain. The adaptive immune system detects the non-human viral protein being expressed by these cells, and then forms antibodies against that protein. This is purported to confer protection against the virus, by training the adaptive immune system to recognize and produce antibodies against the Spike on the actual virus.324,325 The J&J and AstraZeneca vaccines do something similar, but use an adenovirus vector for genetic material delivery instead of a lipid nanoparticle.326 These vaccines were produced or validated with the aid of fetal cell lines HEK-293 and PER.C6, which people with certain religious convictions may object strongly to.327,328

SARS-CoV-2 Spike is a highly pathogenic protein on its own. It is impossible to overstate the danger presented by introducing this protein into the human body.328,329

It is claimed by vaccine manufacturers that the vaccine remains in cells in the shoulder, and that SARS- CoV-2 Spike produced and expressed by these cells from the vaccine's genetic material is harmless and inert, thanks to the insertion of prolines in the Spike sequence to stabilize it in the prefusion conformation, preventing the Spike from becoming active and fusing with other cells.330,331However, a pharmacokinetic study from Japan showed that the lipid nanoparticles and mRNA from the Pfizer vaccine did not stay in the shoulder, and in fact bioaccumulated in many different organs, including the reproductive organs and adrenal glands, meaning that modified Spike is being expressed quite literally all over the place.332 These lipid nanoparticles may trigger anaphylaxis in an unlucky few, but far more concerning is the unregulated expression of Spike in various somatic cell lines far from the injection site and the unknown consequences of that.333,334

Messenger RNA is normally consumed right after it is produced in the body, being translated into a protein by a ribosome.335 COVID-19 vaccine mRNA is produced outside the body, long before a ribosome translates it. In the meantime, it could accumulate damage if inadequately preserved. When a ribosome attempts to translate a damaged strand of mRNA, it can become stalled. When this happens, the ribosome becomes useless for translating proteins because it now has a piece of mRNA stuck in it, like a lace card in an old punch card reader. The whole thing has to be cleaned up and new ribosomes synthesized to replace it.336,337In cells with low ribosome turnover, like nerve cells, this can lead to reduced protein synthesis, cytopathic effects, and neuropathies.338-340

Certain proteins, including SARS-CoV-2 Spike, have proteolytic cleavage sites that are basically like little dotted lines that say "cut here", which attract a living organism's own proteases (essentially, molecular scissors) to cut them.341 There is a possibility that S1 may be proteolytically cleaved from S2, causing active S1 to float away into the bloodstream while leaving the S2 "stalk" embedded in the membrane of the cell that expressed the protein.342-347

SARS-CoV-2 Spike has a Superantigenic region (SAg), which may promote extreme inflammation.348,349 In one study, the Pfizer BNT162b2 vaccine was found to reprogram adaptive and innate immune responses in such a way that TLR4 surveillance is reduced.350 Anti-Spike antibodies were found in one study to function as autoantibodies and attack the body's own cells.351Those who have been immunized with COVID-19 vaccines have developed blood clots, myocarditis, Guillain-Barre Syndrome, Bell's Palsy, and multiple sclerosis flares, indicating that the vaccine promotes autoimmune reactions against healthy tissue.352-355

SARS-CoV-2 Spike does not only bind to ACE2. It was suspected to have regions that bind to basigin, integrins, neuropilin-1, and bacterial lipopolysaccharides as well.356-360SARS-CoV-2 Spike, on its own, can potentially bind any of these things and act as a ligand for them, triggering unspecified and likely highly inflammatory cellular activity.361

SARS-CoV-2 Spike contains an unusual PRRA insert that forms a furin cleavage site. Furin is a ubiquitous human protease, making this an ideal property for the Spike to have, giving it a high degree of cell tropism. No wild-type SARS-like coronaviruses related to SARS-CoV-2 possess this feature, making it highly suspicious, and perhaps a sign of human tampering.362-364

SARS-CoV-2 Spike has a prion-like domain that enhances its infectiousness.365-367 The Spike S1 RBD may bind to heparin-binding proteins and promote amyloid aggregation. In humans, this could lead to Parkinson's, Lewy Body Dementia, premature Alzheimer's, or various other neurodegenerative diseases.368This is very concerning because SARS-CoV-2 S1 is capable of injuring and penetrating the blood-brain barrier and entering the brain. It is also capable of increasing the permeability of the blood- brain barrier to other molecules.369-371

SARS-CoV-2, like other betacoronaviruses, may have Dengue-like ADE, or antibody-dependent enhancement of disease.372-379 For those who aren't aware, some viruses, including betacoronaviruses, have a feature called ADE. There is also something called Original Antigenic Sin, which is the observation that the body prefers to produce antibodies based on previously-encountered strains of a virus over newly-encountered ones.380,381

In ADE, antibodies from a previous infection become non-neutralizing due to mutations in the virus's proteins. These non-neutralizing antibodies then act as trojan horses, allowing live, active virus to be pulled into macrophages through their Fc receptor pathways, allowing the virus to infect immune cells that it would not have been able to infect before. This has been known to happen with Dengue Fever; when someone gets sick with Dengue, recovers, and then contracts a different strain, they can get very, very ill.382,383

If someone is vaccinated with mRNA based on the Spike from the initial Wuhan strain of SARS-CoV-2, and then they become infected with a future, mutated strain of the virus, they may become severely ill. In other words, it is possible for vaccines to sensitize someone to disease. There is a precedent for this in recent history. Sanofi's Dengvaxia vaccine for Dengue failed because it caused immune sensitization in people whose immune systems were Dengue-naïve.384-387

In mice immunized against SARS-CoV and challenged with the virus, a close relative of SARS-CoV-2, they developed immune sensitization, Th2 immunopathology, and eosinophil infiltration in their lungs.388

We have been told that SARS-CoV-2 mRNA vaccines cannot be integrated into the human genome, because messenger RNA cannot be turned back into DNA. This is false. There are elements in human cells called LINE-1 retrotransposons, which can indeed integrate mRNA into a human genome by endogenous reverse transcription. Because the mRNA used in the vaccines is stabilized, it persists inside cells for a longer period of time, increasing the chances for this to happen. If the gene for SARS-CoV-2 Spike is integrated into a portion of the genome that is not silent and actually expresses a protein, it is possible that people who take this vaccine may continuously express SARS-CoV-2 Spike from their somatic cells for the rest of their lives.389-391

By inoculating people with a vaccine that causes their cells to express Spike proteins, they are being inoculated with a pathogenic protein. A toxin that may cause inflammation, heart problems, and a raised risk of cancers. In the long-term, it may also potentially lead to premature neurodegenerative disease. Absolutely nobody should be compelled to take this vaccine under any circumstances, and in actual fact, the vaccination campaign must be stopped immediately.

COVID-19 Criminal Conspiracy

The vaccine and the virus were made by the same people.

In 2014, there was a moratorium on SARS gain-of-function research that lasted until 2017.392-394 This research was not halted. Instead, it was outsourced, with the federal grants being laundered through NGOs. Ralph Baric is a virologist and SARS expert at UNC Chapel Hill in North Carolina. This is who Anthony Fauci was referring to when he insisted, before Congress, that if any gain-of-function research was being conducted, it was being conducted in North Carolina.395,396

This was a lie. Anthony Fauci lied before Congress. A felony.

Ralph Baric and Shi Zhengli are colleagues and have co-written papers together.397 Ralph Baric mentored Shi Zhengli in his gain-of-function manipulation techniques, particularly serial passage, which results in a virus that appears as if it originated naturally. In other words, deniable bioweapons. Serial passage in humanized hACE2 mice may have produced something like SARS-CoV-2.398-401

The funding for the gain-of-function research being conducted at the Wuhan Institute of Virology came from Peter Daszak. Peter Daszak runs an NGO called EcoHealth Alliance. EcoHealth Alliance received millions of dollars in grant money from the National Institutes of Health/National Institute of Allergy and Infectious Diseases (that is, Anthony Fauci), the Defense Threat Reduction Agency (part of the US Department of Defense), and the United States Agency for International Development. NIH/NIAID contributed a few million dollars, and DTRA and USAID each contributed tens of millions of dollars towards this research. Altogether, it was over a hundred million dollars.402-405

EcoHealth Alliance subcontracted these grants to the Wuhan Institute of Virology, a lab in China with a very questionable safety record and poorly trained staff, so that they could conduct gain-of-function research, not in their fancy P4 lab, but in a level-2 lab where technicians wore nothing more sophisticated than perhaps a hairnet, latex gloves, and a surgical mask, instead of the bubble suits used when working with dangerous viruses.406-411 Chinese scientists in Wuhan reported being routinely bitten and urinated on by laboratory animals. Why anyone would outsource this dangerous and delicate work to the People's Republic of China, a country infamous for industrial accidents and massive explosions that have claimed hundreds of lives, is completely beyond me, unless the aim was to start a pandemic on purpose.412

In November of 2019, three technicians at the Wuhan Institute of Virology developed symptoms consistent with a flu-like illness. Anthony Fauci, Peter Daszak, and Ralph Baric knew at once what had happened, because back channels exist between this laboratory and our scientists and officials.413,414

December 12th, 2019, Ralph Baric signed a Material Transfer Agreement (essentially, an NDA) to receive Coronavirus mRNA vaccine-related materials co-owned by Moderna and NIH.415,416It wasn't until a whole month later, on January 11th, 2020, that China allegedly sent us the sequence to what would become known as SARS-CoV-2.417,418Moderna claims, rather absurdly, that they developed a working vaccine from this sequence in under 48 hours.419-421

Stéphane Bancel, the current CEO of Moderna, was formerly the CEO of bioMérieux, a French multinational corporation specializing in medical diagnostic tech, founded by one Alain Mérieux.422,423 Alain Mérieux was one of the individuals who was instrumental in the construction of the Wuhan Institute of Virology's P4 lab.424-426

Comment: Interestingly, there is no mention of Fort Detrick....

The sequence given as the closest relative to SARS-CoV-2, RaTG13, is not a real virus. It is a forgery. It was made by entering a gene sequence by hand into a database, to create a cover story for the existence of SARS-CoV-2, which is very likely a gain-of-function chimera produced at the Wuhan Institute of Virology and was either leaked by accident or intentionally released. For a virus as significant as RaTG13 appears to be to lie fallow for the better part of a decade with no research papers acknowledging its existence at all is an absurdity.427-429

The animal reservoir of SARS-CoV-2 has never been found.430,431

26 of the 27 people involved in penning the Lancet letter decrying the lab leak were connected directly to researchers linked to the Wuhan Institute of Virology, a massive conflict of interest.432 One of those was Peter Daszak himself, who was also a WHO investigator on the ground in Wuhan, and also served as a Facebook fact-checker.433-439 Peter Daszak and Aleksei Chmura penned an absolutely psychotic letter about animal reservoirs of viruses in 2008.440 Aleksei Chmura, for his part, was directly involved in capturing bats and collecting samples from them.441-449

Dr. David E. Martin showed, beyond a shadow of a doubt, with his research into biotech patents with his company, M-CAM, that literally every aspect of SARS and its variations are patented technologies.450

The government response to the pandemic has varied from the farcical to the downright criminal:

Residents in Wuhan were welded inside their apartments by the authorities to enforce a quarantine.451 In New York, sick COVID-19 patients were transferred into nursing homes to keep them out of hospitals, resulting in thousands of elderly and vulnerable people dying of COVID-19 due to nosocomial infections.452-454 In the UK, a whistleblower by the name of Wayne Smith claimed that the elderly were murdered by dosing them with large quantities of midazolam, and then the deaths were blamed on COVID-19; he was later found dead, supposedly of COVID-19.455-457

While the COVID-19 outbreak ravaged Wuhan, officials in the US completely dropped the ball by failing to stockpile N95 masks and other equipment for healthcare workers, leaving them short on supplies.458,459 Many masks sat unused in warehouses.460 Companies in the US offered to manufacture masks locally, but were rebuffed by the government.461,462 Fearing a run on masks, Anthony Fauci deliberately misinformed the public by claiming that N95 masks have no utility against the virus whatsoever, even though their performance is fair, albeit inferior to a proper respirator.463

COVID-19 has been diagnosed with PCR tests with extremely high cycle thresholds. A PCR test cannot actually diagnose an infection. All a PCR test indicates is that a targeted amino acid sequence is present in a sample, indicating that something like a fragment of a virus might exist in a person. A cycle threshold of 40 or greater being used to diagnose a viral infection is fraudulent. The sample is amplified over a trillion times. The targeted AA sequence could appear in practically any organic sample, at that rate. The false positive rate would be enormous.464-469The CDC quietly reduced the Ct to 28 after people started getting vaccinated for COVID-19. This would show a high rate of false negatives, thus causing the vaccine to appear more effective than it really is. In essence, the apparent rate of COVID-19 infections can be adjusted by the authorities by altering the sensitivity of tests.470,471

The FBI raided Allure Medical in Shelby Township north of Detroit for billing insurance for "fraudulent COVID-19 cures". The treatment they were using was Intravenous Vitamin C. An antioxidant. Which, as described above, is an entirely valid treatment for COVID-19-induced sepsis, and indeed, is now part of the MATH+ protocol advanced by Dr. Paul E. Marik.225,472-476

The FDA banned ranitidine (Zantac) due to supposed NDMA (N-nitrosodimethylamine) contamination.477,478 Ranitidine is not only an H2 blocker used as antacid, but also has a powerful antioxidant effect, scavenging hydroxyl radicals. This gives it utility in treating COVID-19.232,479

The FDA also attempted to take N-acetylcysteine, a harmless amino acid supplement and antioxidant, off the shelves, compelling Amazon to remove it from their online storefront.480-483

This leaves us with a chilling question: did the FDA knowingly suppress antioxidants useful for treating COVID-19 sepsis as part of a willful criminal conspiracy against the American public?

The lab leak theory has been suppressed because pulling that thread leads one to inevitably conclude that there is enough circumstantial evidence to link Moderna, the NIH, the WIV, and both the vaccine and the virus's creation together. In a sane world, this would have immediately led to the world's biggest RICO and mass murder case. Anthony Fauci, Peter Daszak, Ralph Baric, Shi Zhengli, and Stéphane Bancel, and their accomplices, would have been indicted and prosecuted to the fullest extent of the law. Instead, billions of our tax dollars were awarded to the perpetrators.

This is not a conspiracy "theory". It is an actual criminal conspiracy, in which people connected to the development of Moderna's mRNA-1273 are directly connected to the Wuhan Institute of Virology and their gain-of-function research by very few degrees of separation, if any. The paper trail is well- established. The establishment is cooperating with, and facilitating, the worst criminals in human history, and are actively suppressing non-vaccine treatments and therapies in order to compel us to inject these criminals' products into our bodies. This is absolutely unacceptable.

COVID-19 Vaccine Development and Links to Transhumanism

This section deals with some more speculative aspects of the pandemic and the medical and scientific establishment's reaction to it, as well as the disturbing links between scientists involved in vaccine research and scientists whose work involved merging nanotechnology with living cells.

On June 9th, 2020, Charles Lieber, a Harvard nanotechnology researcher with decades of experience, was indicted by the DOJ for fraud.484 Charles Lieber received millions of dollars in grant money from the US Department of Defense, specifically the military think tanks DARPA, AFOSR, and ONR, as well as NIH and MITRE.485 His specialty is the use of silicon nanowires in lieu of patch clamp electrodes to monitor and modulate intracellular activity, something he has been working on at Harvard for the past twenty years.486 He was claimed to have been working on silicon nanowire batteries in China, but none of his colleagues can recall him ever having worked on battery technology in his life; all of his research deals with bionanotechnology, or the blending of nanotech with living cells.487-489

The indictment was over his collaboration with the Wuhan University of Technology. He had double- dipped, against the terms of his DOD grants, and taken money from the PRC's Thousand Talents plan, a program which the Chinese government uses to bribe Western scientists into sharing proprietary R&D information that can be exploited by the PLA for strategic advantage.490-496

Charles Lieber's own papers describe the use of silicon nanowires for brain-computer interfaces, or "neural lace" technology. His papers describe how neurons can endocytose whole silicon nanowires or parts of them, monitoring and even modulating neuronal activity.497-499

Charles Lieber was a colleague of Robert Langer. Together, along with Daniel S. Kohane, they worked on a paper describing artificial tissue scaffolds that could be implanted in a human heart to monitor its activity remotely.500,501

Robert Langer, an MIT alumnus and expert in nanotech drug delivery, is one of the co-founders of Moderna.502 His net worth is now $5.1 billion USD thanks to Moderna's mRNA-1273 vaccine sales.503,504

Both Charles Lieber and Robert Langer's bibliographies describe, essentially, techniques for human enhancement, i.e. transhumanism.505,506 Klaus Schwab, the founder of the World Economic Forum and the architect behind the so-called "Great Reset", has long spoken of the "blending of biology and machinery" in his books.507,508

Since these revelations, it has come to the attention of independent researchers that the COVID-19 vaccines may contain reduced graphene oxide nanoparticles.509-515Japanese researchers have also found unexplained contaminants in COVID-19 vaccines.516-518

Graphene oxide is an anxiolytic. It has been shown to reduce the anxiety of laboratory mice when injected into their brains.519,520 Indeed, given SARS-CoV-2 Spike's propensity to compromise the blood- brain barrier and increase its permeability, it is the perfect protein for preparing brain tissue for extravasation of nanoparticles from the bloodstream and into the brain.521-525 Graphene is also highly conductive and, in some circumstances, paramagnetic.526-529

In 2013, under the Obama administration, DARPA launched the BRAIN Initiative; BRAIN is an acronym for Brain Research Through Advancing Innovative Neurotechnologies®. This program involves the development of brain-computer interface technologies for the military, particularly non-invasive, injectable systems that cause minimal damage to brain tissue when removed.530

Supposedly, this technology would be used for healing wounded soldiers with traumatic brain injuries, the direct brain control of prosthetic limbs, and even new abilities such as controlling drones with one's mind. Various methods have been proposed for achieving this, including optogenetics, magnetogenetics, ultrasound, implanted electrodes, and transcranial electromagnetic stimulation. In all instances, the goal is to obtain read or read-write capability over neurons, either by stimulating and probing them, or by rendering them especially sensitive to stimulation and probing.531

However, the notion of the widespread use of BCI technology, such as Elon Musk's Neuralink device, raises many concerns over privacy and personal autonomy. Reading from neurons is problematic enough on its own. Wireless brain-computer interfaces may interact with current or future wireless GSM infrastructure, creating neurological data security concerns. A hacker or other malicious actor may compromise such networks to obtain people's brain data, and then exploit it for nefarious purposes.532-536

However, a device capable of writing to human neurons, not just reading from them, presents another, even more serious set of ethical concerns. A BCI that is capable of altering the contents of one's mind for innocuous purposes, such as projecting a heads-up display onto their brain's visual center or sending audio into one's auditory cortex, would also theoretically be capable of altering mood and personality, or perhaps even subjugating someone's very will, rendering them utterly obedient to authority. This technology would be a tyrant's wet dream. Imagine soldiers who would shoot their own countrymen without hesitation, or helpless serfs who are satisfied to live in literal dog kennels.537,538

BCIs could be used to unscrupulously alter perceptions of basic things such as emotions and values, changing people's thresholds of satiety, happiness, anger, disgust, and so forth. This is not inconsequential. Someone's entire regime of behaviors could be altered by a BCI, including such things as suppressing their appetite or desire for virtually anything on Maslow's Hierarchy of Needs. Anything is possible when you have direct access to someone's brain and its contents. Someone who is obese could be made to feel disgust at the sight of food. Someone who is involuntarily celibate could have their libido disabled so they don't even desire sex to begin with. Someone who is racist could be forced to feel delight over cohabiting with people of other races. Someone who is violent could be forced to be meek and submissive. These things might sound good to you if you are a tyrant, but to normal people, the idea of personal autonomy being overridden to such a degree is appalling.539-541

For the wealthy, neural laces would be an unequaled boon, giving them the opportunity to enhance their intelligence with neuroprosthetics (i.e. an "exocortex"), and to deliver irresistible commands directly into the minds of their BCI-augmented servants, even physically or sexually abusive commands that they would normally refuse.542,543

If the vaccine is a method to surreptitiously introduce an injectable BCI into millions of people without their knowledge or consent, then what we are witnessing is the rise of a tyrannical regime unlike anything ever seen before on the face of this planet, one that fully intends to strip every man, woman, and child of our free will. The people who rule over us are Dark Triad types who cannot be trusted with such unimaginable power.544-549

Our flaws are what make us human. A utopia arrived at by removing people's free will is not a utopia at all. It is a monomaniacal nightmare. Imagine being beaten and sexually assaulted by a wealthy and powerful psychopath and being forced to smile and laugh over it because your neural lace gives you no choice but to obey your master.550

The Elites are forging ahead with this technology without giving people any room to question the social or ethical ramifications, or even bothering to establish regulatory frameworks that ensure that our personal agency and autonomy will not be overridden by these devices. They do this because they secretly dream of a future where they can treat you worse than an animal and you cannot even fight back. If this evil plan is allowed to continue, it will spell the end of humanity as we know it.


The current pandemic was produced and perpetuated by the establishment, through the use of a virus engineered in a PLA-connected Chinese biowarfare laboratory, with the aid of American taxpayer dollars and French expertise.

This research was conducted under the absolutely ridiculous euphemism of "gain-of-function" research, which is supposedly carried out in order to determine which viruses have the highest potential for zoonotic spillover and preemptively vaccinate or guard against them.

Gain-of-function/gain-of-threat research, a.k.a. "Dual-Use Research of Concern", or DURC, is bioweapon research by another, friendlier-sounding name, simply to avoid the taboo of calling it what it actually is. It has always been bioweapon research. The people who are conducting this research fully understand that they are taking wild pathogens that are not infectious in humans and making them more infectious, often taking grants from military think tanks encouraging them to do so.

These virologists conducting this type of research are enemies of their fellow man, like pyromaniac firefighters. GOF research has never protected anyone from any pandemic. In fact, it has now started one, meaning its utility for preventing pandemics is actually negative. It should have been banned globally, and the lunatics performing it should have been put in straitjackets long ago.

Either through a leak or an intentional release from the Wuhan Institute of Virology, a deadly SARS strain is now endemic across the globe, after the WHO and CDC and public officials first downplayed the risks, and then intentionally incited a panic and lockdowns that jeopardized people's health and their livelihoods.

This was then used by the utterly depraved and psychopathic aristocratic class who rule over us as an excuse to coerce people into accepting an injected poison which may be a depopulation agent, a mind control/pacification agent in the form of injectable "smart dust", or both in one. They believe they can get away with this by weaponizing the social stigma of vaccine refusal. They are incorrect.

Their motives are clear and obvious to anyone who has been paying attention. These megalomaniacs have raided the pension funds of the free world. Wall Street is insolvent and has had an ongoing liquidity crisis since the end of 2019. The aim now is to exert total, full-spectrum physical, mental, and financial control over humanity before we realize just how badly we've been extorted by these maniacs.

The pandemic and its response served multiple purposes for the Elite:

  • Concealing a depression brought on by the usurious plunder of our economies conducted by rentier-capitalists and absentee owners who produce absolutely nothing of any value to society whatsoever. Instead of us having a very predictable Occupy Wall Street Part II, the Elites and their stooges got to stand up on television and paint themselves as wise and all-powerful saviors instead of the marauding cabal of despicable land pirates that they are.
  • Destroying small businesses and eroding the middle class.
  • Transferring trillions of dollars of wealth from the American public and into the pockets of billionaires and special interests.
  • Engaging in insider trading, buying stock in biotech companies and shorting brick-and-mortar businesses and travel companies, with the aim of collapsing face-to-face commerce and tourism and replacing it with e-commerce and servitization.
  • Creating a casus belli for war with China, encouraging us to attack them, wasting American lives and treasure and driving us to the brink of nuclear armageddon.
  • Establishing technological and biosecurity frameworks for population control and technocratic- socialist "smart cities" where everyone's movements are despotically tracked, all in anticipation of widespread automation, joblessness, and food shortages, by using the false guise of a vaccine to compel cooperation.

Any one of these things would constitute a vicious rape of Western society. Taken together, they beggar belief; they are a complete inversion of our most treasured values.

What is the purpose of all of this? One can only speculate as to the perpetrators' motives, however, we have some theories.

The Elites are trying to pull up the ladder, erase upward mobility for large segments of the population, cull political opponents and other "undesirables", and put the remainder of humanity on a tight leash, rationing our access to certain goods and services that they have deemed "high-impact", such as automobile use, tourism, meat consumption, and so on. Naturally, they will continue to have their own luxuries, as part of a strict caste system akin to feudalism.

What is the most convenient means of accomplishing this? First, scare the public, globally, with an engineered pandemic virus. Then, convince people that the only way they can have their bread and circuses back is if they agree to have poison injected into their shoulder. Naturally, people would panic if they saw everyone around them dying or becoming infertile, so the shot would also necessarily contain something to keep them docile and content.

Why are they doing this? Simple. The Elites are Neo-Malthusians and believe that we are overpopulated and that resource depletion will collapse civilization in a matter of a few short decades. They are not necessarily incorrect in this belief. We are overpopulated, and we are consuming too many resources. However, orchestrating such a gruesome and murderous power grab in response to a looming crisis demonstrates that they have nothing but the utmost contempt for their fellow man. Depopulating the Earth is atrocious in any context, but doing so without the knowledge or consent of the public is monstrous.

It is the opinion of ICENI, and other independent researchers, that the world's governments are covertly engaged in an act of genocide against their own populations. This will not be tolerated.

To those who are participating in this disgusting farce without any understanding of what they are doing, we have one word for you. Stop. You are causing irreparable harm to your country and to your fellow citizens.

To those who may be reading this warning and have full knowledge and understanding of what they are doing and how it will unjustly harm millions of innocent people, we have a few more words.

Damn you to hell. You will not destroy America and the Free World, and you will not have your New World Order. We will make certain of that.

References 1. Libby P, Lüscher T. COVID-19 is, in the end, an endothelial disease.Eur Heart J.2020;41(32):3038-3044. doi:10.1093/eurheartj/ehaa6232. Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19.TheLancet . 2020;395(10234):1417-1418. doi:10.1016/S0140-6736(20)30937-53. Rapid endotheliitis and vascular damage characterize SARS-CoV-2 infection in a human lung-on-chip model.EMBO Rep. 2021;22(6):e52744. doi:10.15252/embr.2021527444. Cui X, Chen W, Zhou H, et al. Pulmonary Edema in COVID-19 Patients: Mechanisms andTreatment Potential.Front Pharmacol . 2021;12:1444. doi:10.3389/fphar.2021.6643495. Zwaveling S, Wijk RG van, Karim F. Pulmonary edema in COVID-19: Explained by bradykinin? J Allergy Clin Immunol . 2020;146(6):1454-1455. doi:10.1016/j.jaci.2020.08.0386. Frontiers | Parallels in Sepsis and COVID-19 Conditions: Implications for Managing SevereCOVID-19 | Immunology. Accessed September 27, 2021. Vincent J-L. COVID-19: it’s all about sepsis.Future Microbiol . 2021;16(3):131-133.doi:10.2217/fmb-2020-03128. Gómez-Mesa JE, Galindo-Coral S, Montes MC, Muñoz Martin AJ. Thrombosis and Coagulopathyin COVID-19.Curr Probl Cardiol . 2021;46(3):100742. doi:10.1016/j.cpcardiol.2020.1007429. Chan NC, Weitz JI. COVID-19 coagulopathy, thrombosis, and bleeding.Blood . 2020;136(4):381-383. doi:10.1182/blood.202000733510. Ortega-Paz L, Capodanno D, Montalescot G, Angiolillo DJ. Coronavirus Disease 2019–AssociatedThrombosis and Coagulopathy: Review of the Pathophysiological Characteristics and Implications forAntithrombotic Management. J Am Heart Assoc. 2021;10(3):e019650. doi:10.1161/JAHA.120.01965011. Mokhtari T, Hassani F, Ghaffari N, Ebrahimi B, Yarahmadi A, Hassanzadeh G. COVID-19 andmultiorgan failure: A narrative review on potential mechanisms. J Mol Histol . Published online October4, 2020:1-16. doi:10.1007/s10735-020-09915-312. Zaim S, Chong JH, Sankaranarayanan V, Harky A. COVID-19 and Multiorgan Response.Curr ProblCardiol . 2020;45(8):100618. doi:10.1016/j.cpcardiol.2020.10061813. Frontiers | Pathogenesis of Multiple Organ Injury in COVID-19 and Potential TherapeuticStrategies | Physiology. Accessed September 27, 2021. Boldrini M, Canoll PD, Klein RS. How COVID-19 Affects the Brain. JAMA Psychiatry .2021;78(6):682-683. doi:10.1001/jamapsychiatry.2021.0500 15. Parry AH, Wani AH, Yaseen M. Neurological Dysfunction in Coronavirus Disease-19 (COVID-19). Acad Radiol . 2020;27(9):1329-1330. doi:10.1016/j.acra.2020.05.02416. Schwabenland M, Salié H, Tanevski J, et al. Deep spatial profiling of human COVID-19 brainsreveals neuroinflammation with distinct microanatomical microglia-T-cell interactions.Immunity .2021;54(7):1594-1610.e11. doi:10.1016/j.immuni.2021.06.00217. Rogers JP, Watson CJ, Badenoch J, et al. Neurology and neuropsychiatry of COVID-19: asystematic review and meta-analysis of the early literature reveals frequent CNS manifestations and keyemerging narratives. J Neurol Neurosurg Psychiatry . 2021;92(9):932-941. doi:10.1136/jnnp-2021-32640518. Abbasi J. Researchers Investigate What COVID-19 Does to the Heart. JAMA. 2021;325(9):808-811. doi:10.1001/jama.2021.010719. COVID-19 as a Possible Cause of Myocarditis and Pericarditis. American College of Cardiology.Accessed September 27, 2021. Bzeizi K, Abdulla M, Mohammed N, Alqamish J, Jamshidi N, Broering D. Effect of COVID-19 onliver abnormalities: a systematic review and meta-analysis.Sci Rep. 2021;11(1):10599.doi:10.1038/s41598-021-89513-921. Moon AM, Barritt AS. Elevated Liver Enzymes in Patients with COVID-19: Look, but Not TooHard.Dig Dis Sci . Published online September 2, 2020:1-3. doi:10.1007/s10620-020-06585-922. Iqbal Z, Ho JH, Adam S, et al. Managing hyperlipidaemia in patients with COVID-19 and during itspandemic: An expert panel position statement from HEART UK. Atherosclerosis. 2020;313:126-136.doi:10.1016/j.atherosclerosis.2020.09.00823. Steenblock C, Richter S, Berger I, et al. Viral infiltration of pancreatic islets in patients withCOVID-19.Nat Commun. 2021;12(1):3534. doi:10.1038/s41467-021-23886-324. Hayden MR. An Immediate and Long-Term Complication of COVID-19 May Be Type 2 DiabetesMellitus: The Central Role of β-Cell Dysfunction, Apoptosis and Exploration of Possible Mechanisms.Cells. 2020;9(11):2475. doi:10.3390/cells911247525. Mukherjee S, Banerjee O, Singh S, Maji BK. COVID 19 could trigger global diabetes burden – Ahypothesis.Diabetes Metab Syndr . 2020;14(5):963-964. doi:10.1016/j.dsx.2020.06.04926. Wu C-T, Lidsky PV, Xiao Y, et al. SARS-CoV-2 infects human pancreatic β cells and elicits β cellimpairment.Cell Metab. 2021;33(8):1565-1576.e5. doi:10.1016/j.cmet.2021.05.01327. Legrand M, Bell S, Forni L, et al. Pathophysiology of COVID-19-associated acute kidney injury.Nat Rev Nephrol . Published online July 5, 2021:1-14. doi:10.1038/s41581-021-00452-028. Nugent J, Aklilu A, Yamamoto Y, et al. Assessment of Acute Kidney Injury and LongitudinalKidney Function After Hospital Discharge Among Patients With and Without COVID-19. JAMA NetwOpen. 2021;4(3):e211095. doi:10.1001/jamanetworkopen.2021.109529. Chen Z, Hu J, Liu L, et al. SARS-CoV-2 Causes Acute Kidney Injury by Directly Infecting RenalTubules.Front Cell Dev Biol . 2021;9:1245. doi:10.3389/fcell.2021.66486830. Gu J, Han B, Wang J. COVID-19: Gastrointestinal Manifestations and Potential Fecal–OralTransmission.Gastroenterology . 2020;158(6):1518-1519. doi:10.1053/j.gastro.2020.02.05431. Lehmann M, Allers K, Heldt C, et al. Human small intestinal infection by SARS-CoV-2 ischaracterized by a mucosal infiltration with activated CD8+ T cells.Mucosal Immunol . Published onlineAugust 21, 2021:1-12. doi:10.1038/s41385-021-00437-z32. Zhang H, Kang Z, Gong H, et al. Digestive system is a potential route of COVID-19: an analysis ofsingle-cell coexpression pattern of key proteins in viral entry process.Gut . 2020;69(6):1010-1018.doi:10.1136/gutjnl-2020-320953 33. Pourbagheri-Sigaroodi A, Bashash D, Fateh F, Abolghasemi H. Laboratory findings in COVID-19diagnosis and prognosis.Clin Chim Acta Int J Clin Chem. 2020;510:475-482.doi:10.1016/j.cca.2020.08.01934. Zhang Z-L, Hou Y-L, Li D-T, Li F-Z. Laboratory findings of COVID-19: a systematic review andmeta-analysis.Scand J Clin Lab Invest . 2020;80(6):441-447. doi:10.1080/00365513.2020.176858735. Xie Y, Wang Z, Liao H, Marley G, Wu D, Tang W. Epidemiologic, clinical, and laboratory findingsof the COVID-19 in the current pandemic: systematic review and meta-analysis.BMC Infect Dis.2020;20(1):640. doi:10.1186/s12879-020-05371-236. Xiang Q, Feng Z, Diao B, et al. SARS-CoV-2 Induces Lymphocytopenia by Promoting Inflammationand Decimates Secondary Lymphoid Organs.Front Immunol . 2021;12:1292.doi:10.3389/fimmu.2021.66105237. Rha M-S, Shin E-C. Activation or exhaustion of CD8+ T cells in patients with COVID-19.Cell MolImmunol . Published online August 19, 2021:1-9. doi:10.1038/s41423-021-00750-438. Kusnadi A, Ramírez-Suástegui C, Fajardo V, et al. Severely ill patients with COVID-19 displayimpaired exhaustion features in SARS-CoV-2–reactive CD8+ T cells.Sci Immunol . 2021;6(55):eabe4782.doi:10.1126/sciimmunol.abe478239. Del Valle DM, Kim-Schulze S, Huang H-H, et al. An inflammatory cytokine signature predictsCOVID-19 severity and survival.Nat Med . 2020;26(10):1636-1643. doi:10.1038/s41591-020-1051-940. What explains the non-respiratory symptoms seen in some COVID-19 patients? Chemical &Engineering News. Accessed September 28, 2021. Protean manifestations of COVID-19: “Our ignorance is profound.” Accessed September 28,2021. Jarrahi A, Ahluwalia M, Khodadadi H, et al. Neurological consequences of COVID-19: what havewe learned and where do we go from here? J Neuroinflammation. 2020;17(1):286. doi:10.1186/s12974-020-01957-443. Zubair AS, McAlpine LS, Gardin T, Farhadian S, Kuruvilla DE, Spudich S. Neuropathogenesis andNeurologic Manifestations of the Coronaviruses in the Age of Coronavirus Disease 2019: A Review. JAMANeurol . 2020;77(8):1018-1027. doi:10.1001/jamaneurol.2020.206544. Qureshi AI, Baskett WI, Huang W, et al. Acute Ischemic Stroke and COVID-19.Stroke.2021;52(3):905-912. doi:10.1161/STROKEAHA.120.03178645. Riyahi S, Dev H, Behzadi A, et al. Pulmonary Embolism in Hospitalized Patients with COVID-19: AMulticenter Study.Radiology . Published online July 13, 2021:210777. doi:10.1148/radiol.202121077746. Zhong P, Xu J, Yang D, et al. COVID-19-associated gastrointestinal and liver injury: clinicalfeatures and potential mechanisms.Signal Transduct Target Ther . 2020;5(1):1-8. doi:10.1038/s41392-020-00373-747. Nishiga M, Wang DW, Han Y, Lewis DB, Wu JC. COVID-19 and cardiovascular disease: from basicmechanisms to clinical perspectives.Nat Rev Cardiol . 2020;17(9):543-558. doi:10.1038/s41569-020-0413-948. Al-Sabah S, Al-Haddad M, Al-Youha S, Jamal M, Almazeedi S. COVID-19: Impact of obesity anddiabetes on disease severity.Clin Obes. Published online October 20, 2020:e12414.doi:10.1111/cob.1241449. Gao M, Piernas C, Astbury NM, et al. Associations between body-mass index and COVID-19severity in 6·9 million people in England: a prospective, community-based, cohort study.Lancet DiabetesEndocrinol . 2021;9(6):350-359. doi:10.1016/S2213-8587(21)00089-9 50. Jin Y, Ji W, Yang H, Chen S, Zhang W, Duan G. Endothelial activation and dysfunction in COVID-19: from basic mechanisms to potential therapeutic approaches.Signal Transduct Target Ther .2020;5(1):1-13. doi:10.1038/s41392-020-00454-751. Green SJ. Covid-19 accelerates endothelial dysfunction and nitric oxide deficiency.MicrobesInfect . 2020;22(4):149-150. doi:10.1016/j.micinf.2020.05.00652. Levin AT, Hanage WP, Owusu-Boaitey N, Cochran KB, Walsh SP, Meyerowitz-Katz G. Assessingthe age specificity of infection fatality rates for COVID-19: systematic review, meta-analysis, and publicpolicy implications.Eur J Epidemiol . 2020;35(12):1123-1138. doi:10.1007/s10654-020-00698-153. CDC. Cases, Data, and Surveillance. Centers for Disease Control and Prevention. PublishedFebruary 11, 2020. Accessed September 28, 2021. Covid IFR Analysis. Accessed September 28, 2021. Seoane B. A scaling approach to estimate the age-dependent COVID-19 infection fatality ratiofrom incomplete data.PLOS ONE . 2021;16(2):e0246831. doi:10.1371/journal.pone.024683156. Hu B, Guo H, Zhou P, Shi Z-L. Characteristics of SARS-CoV-2 and COVID-19.Nat Rev Microbiol .2021;19(3):141-154. doi:10.1038/s41579-020-00459-757. Xia L, Chen J, Friedemann T, et al. The Course of Mild and Moderate COVID-19 Infections—TheUnexpected Long-Lasting Challenge.Open Forum Infect Dis. 2020;7(9). doi:10.1093/ofid/ofaa28658. Han C, Duan C, Zhang S, et al. Digestive Symptoms in COVID-19 Patients With Mild DiseaseSeverity: Clinical Presentation, Stool Viral RNA Testing, and Outcomes. Am J Gastroenterol . Publishedonline April 15, 2020:10.14309/ajg.0000000000000664. doi:10.14309/ajg.000000000000066459. CDC. Cases, Data, and Surveillance. Centers for Disease Control and Prevention. PublishedFebruary 11, 2020. Accessed September 28, 2021. Wu SL, Mertens AN, Crider YS, et al. Substantial underestimation of SARS-CoV-2 infection in theUnited States.Nat Commun. 2020;11(1):4507. doi:10.1038/s41467-020-18272-461. Irons NJ, Raftery AE. Estimating SARS-CoV-2 infections from deaths, confirmed cases, tests, andrandom surveys.Proc Natl Acad Sci . 2021;118(31). doi:10.1073/pnas.210327211862. Achaiah NC, Subbarajasetty SB, Shetty RM. R0 and Re of COVID-19: Can We Predict When thePandemic Outbreak will be Contained?Indian J Crit Care Med Peer-Rev Off Publ Indian Soc Crit CareMed . 2020;24(11):1125-1127. doi:10.5005/jp-journals-10071-2364963. Ives AR, Bozzuto C. Estimating and explaining the spread of COVID-19 at the county level in theUSA.Commun Biol . 2021;4(1):1-9. doi:10.1038/s42003-020-01609-664. Lan J, Ge J, Yu J, et al. Structure of the SARS-CoV-2 spike receptor-binding domain bound to theACE2 receptor.Nature. 2020;581(7807):215-220. doi:10.1038/s41586-020-2180-565. Yang J, Petitjean SJL, Koehler M, et al. Molecular interaction and inhibition of SARS-CoV-2binding to the ACE2 receptor.Nat Commun. 2020;11(1):4541. doi:10.1038/s41467-020-18319-666. ACE2 angiotensin converting enzyme 2 [Homo sapiens (human)] - Gene - NCBI. AccessedSeptember 28, 2021. Samavati L, Uhal BD. ACE2, Much More Than Just a Receptor for SARS-COV-2.Front Cell InfectMicrobiol . 2020;10:317. doi:10.3389/fcimb.2020.0031768. Patel S, Rauf A, Khan H, Abu-Izneid T. Renin-angiotensin-aldosterone (RAAS): The ubiquitoussystem for homeostasis and pathologies.Biomed Pharmacother . 2017;94:317-325.doi:10.1016/j.biopha.2017.07.09169. Romero CA, Orias M, Weir MR. Novel RAAS agonists and antagonists: clinical applications andcontroversies.Nat Rev Endocrinol . 2015;11(4):242-252. doi:10.1038/nrendo.2015.670. The Renin-Angiotensin-Aldosterone-System. TeachMePhysiology. Accessed September 28, 2021. 71. Fountain JH, Lappin SL. Physiology, Renin Angiotensin System. In:StatPearls. StatPearlsPublishing; 2021. Accessed September 28, 2021. Renin Angiotensin Aldosterone System - an overview | ScienceDirect Topics. AccessedSeptember 28, 2021. Hamming I, Timens W, Bulthuis M, Lely A, Navis G, van Goor H. Tissue distribution of ACE2protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. JPathol . 2004;203(2):631-637. doi:10.1002/path.157074. Tissue expression of ACE2 - Summary - The Human Protein Atlas. Accessed September 28, 2021. The protein expression profile of ACE2 in human tissues.Mol Syst Biol . 2020;16(7):e9610.doi:10.15252/msb.2020961076. Huang Y, Yang C, Xu X, Xu W, Liu S. Structural and functional properties of SARS-CoV-2 spikeprotein: potential antivirus drug development for COVID-19. Acta Pharmacol Sin. 2020;41(9):1141-1149.doi:10.1038/s41401-020-0485-477. Shang J, Wan Y, Luo C, et al. Cell entry mechanisms of SARS-CoV-2.Proc Natl Acad Sci .2020;117(21):11727-11734. doi:10.1073/pnas.200313811778. Xie Y, Karki CB, Du D, et al. Spike Proteins of SARS-CoV and SARS-CoV-2 Utilize DifferentMechanisms to Bind With Human ACE2.Front Mol Biosci . 2020;7:392. doi:10.3389/fmolb.2020.59187379. Syncytia formation by SARS-CoV-2-infected cells.EMBO J. 2020;39(23):e106267.doi:10.15252/embj.202010626780. Ma H, Zhu Z, Lin H, et al. Pyroptosis of syncytia formed by fusion of SARS-CoV-2 spike and ACE2-expressing cells.Cell Discov . 2021;7(1):1-4. doi:10.1038/s41421-021-00310-081. Xia B, Shen X, He Y, et al. SARS-CoV-2 envelope protein causes acute respiratory distresssyndrome (ARDS)-like pathological damages and constitutes an antiviral target.Cell Res. 2021;31(8):847-860. doi:10.1038/s41422-021-00519-482. Nieto-Torres JL, Verdiá-Báguena C, Jimenez-Guardeño JM, et al. Severe acute respiratorysyndrome coronavirus E protein transports calcium ions and activates the NLRP3 inflammasome.Virology . 2015;485:330-339. doi:10.1016/j.virol.2015.08.01083. Minakshi R, Padhan K, Rehman S, Hassan MdI, Ahmad F. The SARS Coronavirus 3a protein bindscalcium in its cytoplasmic domain.Virus Res. 2014;191:180-183. doi:10.1016/j.virusres.2014.08.00184. Pan P, Shen M, Yu Z, et al. SARS-CoV-2 N protein promotes NLRP3 inflammasome activation toinduce hyperinflammation.Nat Commun. 2021;12(1):4664. doi:10.1038/s41467-021-25015-685. Shah A. Novel Coronavirus-Induced NLRP3 Inflammasome Activation: A Potential Drug Target inthe Treatment of COVID-19.Front Immunol . 2020;11:1021. doi:10.3389/fimmu.2020.0102186. Xu H, Chitre SA, Akinyemi IA, et al.SARS-CoV-2 Viroporin Triggers the NLRP3 InflammatoryPathway .; 2020:2020.10.27.357731. doi:10.1101/2020.10.27.35773187. Olagnier D, Farahani E, Thyrsted J, et al. SARS-CoV2-mediated suppression of NRF2-signalingreveals potent antiviral and anti-inflammatory activity of 4-octyl-itaconate and dimethyl fumarate.NatCommun. 2020;11(1):4938. doi:10.1038/s41467-020-18764-388. Bousquet J, Cristol J-P, Czarlewski W, et al. Nrf2-interacting nutrients and COVID-19: time forresearch to develop adaptation strategies.Clin Transl Allergy . 2020;10(1):58. doi:10.1186/s13601-020-00362-789. Cuadrado A, Pajares M, Benito C, et al. Can Activation of NRF2 Be a Strategy against COVID-19?Trends Pharmacol Sci . 2020;41(9):598-610. doi:10.1016/ Bousquet J, Czarlewski W, Zuberbier T, et al. Potential Interplay between Nrf2, TRPA1, andTRPV1 in Nutrients for the Control of COVID-19.Int Arch Allergy Immunol . 2021;182(4):324-338.doi:10.1159/000514204 91. McCarthy CG, Wilczynski S, Wenceslau CF, Webb RC. A new storm on the horizon in COVID-19:Bradykinin-induced vascular complications.Vascul Pharmacol . 2021;137:106826.doi:10.1016/j.vph.2020.10682692. Lei Y, Zhang J, Schiavon CR, et al. SARS-CoV-2 Spike Protein Impairs Endothelial Function viaDownregulation of ACE 2.Circ Res. 2021;128(9):1323-1326. doi:10.1161/CIRCRESAHA.121.31890293. Silhol F, Sarlon G, Deharo J-C, Vaïsse B. Downregulation of ACE2 induces overstimulation of therenin–angiotensin system in COVID-19: should we block the renin–angiotensin system?Hypertens Res.2020;43(8):854-856. doi:10.1038/s41440-020-0476-394. Ciulla MM. SARS-CoV-2 downregulation of ACE2 and pleiotropic effects of ACEIs/ARBs.Hypertens Res. 2020;43(9):985-986. doi:10.1038/s41440-020-0488-z95. Lu J, Sun PD. High affinity binding of SARS-CoV-2 spike protein enhances ACE2 carboxypeptidaseactivity. J Biol Chem. 2020;295(52):18579-18588. doi:10.1074/jbc.RA120.01530396. Osman W, Fahdi FA, Salmi IA, Khalili HA, Gokhale A, Khamis F. Serum Calcium and Vitamin Dlevels: Correlation with severity of COVID-19 in hospitalized patients in Royal Hospital, Oman.Int J InfectDis. 2021;107:153-163. doi:10.1016/j.ijid.2021.04.05097. Raesi A, Saedi Dezaki E, Moosapour H, et al. Hypocalcemia in Covid-19: A Prognostic Marker forSevere Disease.Iran J Pathol . 2021;16(2):144-153. doi:10.30699/IJP.2020.130491.244298. Bennouar S, Cherif AB, Kessira A, Bennouar D-E, Abdi S. Vitamin D Deficiency and Low SerumCalcium as Predictors of Poor Prognosis in Patients with Severe COVID-19. J Am Coll Nutr .2021;40(2):104-110. doi:10.1080/07315724.2020.185601399. Blaes N, Girolami J-P. Targeting the “Janus face” of the B2-bradykinin receptor.Expert Opin TherTargets. 2013;17. doi:10.1517/14728222.2013.827664100. Siragy H, Jaffa A, Margolius H. Bradykinin B2 receptor modulates renal prostaglandin E2 andnitric oxide.Hypertension. Published online 1997. doi:10.1161/01.HYP.29.3.757101. Pyne NJ, Tolan D, Pyne S. Bradykinin stimulates cAMP synthesis via mitogen-activated proteinkinase-dependent regulation of cytosolic phospholipase A2 and prostaglandin E2 release in airwaysmooth muscle.Biochem J. 1997;328(Pt 2):689-694. Accessed September 28, 2021. Dixon BS, Breckon R, Fortune J, Sutherland E, Simon FR, Anderson RJ. Bradykinin activatesprotein kinase C in cultured cortical collecting tubular cells. Am J Physiol-Ren Physiol . 1989;257(5):F808-F817. doi:10.1152/ajprenal.1989.257.5.F808103. Schini VB, Boulanger C, Regoli D, Vanhoutte PM. Bradykinin stimulates the production of cyclicGMP via activation of B2 kinin receptors in cultured porcine aortic endothelial cells. J Pharmacol ExpTher . 1990;252(2):581-585.104. Gholamreza-Fahimi E, Bisha M, Hahn J, et al. Cyclooxygenase activity in bradykinin-induceddermal extravasation. A study in mice and humans.Biomed Pharmacother . 2020;123:109797.doi:10.1016/j.biopha.2019.109797105. Fong P, Stafforini DM, Brown NJ, Pretorius M. Increased blood flow induces oxidative stressthrough an endothelium- and nitric oxide-independent mechanism.Free Radic Biol Med .2010;49(2):301-305. doi:10.1016/j.freeradbiomed.2010.04.023106. Portilla D, Morrissey J, Morrison AR. Bradykinin-activated membrane-associated phospholipaseC in Madin-Darby canine kidney cells. J Clin Invest . 1988;81(6):1896-1902. doi:10.1172/JCI113536107. Cruzblanca H, Koh D-S, Hille B. Bradykinin inhibits M current via phospholipase C and Ca2+release from IP3-sensitive Ca2+ stores in rat sympathetic neurons.Proc Natl Acad Sci . 1998;95(12):7151-7156. doi:10.1073/pnas.95.12.7151108. Bradykinin - an overview | ScienceDirect Topics. Accessed September 28, 2021. 109. Banerjee A, Czinn SJ, Reiter RJ, Blanchard TG. Crosstalk between endoplasmic reticulum stressand anti-viral activities: A novel therapeutic target for COVID-19.Life Sci . 2020;255:117842.doi:10.1016/j.lfs.2020.117842110. Danta CC. SARS-CoV-2, Hypoxia, and Calcium Signaling: The Consequences and TherapeuticOptions. ACS Pharmacol Transl Sci . 2021;4(1):400-402. doi:10.1021/acsptsci.0c00219111. Shaban MS, Müller C, Mayr-Buro C, et al. Multi-level inhibition of coronavirus replication bychemical ER stress.Nat Commun. 2021;12(1):5536. doi:10.1038/s41467-021-25551-1112. Sabirli R, Koseler A, Goren T, Turkcuer I, Kurt O. High GRP78 levels in Covid-19 infection: A case-control study.Life Sci . 2021;265:118781. doi:10.1016/j.lfs.2020.118781113. Dubiella U, Seybold H, Durian G, et al. Calcium-dependent protein kinase/NADPH oxidaseactivation circuit is required for rapid defense signal propagation.Proc Natl Acad Sci .2013;110(21):8744-8749. doi:10.1073/pnas.1221294110114. Görlach A, Bertram K, Hudecova S, Krizanova O. Calcium and ROS: A mutual interplay.RedoxBiol . 2015;6:260-271. doi:10.1016/j.redox.2015.08.010115. Feno S, Butera G, Vecellio Reane D, Rizzuto R, Raffaello A. Crosstalk between Calcium and ROS inPathophysiological Conditions.Oxid Med Cell Longev . 2019;2019:e9324018. doi:10.1155/2019/9324018116. Beckman JS, Koppenol WH. Nitric oxide, superoxide, and peroxynitrite: the good, the bad, andugly. Am J Physiol . 1996;271(5 Pt 1):C1424-1437. doi:10.1152/ajpcell.1996.271.5.C1424117. PACHER P, BECKMAN JS, LIAUDET L. Nitric Oxide and Peroxynitrite in Health and Disease.PhysiolRev . 2007;87(1):315-424. doi:10.1152/physrev.00029.2006118. Radi R. Oxygen radicals, nitric oxide, and peroxynitrite: Redox pathways in molecular medicine.Proc Natl Acad Sci . 2018;115(23):5839-5848. doi:10.1073/pnas.1804932115119. Guzik TJ, West NEJ, Pillai R, Taggart DP, Channon KM. Nitric Oxide Modulates SuperoxideRelease and Peroxynitrite Formation in Human Blood Vessels.Hypertension. 2002;39(6):1088-1094.doi:10.1161/01.HYP.0000018041.48432.B5120. Roe ND, Ren J. Nitric oxide synthase uncoupling: A therapeutic target in cardiovascular diseases.Vascul Pharmacol . 2012;57(5):168-172. doi:10.1016/j.vph.2012.02.004121. Luo S, Lei H, Qin H, Xia Y. Molecular mechanisms of endothelial NO synthase uncoupling.CurrPharm Des. 2014;20(22):3548-3553. doi:10.2174/13816128113196660746122. Chen W, Druhan LJ, Chen C-A, et al. Peroxynitrite induces destruction of the tetrahydrobiopterinand heme in endothelial nitric oxide synthase: transition from reversible to irreversible enzymeinhibition.Biochemistry . 2010;49(14):3129-3137. doi:10.1021/bi9016632123. Ozdemir B, Yazici A. Could the decrease in the endothelial nitric oxide (NO) production and NObioavailability be the crucial cause of COVID-19 related deaths?Med Hypotheses. 2020;144:109970.doi:10.1016/j.mehy.2020.109970124. Guan SP, Seet RCS, Kennedy BK. Does eNOS derived nitric oxide protect the young from severeCOVID-19 complications? Ageing Res Rev . 2020;64:101201. doi:10.1016/j.arr.2020.101201125. Nitric Oxide - an overview | ScienceDirect Topics. Accessed September 28, 2021. Levine AB, Punihaole D, Levine TB. Characterization of the Role of Nitric Oxide and Its ClinicalApplications.Cardiology . 2012;122(1):55-68. doi:10.1159/000338150127. Rosselli M, Keller PJ, Dubey RK. Role of nitric oxide in the biology, physiology andpathophysiology of reproduction.Hum Reprod Update. 1998;4(1):3-24. doi:10.1093/humupd/4.1.3128. Mel A de. Potential roles of nitric oxide in COVID-19: A perspective.Integr Mol Med . 2020;7(3).doi:10.15761/IMM.1000403129. Ricciardolo FLM, Bertolini F, Carriero V, Högman M. Nitric oxide’s physiologic effects andpotential as a therapeutic agent against COVID-19. J Breath Res. 2020;15(1):014001. doi:10.1088/1752-7163/abc302 130. Åkerström S, Gunalan V, Keng CT, Tan Y-J, Mirazimi A. Dual effect of nitric oxide on SARS-CoVreplication: Viral RNA production and palmitoylation of the S protein are affected.Virology .2009;395(1):1-9. doi:10.1016/j.virol.2009.09.007131. Hadi HA, Carr CS, Al Suwaidi J. Endothelial Dysfunction: Cardiovascular Risk Factors, Therapy,and Outcome.Vasc Health Risk Manag. 2005;1(3):183-198. Accessed September 28, 2021. Bonetti PO, Lerman LO, Lerman A. Endothelial Dysfunction. Arterioscler Thromb Vasc Biol .2003;23(2):168-175. doi:10.1161/01.ATV.0000051384.43104.FC133. Endothelial Dysfunction in Diabetes | Diabetes Care. Accessed September 28, 2021. Patel PD, Velazquez JL, Arora RR. Endothelial dysfunction in African-Americans.Int J Cardiol .2009;132(2):157-172. doi:10.1016/j.ijcard.2008.10.007135. Kalinowski L, Dobrucki IT, Malinski T. Race-specific differences in endothelial function:predisposition of African Americans to vascular diseases.Circulation. 2004;109(21):2511-2517.doi:10.1161/01.CIR.0000129087.81352.7A136. Ungvari Z, Tarantini S, Kiss T, et al. Endothelial dysfunction and angiogenesis impairment in theageing vasculature.Nat Rev Cardiol . 2018;15(9):555-565. doi:10.1038/s41569-018-0030-z137. Reusch N, De Domenico E, Bonaguro L, et al. Neutrophils in COVID-19.Front Immunol .2021;12:952. doi:10.3389/fimmu.2021.652470138. Cavalcante-Silva LHA, Carvalho DCM, Lima É de A, et al. Neutrophils and COVID-19: The road sofar.Int Immunopharmacol . 2021;90:107233. doi:10.1016/j.intimp.2020.107233139. Knoll R, Schultze JL, Schulte-Schrepping J. Monocytes and Macrophages in COVID-19.FrontImmunol . 2021;12:2952. doi:10.3389/fimmu.2021.720109140. Meidaninikjeh S, Sabouni N, Marzouni HZ, Bengar S, Khalili A, Jafari R. Monocytes andmacrophages in COVID-19: Friends and foes.Life Sci . 2021;269:119010. doi:10.1016/j.lfs.2020.119010141. Phagocytes - an overview | ScienceDirect Topics. Accessed September 28, 2021. Respiratory Burst - an overview | ScienceDirect Topics. Accessed September 28, 2021. Superoxide Dismutase - an overview | ScienceDirect Topics. Accessed September 28, 2021. Myeloperoxidase - an overview | ScienceDirect Topics. Accessed September 28, 2021. Spickett CM, Jerlich A, Panasenko OM, et al. The reactions of hypochlorous acid, the reactiveoxygen species produced by myeloperoxidase, with lipids. Acta Biochim Pol . 2000;47(4):889-899.146. Hypochlorous_acid. Accessed September 28, 2021. Neutrophil extracellular traps in immunity and disease | Nature Reviews Immunology. AccessedSeptember 28, 2021. Kaplan MJ, Radic M. Neutrophil extracellular traps (NETs): Double-edged swords of innateimmunity. J Immunol Baltim Md 1950. 2012;189(6):2689-2695. doi:10.4049/jimmunol.1201719149. Gillot C, Favresse J, Mullier F, Lecompte T, Dogné J-M, Douxfils J. NETosis and the ImmuneSystem in COVID-19: Mechanisms and Potential Treatments.Front Pharmacol . 2021;12:1999.doi:10.3389/fphar.2021.708302150. Arcanjo A, Logullo J, Menezes CCB, et al. The emerging role of neutrophil extracellular traps insevere acute respiratory syndrome coronavirus 2 (COVID-19).Sci Rep. 2020;10(1):19630.doi:10.1038/s41598-020-76781-0 151. Middleton EA, He X-Y, Denorme F, et al. Neutrophil extracellular traps contribute toimmunothrombosis in COVID-19 acute respiratory distress syndrome.Blood . 2020;136(10):1169-1179.doi:10.1182/blood.2020007008152. Schönrich G, Raftery MJ, Samstag Y. Devilishly radical NETwork in COVID-19: Oxidative stress,neutrophil extracellular traps (NETs), and T cell suppression. Adv Biol Regul . 2020;77:100741.doi:10.1016/j.jbior.2020.100741153. Goud PT, Bai D, Abu-Soud HM. A Multiple-Hit Hypothesis Involving Reactive Oxygen Species andMyeloperoxidase Explains Clinical Deterioration and Fatality in COVID-19.Int J Biol Sci . 2021;17(1):62-72.doi:10.7150/ijbs.51811154. Edeas M, Saleh J, Peyssonnaux C. Iron: Innocent bystander or vicious culprit in COVID-19pathogenesis?Int J Infect Dis. 2020;97:303-305. doi:10.1016/j.ijid.2020.05.110155. Habib HM, Ibrahim S, Zaim A, Ibrahim WH. The role of iron in the pathogenesis of COVID-19 andpossible treatment with lactoferrin and other iron chelators.Biomed Pharmacother . 2021;136:111228.doi:10.1016/j.biopha.2021.111228156. Rahman A, Tabassum T, Araf Y, Al Nahid A, Ullah MdA, Hosen MJ. Silent hypoxia in COVID-19:pathomechanism and possible management strategy.Mol Biol Rep. Published online April 23, 2021:1-7.doi:10.1007/s11033-021-06358-1157. Tobin MJ, Laghi F, Jubran A. Why COVID-19 Silent Hypoxemia Is Baffling to Physicians. Am JRespir Crit Care Med . 2020;202(3):356-360. doi:10.1164/rccm.202006-2157CP158. Kehrer JP. The Haber-Weiss reaction and mechanisms of toxicity.Toxicology . 2000;149(1):43-50.doi:10.1016/s0300-483x(00)00231-6159. Wardman P, Candeias LP. Fenton Chemistry: An Introduction.Radiat Res. 1996;145(5):523-531.doi:10.2307/3579270160. Sharpe MA, Robb SJ, Clark JB. Nitric oxide and Fenton/Haber–Weiss chemistry: nitric oxide is apotent antioxidant at physiological concentrations. J Neurochem. 2003;87(2):386-394.doi:10.1046/j.1471-4159.2003.02001.x161. Kanti Das T, Wati MR, Fatima-Shad K. Oxidative Stress Gated by Fenton and Haber WeissReactions and Its Association With Alzheimer’s Disease. Arch Neurosci . 2015;2(2).doi:10.5812/archneurosci.20078162. Barciszewska A-M. Elucidating of oxidative distress in COVID-19 and methods of its prevention.Chem Biol Interact . 2021;344:109501. doi:10.1016/j.cbi.2021.109501163. Ntyonga-Pono M-P. COVID-19 infection and oxidative stress: an under-explored approach forprevention and treatment?Pan Afr Med J. 2020;35(Suppl 2):12. doi:10.11604/pamj.2020.35.2.22877164. Forcados GE, Muhammad A, Oladipo OO, Makama S, Meseko CA. Metabolic Implications ofOxidative Stress and Inflammatory Process in SARS-CoV-2 Pathogenesis: Therapeutic Potential of NaturalAntioxidants.Front Cell Infect Microbiol . 2021;11:457. doi:10.3389/fcimb.2021.654813165. Cumpstey AF, Clark AD, Santolini J, Jackson AA, Feelisch M. COVID-19: A Redox Disease—What aStress Pandemic Can Teach Us About Resilience and What We May Learn from the Reactive SpeciesInteractome About Its Treatment. Antioxid Redox Signal . Published online June 29, 2021.doi:10.1089/ars.2021.0017166. Hydroxyl Radical - an overview | ScienceDirect Topics. Accessed September 28, 2021. Gligorovski S, Strekowski R, Barbati S, Vione D. Environmental Implications of Hydroxyl Radicals(•OH).Chem Rev . 2015;115(24):13051-13092. doi:10.1021/cr500310b168. Lyngsie G, Krumina L, Tunlid A, Persson P. Generation of hydroxyl radicals from reactionsbetween a dimethoxyhydroquinone and iron oxide nanoparticles.Sci Rep. 2018;8(1):10834.doi:10.1038/s41598-018-29075-5 169. Takeda K, Fujisawa K, Nojima H, Kato R, Ueki R, Sakugawa H. Hydroxyl radical generation with ahigh power ultraviolet light emitting diode (UV-LED) and application for determination of hydroxylradical reaction rate constants. J Photochem Photobiol Chem. 2017;340:8-14.doi:10.1016/j.jphotochem.2017.02.020170. Kord Forooshani P, Pinnaratip R, Polega E, et al. Hydroxyl Radical Generation through theFenton-like Reaction of Hematin- and Catechol-Functionalized Microgels.Chem Mater .2020;32(19):8182-8194. doi:10.1021/acs.chemmater.0c01551171. Deng Y, Zhao R. Advanced Oxidation Processes (AOPs) in Wastewater Treatment.Curr PollutRep. 2015;1(3):167-176. doi:10.1007/s40726-015-0015-z172. Hypoxanthine - an overview | ScienceDirect Topics. Accessed September 28, 2021. Dowell FJ, Hamilton CA, McMurray J, Reid JL. Effects of a xanthine oxidase/hypoxanthine freeradical and reactive oxygen species generating system on endothelial function in New Zealand whiterabbit aortic rings. J Cardiovasc Pharmacol . 1993;22(6):792-797. doi:10.1097/00005344-199312000-00003174. Fig. 1. Generation of superoxide by xanthine-hypoxanthine oxidase and... ResearchGate.Accessed September 28, 2021. Granger DN. Role of xanthine oxidase and granulocytes in ischemia-reperfusion injury. Am JPhysiol . 1988;255(6 Pt 2):H1269-1275. doi:10.1152/ajpheart.1988.255.6.H1269176. Mao H, Yang A, Zhao Y, Lei L, Li H. Succinate Supplement Elicited “Pseudohypoxia” Condition toPromote Proliferation, Migration, and Osteogenesis of Periodontal Ligament Cells.Stem Cells Int .2020;2020:e2016809. doi:10.1155/2020/2016809177. Lukyanova LD, Kirova YI. Mitochondria-controlled signaling mechanisms of brain protection inhypoxia.Front Neurosci . 2015;9:320. doi:10.3389/fnins.2015.00320178. Messner KR, Imlay JA. Mechanism of superoxide and hydrogen peroxide formation by fumaratereductase, succinate dehydrogenase, and aspartate oxidase. J Biol Chem. 2002;277(45):42563-42571.doi:10.1074/jbc.M204958200179. Quinlan CL, Orr AL, Perevoshchikova IV, Treberg JR, Ackrell BA, Brand MD. MitochondrialComplex II Can Generate Reactive Oxygen Species at High Rates in Both the Forward and ReverseReactions. J Biol Chem. 2012;287(32):27255-27264. doi:10.1074/jbc.M112.374629180. Cowled P, Fitridge R. Pathophysiology of Reperfusion Injury. In: Fitridge R, Thompson M, eds.Mechanisms of Vascular Disease: A Reference Book for Vascular Specialists. University of Adelaide Press;2011. Accessed September 28, 2021. Sun Z-Y, Xia H-G, Zhu D-Q, Deng L-M, Zhu P-Z, Wang D-B. Clinical significance of mechanicalventilation on ischemic-reperfusion injury caused by lung chest trauma and VEGF expression levels inperipheral blood.Exp Ther Med . 2017;14(3):2531-2535. doi:10.3892/etm.2017.4825182. Gielis JF, Beckers PAJ, Briedé JJ, Cos P, Schil PEV. Oxidative and nitrosative stressduring pulmonary ischemia-reperfusion injury: from the lab to the OR. Ann Transl Med .2017;5(6):4-4. doi:10.21037/atm.2017.03.32183. Wu N-C, Liao F-T, Cheng H, Sung S-H, Yang Y-C, Wang J-J. Intravenous superoxide dismutase as aprotective agent to prevent impairment of lung function induced by high tidal volume ventilation.BMCPulm Med . 2017;17:105. doi:10.1186/s12890-017-0448-9184. Lipid Peroxidation - an overview | ScienceDirect Topics. Accessed September 28, 2021. Ayala A, Muñoz MF, Argüelles S. Lipid Peroxidation: Production, Metabolism, and SignalingMechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal.Oxid Med Cell Longev . 2014;2014:360438.doi:10.1155/2014/360438 186. Binder CJ, Papac-Milicevic N, Witztum JL. Innate sensing of oxidation-specific epitopes in healthand disease.Nat Rev Immunol . 2016;16(8):485-497. doi:10.1038/nri.2016.63187. Leibundgut G, Witztum JL, Tsimikas S. Oxidation-specific epitopes and immunological responses:Translational biotheranostic implications for atherosclerosis.Curr Opin Pharmacol .2013;13(2):10.1016/j.coph.2013.02.005. doi:10.1016/j.coph.2013.02.005188. Miller YI, Choi S-H, Wiesner P, et al. Oxidation-Specific Epitopes Are Danger-AssociatedMolecular Patterns Recognized by Pattern Recognition Receptors of Innate Immunity.Circ Res.2011;108(2):235-248. doi:10.1161/CIRCRESAHA.110.223875189. Zhivaki D, Kagan JC. Innate immune detection of lipid oxidation as a threat assessment strategy.Nat Rev Immunol . Published online September 21, 2021:1-9. doi:10.1038/s41577-021-00618-8190. Macdonald J, Galley HF, Webster NR. Oxidative stress and gene expression in sepsis.Br J Anaesth. 2003;90(2):221-232. doi:10.1093/bja/aeg034191. Mantzarlis K, Tsolaki V, Zakynthinos E. Role of Oxidative Stress and Mitochondrial Dysfunction inSepsis and Potential Therapies.Oxid Med Cell Longev . 2017;2017:e5985209. doi:10.1155/2017/5985209192. Toufekoula C, Papadakis V, Tsaganos T, et al. Compartmentalization of lipid peroxidation insepsis by multidrug-resistant gram-negative bacteria: experimental and clinical evidence.Crit Care.2013;17(1):R6. doi:10.1186/cc11930193. Dominic P, Ahmad J, Bhandari R, et al. Decreased availability of nitric oxide and hydrogen sulfideis a hallmark of COVID-19.Redox Biol . 2021;43:101982. doi:10.1016/j.redox.2021.101982194. Yang M, Lai CL. SARS-CoV-2 infection: can ferroptosis be a potential treatment target formultiple organ involvement?Cell Death Discov . 2020;6(1):1-6. doi:10.1038/s41420-020-00369-w195. Jacobs W, Lammens M, Kerckhofs A, et al. Fatal lymphocytic cardiac damage in coronavirusdisease 2019 (COVID-19): autopsy reveals a ferroptosis signature.ESC Heart Fail . 2020;7(6):3772-3781.doi:10.1002/ehf2.12958196. Tavakol S, Seifalian AM. Vitamin E at a high dose as an anti-ferroptosis drug and not just asupplement for COVID-19 treatment.Biotechnol Appl Biochem. n/a(n/a). doi:10.1002/bab.2176197. Sonnweber T, Boehm A, Sahanic S, et al. Persisting alterations of iron homeostasis in COVID-19are associated with non-resolving lung pathologies and poor patients’ performance: a prospectiveobservational cohort study.Respir Res. 2020;21(1):276. doi:10.1186/s12931-020-01546-2198. Žarković N, Orehovec B, Milković L, et al. Preliminary Findings on the Association of the LipidPeroxidation Product 4-Hydroxynonenal with the Lethal Outcome of Aggressive COVID-19. Antioxidants.2021;10(9):1341. doi:10.3390/antiox10091341199. Mehri F, Rahbar AH, Ghane ET, Souri B, Esfahani M. The comparison of oxidative markersbetween Covid-19 patients and healthy subjects. Arch Med Res. Published online June 7, 2021.doi:10.1016/j.arcmed.2021.06.004200. Cao Z, Xia H, Rajsbaum R, Xia X, Wang H, Shi P-Y. Ubiquitination of SARS-CoV-2 ORF7a promotesantagonism of interferon response.Cell Mol Immunol . 2021;18(3):746-748. doi:10.1038/s41423-020-00603-6201. Zhang H, Zheng H, Zhu J, et al. Ubiquitin-Modified Proteome of SARS-CoV-2-Infected Host CellsReveals Insights into Virus–Host Interaction and Pathogenesis. J Proteome Res. Published online March5, 2021:acs.jproteome.0c00758. doi:10.1021/acs.jproteome.0c00758202. Shi H, Zuo Y, Navaz S, et al. Endothelial cell-activating antibodies in COVID-19.MedRxiv PreprServ Health Sci . Published online July 9, 2021:2021.01.18.21250041. doi:10.1101/2021.01.18.21250041203. Chang R, Mamun A, Dominic A, Le N-T. SARS-CoV-2 Mediated Endothelial Dysfunction: ThePotential Role of Chronic Oxidative Stress.Front Physiol . 2021;11:1752. doi:10.3389/fphys.2020.605908204. Mei ZW, van Wijk XMR, Pham HP, Marin MJ. Role of von Willebrand Factor in COVID-19Associated Coagulopathy. J Appl Lab Med . 2021;6(5):1305-1315. doi:10.1093/jalm/jfab042 205. Mancini I, Baronciani L, Artoni A, et al. The ADAMTS13-von Willebrand factor axis in COVID-19patients. J Thromb Haemost JTH. 2021;19(2):513-521. doi:10.1111/jth.15191206. Ladikou EE, Sivaloganathan H, Milne KM, et al. Von Willebrand factor (vWF): marker ofendothelial damage and thrombotic risk in COVID-19?Clin Med . 2020;20(5):e178-e182.doi:10.7861/clinmed.2020-0346207. Afrin LB, Weinstock LB, Molderings GJ. Covid-19 hyperinflammation and post-Covid-19 illnessmay be rooted in mast cell activation syndrome.Int J Infect Dis IJID Off Publ Int Soc Infect Dis.2020;100:327-332. doi:10.1016/j.ijid.2020.09.016208. Gebremeskel S, Schanin J, Coyle KM, et al. Mast Cell and Eosinophil Activation Are AssociatedWith COVID-19 and TLR-Mediated Viral Inflammation: Implications for an Anti-Siglec-8 Antibody.FrontImmunol . 2021;12:641. doi:10.3389/fimmu.2021.650331209. Java A, Apicelli AJ, Liszewski MK, et al. The complement system in COVID-19: friend and foe? JCIInsight . 5(15):e140711. doi:10.1172/jci.insight.140711210. Noris M, Benigni A, Remuzzi G. The case of complement activation in COVID-19 multiorganimpact.Kidney Int . 2020;98(2):314-322. doi:10.1016/j.kint.2020.05.013211. Holter JC, Pischke SE, Boer E de, et al. Systemic complement activation is associated withrespiratory failure in COVID-19 hospitalized patients.Proc Natl Acad Sci . 2020;117(40):25018-25025.doi:10.1073/pnas.2010540117212. Chouaki Benmansour N, Carvelli J, Vivier E. Complement cascade in severe forms of COVID-19:Recent advances in therapy.Eur J Immunol . 2021;51(7):1652-1659. doi:10.1002/eji.202048959213. López-Pedrera C, Barbarroja N, Jimenez-Gomez Y, Collantes-Estevez E, Aguirre MA, CuadradoMJ. Oxidative stress in the pathogenesis of atherothrombosis associated with anti-phospholipidsyndrome and systemic lupus erythematosus: new therapeutic approaches.Rheumatol Oxf Engl .2016;55(12):2096-2108. doi:10.1093/rheumatology/kew054214. Farris AD, Guthridge JM. Overlapping B cell pathways in severe COVID-19 and lupus.NatImmunol . 2020;21(12):1478-1480. doi:10.1038/s41590-020-00822-z215. MacDonald L, Alivernini S, Tolusso B, et al. COVID-19 and RA share an SPP1 myeloid pathwaythat drives PD-L1+ neutrophils and CD14+ monocytes. JCI Insight . 2021;6(13).doi:10.1172/jci.insight.147413216. Schett G, Manger B, Simon D, Caporali R. COVID-19 revisiting inflammatory pathways ofarthritis.Nat Rev Rheumatol . 2020;16(8):465-470. doi:10.1038/s41584-020-0451-z217. Luo M, Cao S, Wei L, et al. Intubation, mortality, and risk factors in critically ill Covid-19 patients:A pilot study. J Clin Anesth. 2020;67:110039. doi:10.1016/j.jclinane.2020.110039218. Tandon A, Pandey L. COVID-19, steroids, and mucormycosis: What an ophthalmologist shouldknow.Indian J Ophthalmol . 2021;69(7):1970. doi:10.4103/ijo.IJO_1143_21219. Therapeutic Anticoagulation with Heparin in Critically Ill Patients with Covid-19.N Engl J Med .2021;385(9):777-789. doi:10.1056/NEJMoa2103417220. Free radicals: What are they and why should nurses care about them? American Nurse.Published April 11, 2011. Accessed September 28, 2021. Ahsan H, Ali A, Ali R. Oxygen free radicals and systemic autoimmunity.Clin Exp Immunol .2003;131(3):398-404. doi:10.1046/j.1365-2249.2003.02104.x222. 8.2: Generation of Free Radicals in the Body. Medicine LibreTexts. Published July 29, 2016.Accessed September 28, 2021. 223. Daiber A, Oelze M, Daub S, et al. Vascular Redox Signaling, Redox Switches in Endothelial NitricOxide Synthase (eNOS Uncoupling), and Endothelial Dysfunction. In: Laher I, ed.Systems Biology of FreeRadicals and Antioxidants. Springer; 2014:1177-1211. doi:10.1007/978-3-642-30018-9_48224. Gladyshev VN. The Free Radical Theory of Aging Is Dead. Long Live the Damage Theory! AntioxidRedox Signal . 2014;20(4):727-731. doi:10.1089/ars.2013.5228225. Junghanns FB. MATH+ Protocol. FLCCC | Front Line COVID-19 Critical Care Alliance. AccessedSeptember 28, 2021. Lammi C, Arnoldi A. Food-derived antioxidants and COVID-19. J Food Biochem.2021;45(1):e13557. doi:10.1111/jfbc.13557227. Żukowski P, Maciejczyk M, Matczuk J, et al. Effect of N-Acetylcysteine on Antioxidant Defense,Oxidative Modification, and Salivary Gland Function in a Rat Model of Insulin Resistance.Oxid Med CellLongev . 2018;2018:e6581970. doi:10.1155/2018/6581970228. Aldini G, Altomare A, Baron G, et al. N-Acetylcysteine as an antioxidant and disulphide breakingagent: the reasons why.Free Radic Res. 2018;52(7):751-762. doi:10.1080/10715762.2018.1468564229. Zhitkovich A. N-Acetylcysteine: Antioxidant, Aldehyde Scavenger, and More.Chem Res Toxicol .2019;32(7):1318-1319. doi:10.1021/acs.chemrestox.9b00152230. Gilad E, Cuzzocrea S, Zingarelli B, Salzman AL, Szabó C. Melatonin is a scavenger of peroxynitrite.Life Sci . 1997;60(10):PL169-174. doi:10.1016/s0024-3205(97)00008-8231. Shaeib F, Khan SN, Ali I, et al. Melatonin Prevents Myeloperoxidase Heme Destruction and theGeneration of Free Iron Mediated by Self-Generated Hypochlorous Acid.PLOS ONE .2015;10(4):e0120737. doi:10.1371/journal.pone.0120737232. Elsaed WM, Alahmadi AM, Al-Ahmadi BT, Taha JA, Tarabishi RM. Gastroprotective andantioxidant effects of fluvoxamine on stress-induced peptic ulcer in rats. J Taibah Univ Med Sci .2018;13(5):422-431. doi:10.1016/j.jtumed.2018.04.010233. Dallé E, Daniels WMU, Mabandla MV. Long-Term Treatment with Fluvoxamine DecreasesNonmotor Symptoms and Dopamine Depletion in a Postnatal Stress Rat Model of Parkinson’s Disease.Oxid Med Cell Longev . 2020;2020:e1941480. doi:10.1155/2020/1941480234. Braga PC, Dal Sasso M, Culici M, Bianchi T, Guffanti EE. Budesonide reduces superoxide andperoxynitrite anion chemiluminescence during human neutrophil bursts.Pharmacology . 2005;75(4):179-186. doi:10.1159/000088623235. Mikolka P, Kopincova J, Tomcikova Mikusiakova L, et al. Effects of surfactant/budesonidetherapy on oxidative modifications in the lung in experimental meconium-induced lung injury. J PhysiolPharmacol Off J Pol Physiol Soc. 2016;67(1):57-65.236. Lamothe PH, Rao E, Serra AJ, et al. Comparative efficacy of cimetidine, famotidine, ranitidine,and mylanta in postoperative stress ulcers. Gastric pH control and ulcer prevention in patientsundergoing coronary artery bypass graft surgery.Gastroenterology . 1991;100(6):1515-1520.doi:10.1016/0016-5085(91)90647-4237. van Zyl JM, Kriegler A, van der Walt BJ. Anti-oxidant properties of H2-receptor antagonists.Effects on myeloperoxidase-catalysed reactions and hydroxyl radical generation in a ferrous-hydrogenperoxide system.Biochem Pharmacol . 1993;45(12):2389-2397. doi:10.1016/0006-2952(93)90218-l238. Ching T-L, Haenen GRMM, Bast A. Cimetidine and other H2 receptor antagonists as powerfulhydroxyl radical scavengers.Chem Biol Interact . 1993;86(2):119-127. doi:10.1016/0009-2797(93)90116-G239. Peterson DA, Gerrard JM, Rao GHR, White JG. Inhibition of ferrous iron induced oxidation ofarachidonic acid by indomethacin.Prostaglandins Med . 1979;2(2):97-108. doi:10.1016/0161-4630(79)90044-2240. Cross AL, Hawkes J, Wright HL, Moots RJ, Edwards SW. APPA (apocynin and paeonol) modulatespathological aspects of human neutrophil function, without supressing antimicrobial ability, and inhibits TNFα expression and signalling.Inflammopharmacology . 2020;28(5):1223-1235. doi:10.1007/s10787-020-00715-5241. Heumüller S, Wind S, Barbosa-Sicard E, et al. Apocynin Is Not an Inhibitor of Vascular NADPHOxidases but an Antioxidant.Hypertension. 2008;51(2):211-217.doi:10.1161/HYPERTENSIONAHA.107.100214242. de Almeida AC, dos Santos Vilela MM, Condino-Neto A, Ximenes VF. The Importance ofMyeloperoxidase in Apocynin-Mediated NADPH Oxidase Inhibition.ISRN Inflamm. 2012;2012:260453.doi:10.5402/2012/260453243. NADPH oxidase Covid-19 Oxygen treatment? ResearchGate. Accessed September 28, 2021. Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19.TheLancet . 2020;395(10234):1417-1418. doi:10.1016/S0140-6736(20)30937-5245. COVID19. Global Sepsis Alliance. Accessed September 28, 2021. HealthLeaders. Expert: Severe COVID-19 Illness Is Viral Sepsis. Accessed September 28, 2021. Aisa-Alvarez A, Soto ME, Guarner-Lans V, et al. Usefulness of Antioxidants as Adjuvant Therapyfor Septic Shock: A Randomized Clinical Trial.Med Kaunas Lith. 2020;56(11):E619.doi:10.3390/medicina56110619248. Aisa-Alvarez A, Perez-Torres I, Camarena-Alejo G, et al. A Randomized clinical trial of antioxidanttherapy in patients with septic shock. Reference study to propose adjuvant therapy in patients withcritical organic damage by COVID-19. Published online September 28, 2021. doi:10.21203/ Kashiouris MG, L’Heureux M, Cable CA, Fisher BJ, Leichtle SW, Fowler AA. The Emerging Role ofVitamin C as a Treatment for Sepsis.Nutrients. 2020;12(2):E292. doi:10.3390/nu12020292250. That “damn machine”: mechanical ventilators in the ICU. STAT. Published August 20, 2021.Accessed September 28, 2021. Ferreira JC, Ho Y-L, Besen BAMP, et al. Protective ventilation and outcomes of critically illpatients with COVID-19: a cohort study. Ann Intensive Care. 2021;11(1):92. doi:10.1186/s13613-021-00882-w252. Effect of Hydroxychloroquine in Hospitalized Patients with Covid-19.N Engl J Med .2020;383(21):2030-2040. doi:10.1056/NEJMoa2022926253. Popp M, Stegemann M, Metzendorf M-I, et al. Ivermectin for preventing and treating COVID-19.Cochrane Database Syst Rev . 2021;7:CD015017. doi:10.1002/14651858.CD015017.pub2254. Acosta MAT, Singer BD. Pathogenesis of COVID-19-induced ARDS: implications for an agingpopulation.Eur Respir J. Published online January 1, 2020. doi:10.1183/13993003.02049-2020255. dos Santos WG. Natural history of COVID-19 and current knowledge on treatment therapeuticoptions.Biomed Pharmacother . 2020;129:110493. doi:10.1016/j.biopha.2020.110493256. Dölken L, Stich A, Spinner CD. Remdesivir for Early COVID-19 Treatment of High-Risk IndividualsPrior to or at Early Disease Onset—Lessons Learned.Viruses. 2021;13(6):963. doi:10.3390/v13060963257. Hydroxychloroquine does not benefit adults hospitalized with COVID-19. National Institutes ofHealth (NIH). Published November 9, 2020. Accessed September 28, 2021. Ivermectin Won’t Treat Covid-19 but Demand for Drug Surges - The New York Times. AccessedSeptember 28, 2021. 259. What the FDA wants doctors to tell patients asking for ivermectin. American MedicalAssociation. Accessed September 28, 2021. AbbVie’s Kaletra doesn’t work in COVID-19, say Chinese scientists -. Accessed September 28,2021. Chamary JV. The Strange Story Of Remdesivir, A Covid Drug That Doesn’t Work. Forbes.Accessed September 28, 2021. Uttar Pradesh government says early use of Ivermectin helped to keep positivity, deaths low.The Indian Express. Published May 12, 2021. Accessed September 28, 2021. India Claims Ivermectin is Effective Against COVID – Orion’s Cold Fire. Accessed September 28,2021. Dr. Soumya Swaminathan deletes her controversial tweet - Indian Bar Association. AccessedSeptember 28, 2021. Indian Bar Association Charges WHO Chief Scientist for Mass Murder - September 28, 2021. Ivomec® (ivermectin) – Effective dewormer, trusted for more than 35 years. BoehringerIngelheim Vetmedica. Published April 10, 2019. Accessed September 28, 2021. CRUMP A, ŌMURA S. Ivermectin, ‘Wonder drug’ from Japan: the human use perspective.Proc Jpn Acad Ser B Phys Biol Sci . 2011;87(2):13-28. doi:10.2183/pjab.87.13268. Camero K. Some people are taking an anti-parasitic to treat COVID. Here’s why that’s a bad idea.Miami Herald. Accessed September 28, 2021. Editor AD News. University experts weigh in on using ivermectin ‘horse dewormer’ as COVID-19treatment. Technician. Accessed September 28, 2021. Yang SNY, Atkinson SC, Wang C, et al. The broad spectrum antiviral ivermectin targets the hostnuclear transport importin α/β1 heterodimer. Antiviral Res. 2020;177:104760.doi:10.1016/j.antiviral.2020.104760271. Kosyna FK, Nagel M, Kluxen L, Kraushaar K, Depping R. The importin α/β-specific inhibitorIvermectin affects HIF-dependent hypoxia response pathways.Biol Chem. 2015;396(12):1357-1367.doi:10.1515/hsz-2015-0171272. Shahbaznejad L, Davoudi A, Eslami G, et al. Effects of Ivermectin in Patients With COVID-19: AMulticenter, Double-blind, Randomized, Controlled Clinical Trial.Clin Ther . 2021;43(6):1007-1019.doi:10.1016/j.clinthera.2021.04.007273. Zaidi AK, Dehgani-Mobaraki P. The mechanisms of action of Ivermectin against SARS-CoV-2: Anevidence-based clinical review article. J Antibiot (Tokyo). Published online June 15, 2021:1-13.doi:10.1038/s41429-021-00430-5274. Ivermectin for COVID-19: real-time meta analysis of 65 studies. Accessed September 28, 2021. 275. Israeli scientist says COVID-19 could be treated for under $1/day. The Jerusalem Post | Accessed September 28, 2021. Feuer W. Gilead’s coronavirus treatment remdesivir to cost $3,120 per U.S. patient with privateinsurance. CNBC. Published June 29, 2020. Accessed September 28, 2021. Pharmaceutical companies pay low taxes and reap enormous profit from COVID vaccines.American Friends Service Committee. Published September 15, 2021. Accessed September 28, 2021. Obscene global vaccine profiteering by pharmaceutical companies. World Socialist Web Site.Accessed September 28, 2021. Pharmaceutical Companies Reaping Immoral Profits From COVID Vaccines Yet Paying Low TaxRates. Common Dreams. Accessed September 28, 2021. Ennis M, Tiligada K. Histamine receptors and COVID-19.Inflamm Res. Published onlineNovember 18, 2020:1-9. doi:10.1007/s00011-020-01422-1281. Hogan II RB, Hogan III RB, Cannon T, et al. Dual-histamine receptor blockade with cetirizine -famotidine reduces pulmonary symptoms in COVID-19 patients.Pulm Pharmacol Ther . 2020;63:101942.doi:10.1016/j.pupt.2020.101942282. Mura C, Preissner S, Nahles S, Heiland M, Bourne PE, Preissner R. Real-world evidence forimproved outcomes with histamine antagonists and aspirin in 22,560 COVID-19 patients.SignalTransduct Target Ther . 2021;6(1):1-3. doi:10.1038/s41392-021-00689-y283. Ishola AA, Joshi T, Abdulai SI, Tijjani H, Pundir H, Chandra S. Molecular basis for the repurposingof histamine H2-receptor antagonist to treat COVID-19. J Biomol Struct Dyn. 2021;0(0):1-18.doi:10.1080/07391102.2021.1873191284. Cross KM, Landis DM, Sehgal L, Payne JD. Melatonin for the Early Treatment of COVID-19: ANarrative Review of Current Evidence and Possible Efficacy.Endocr Pract . 2021;27(8):850-855.doi:10.1016/j.eprac.2021.06.001285. Camp OG, Bai D, Gonullu DC, Nayak N, Abu-Soud HM. Melatonin interferes with COVID-19 atseveral distinct ROS-related steps. J Inorg Biochem. 2021;223:111546.doi:10.1016/j.jinorgbio.2021.111546286. Marinella MA. Indomethacin and resveratrol as potential treatment adjuncts for SARS-CoV-2/COVID-19.Int J Clin Pract . 2020;74(9):e13535. doi:10.1111/ijcp.13535287. Yu L-M, Bafadhel M, Dorward J, et al. Inhaled budesonide for COVID-19 in people at high risk ofcomplications in the community in the UK (PRINCIPLE): a randomised, controlled, open-label, adaptiveplatform trial.The Lancet . 2021;398(10303):843-855. doi:10.1016/S0140-6736(21)01744-X288. Ebell MH. Inhaled Budesonide Reduces the Risk of Emergency Department Evaluation orHospitalization in Early COVID-19. Am Fam Physician. 2021;104(2):207-208. Accessed September 28,2021. Amici C, Di Caro A, Ciucci A, et al. Indomethacin has a potent antiviral activity against SARScoronavirus. Antivir Ther . 2006;11(8):1021-1030.290. Droplets vs Aerosols: What’s More Important in COVID-19 Spread? Published May 13, 2021.Accessed September 28, 2021. 291. COVID-19: Droplet or Airborne Transmission? Penn Medicine Epidemiologists Issue Statement -Penn Medicine. Accessed September 28, 2021. 239 Experts With One Big Claim: The Coronavirus Is Airborne - The New York Times. AccessedSeptember 28, 2021. Goldman E. Exaggerated risk of transmission of COVID-19 by fomites.Lancet Infect Dis.2020;20(8):892-893. doi:10.1016/S1473-3099(20)30561-2294. Lewis D. COVID-19 rarely spreads through surfaces. So why are we still deep cleaning?Nature.2021;590(7844):26-28. doi:10.1038/d41586-021-00251-4295. Viable SARS-CoV-2 in the air of a hospital room with COVID-19 patients | medRxiv. AccessedSeptember 28, 2021. PolitiFact JG. What We Know About the Airborne Spread of the Coronavirus. Kaiser HealthNews. Published September 30, 2020. Accessed September 28, 2021. A guideline to limit indoor airborne transmission of COVID-19 | PNAS. Accessed September 28,2021. Chen CC, Willeke K. Aerosol penetration through surgical masks. Am J Infect Control .1992;20(4):177-184. doi:10.1016/s0196-6553(05)80143-9299. Konda A, Prakash A, Moss GA, Schmoldt M, Grant GD, Guha S. Aerosol Filtration Efficiency ofCommon Fabrics Used in Respiratory Cloth Masks. ACS Nano. 2020;14(5):6339-6347.doi:10.1021/acsnano.0c03252300. Guide for the Selection of Personal Protective Equipment for Emergency First Responders(Percutaneous Protection--Apparel), NIJ Guide 102-00, Volume IIc. National Institute of Justice. AccessedSeptember 28, 2021. US EPA O. EPA Researchers Test Effectiveness of Face Masks, Disinfection Methods AgainstCOVID-19. Published April 5, 2021. Accessed September 28, 2021. Caruhel J-B, Sigaux N, Crambert A, et al. Military gas mask to protect surgeons when performingtracheotomies on patients with COVID-19.BMJ Mil Health. Published online August 2020:bmjmilitary-2020-001547. doi:10.1136/bmjmilitary-2020-001547303. Coronavirus Protection Made Easy with the MaxAir CAPR®. Mopec. Published March 2, 2020.Accessed September 28, 2021. Kitajima M, Ahmed W, Bibby K, et al. SARS-CoV-2 in wastewater: State of the knowledge andresearch needs.Sci Total Environ. 2020;739:139076. doi:10.1016/j.scitotenv.2020.139076305. Sharif S, Ikram A, Khurshid A, et al. Detection of SARs-CoV-2 in wastewater using the existingenvironmental surveillance network: A potential supplementary system for monitoring COVID-19transmission.PLOS ONE . 2021;16(6):e0249568. doi:10.1371/journal.pone.0249568306. Peccia J, Zulli A, Brackney DE, et al. Measurement of SARS-CoV-2 RNA in wastewater trackscommunity infection dynamics.Nat Biotechnol . 2020;38(10):1164-1167. doi:10.1038/s41587-020-0684-z307. McKinney KR, Gong YY, Lewis TG. Environmental transmission of SARS at Amoy Gardens. JEnviron Health. 2006;68(9):26-30; quiz 51-52.308. Hung LS. The SARS epidemic in Hong Kong: what lessons have we learned? J R Soc Med .2003;96(8):374-378. Accessed September 28, 2021. 309. COVID-19 Could Spread Through Dry Floor Drains. CleanLink. Accessed September 28, 2021. ‘Leaky’ Vaccines Can Produce Stronger Versions of Viruses. Healthline. Published July 27, 2015.Accessed September 28, 2021. MD BH. Let’s Stop Pretending About the Covid-19 Vaccines | RealClearScience. Published August23, 2021. Accessed September 28, 2021. CDC Newsroom. CDC. Published January 1, 2016. Accessed September 28, 2021. Brueck H. CDC: Everyone should mask up indoors — whether they’re fully vaccinated or not —as the Delta variant sweeps the US. Business Insider. Accessed September 28, 2021. Lasting immunity found after recovery from COVID-19. National Institutes of Health (NIH).Published January 25, 2021. Accessed September 28, 2021. Gazit S, Shlezinger R, Perez G, et al.Comparing SARS-CoV-2 Natural Immunity to Vaccine-Induced Immunity: Reinfections versus Breakthrough Infections.; 2021:2021.08.24.21262415.doi:10.1101/2021.08.24.21262415316. Accelerated Covid-19 Vaccine Clinical Trials. JD Supra. Accessed September 28, 2021. Were the COVID-19 vaccines rushed? Here’s how the vaccines were developed so fast. AccessedSeptember 28, 2021. Reichmuth AM, Oberli MA, Jaklenec A, Langer R, Blankschtein D. mRNA vaccine delivery usinglipid nanoparticles.Ther Deliv . 2016;7(5):319-334. doi:10.4155/tde-2016-0006319. Without these lipid shells, there would be no mRNA vaccines for COVID-19. Chemical &Engineering News. Accessed September 28, 2021. CDC. Understanding mRNA COVID-19 Vaccines. Centers for Disease Control and Prevention.Published March 4, 2021. Accessed September 28, 2021. What are mRNA vaccines and how do they work?: MedlinePlus Genetics. Accessed September28, 2021. Corbett KS, Edwards DK, Leist SR, et al. SARS-CoV-2 mRNA vaccine design enabled by prototypepathogen preparedness.Nature. 2020;586(7830):567-571. doi:10.1038/s41586-020-2622-0323. PhD SM. How mRNA vaccines from Pfizer and Moderna work, why they’re a breakthrough andwhy they need to be kept so cold. The Conversation. Accessed September 28, 2021. Martínez-Flores D, Zepeda-Cervantes J, Cruz-Reséndiz A, Aguirre-Sampieri S, Sampieri A, Vaca L.SARS-CoV-2 Vaccines Based on the Spike Glycoprotein and Implications of New Viral Variants.FrontImmunol . 2021;12:2774. doi:10.3389/fimmu.2021.701501325. Prompetchara E, Ketloy C, Tharakhet K, et al. DNA vaccine candidate encoding SARS-CoV-2 spikeproteins elicited potent humoral and Th1 cell-mediated immune responses in mice.PLOS ONE .2021;16(3):e0248007. doi:10.1371/journal.pone.0248007 326. COVID-19 Viral Vector Vaccines. Accessed September 28, 2021. Zimmerman RK. Helping patients with ethical concerns about COVID-19 vaccines in light of fetalcell lines used in some COVID-19 vaccines.Vaccine. 2021;39(31):4242-4244.doi:10.1016/j.vaccine.2021.06.027328. The Ethics of the SARS-CoV-2 Vaccines Revisited. Christian Medical & Dental Associations®(CMDA). Published September 15, 2021. Accessed September 28, 2021. Canadian Covid Care Alliance. Accessed September 28, 2021. Juraszek J, Rutten L, Blokland S, et al. Stabilizing the closed SARS-CoV-2 spike trimer.NatCommun. 2021;12(1):244. doi:10.1038/s41467-020-20321-x331. The tiny tweak behind COVID-19 vaccines. Chemical & Engineering News. Accessed September28, 2021. SARS-COV-2 mRNA Vaccine (BNT162, PF-07302048) 2.6.4 Overview of Pharmacokinetic Test |BibSonomy. Accessed September 28, 2021. Krantz MS, Liu Y, Phillips EJ, Stone CA. COVID-19 vaccine anaphylaxis: PEG or not? Allergy .2021;76(6):1934-1937. doi:10.1111/all.14722334. Moghimi SM. Allergic Reactions and Anaphylaxis to LNP-Based COVID-19 Vaccines.Mol Ther .2021;29(3):898-900. doi:10.1016/j.ymthe.2021.01.030335. Overview of translation (article). Khan Academy. Accessed September 28, 2021. Thomas EN, Kim KQ, McHugh EP, Marcinkiewicz T, Zaher HS. Alkylative damage of mRNA leadsto ribosome stalling and rescue by trans translation in bacteria. Dever TE, Storz G, eds.eLife.2020;9:e61984. doi:10.7554/eLife.61984337. Karamyshev AL, Karamysheva ZN. Lost in Translation: Ribosome-Associated mRNA and ProteinQuality Controls.Front Genet . 2018;9:431. doi:10.3389/fgene.2018.00431338. Mendonsa S, von Kuegelgen N, Bujanic L, Chekulaeva M. Charcot–Marie–Tooth mutation inglycyl-tRNA synthetase stalls ribosomes in a pre-accommodation state and activates integrated stressresponse.Nucleic Acids Res. 2021;49(17):10007-10017. doi:10.1093/nar/gkab730339. Zuko A, Mallik M, Thompson R, et al. tRNA overexpression rescues peripheral neuropathycaused by mutations in tRNA synthetase.Science. 2021;373(6559):1161-1166.doi:10.1126/science.abb3356340. Zhang S, Chen Y, Wang Y, Zhang P, Chen G, Zhou Y. Insights Into Translatomics in the NervousSystem.Front Genet . 2020;11:1682. doi:10.3389/fgene.2020.599548341. Klein T, Eckhard U, Dufour A, Solis N, Overall CM. Proteolytic Cleavage—Mechanisms, Function,and “Omic” Approaches for a Near-Ubiquitous Posttranslational Modification.Chem Rev .2018;118(3):1137-1168. doi:10.1021/acs.chemrev.7b00120342. Örd M, Faustova I, Loog M. The sequence at Spike S1/S2 site enables cleavage by furin andphospho-regulation in SARS-CoV2 but not in SARS-CoV1 or MERS-CoV.Sci Rep. 2020;10(1):16944.doi:10.1038/s41598-020-74101-0343. Lemmin T, Kalbermatter D, Harder D, Plattet P, Fotiadis D. Structures and dynamics of the novelS1/S2 protease cleavage site loop of the SARS-CoV-2 spike glycoprotein. J Struct Biol X . 2020;4:100038.doi:10.1016/j.yjsbx.2020.100038 344. Belouzard S, Chu VC, Whittaker GR. Activation of the SARS coronavirus spike protein viasequential proteolytic cleavage at two distinct sites.Proc Natl Acad Sci . 2009;106(14):5871-5876.doi:10.1073/pnas.0809524106345. Ogata AF, Cheng C-A, Desjardins M, et al. Circulating Severe Acute Respiratory SyndromeCoronavirus 2 (SARS-CoV-2) Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients.Clin Infect Dis. 2021;(ciab465). doi:10.1093/cid/ciab465346. Peacock TP, Goldhill DH, Zhou J, et al. The furin cleavage site in the SARS-CoV-2 spike protein isrequired for transmission in ferrets.Nat Microbiol . 2021;6(7):899-909. doi:10.1038/s41564-021-00908-w347. Bestle D, Heindl MR, Limburg H, et al. TMPRSS2 and furin are both essential for proteolyticactivation of SARS-CoV-2 in human airway cells.Life Sci Alliance. 2020;3(9). doi:10.26508/lsa.202000786348. Cheng MH, Zhang S, Porritt RA, et al. Superantigenic character of an insert unique to SARS-CoV-2spike supported by skewed TCR repertoire in patients with hyperinflammation.Proc Natl Acad Sci .2020;117(41):25254-25262. doi:10.1073/pnas.2010722117349. Brown M, Bhardwaj N. Super(antigen) target for SARS-CoV-2.Nat Rev Immunol . 2021;21(2):72-72. doi:10.1038/s41577-021-00502-5350. Föhse K, Geckin B, Overheul G, et al. The BNT162b2 mRNA vaccine against SARS-CoV-2reprograms both adaptive and innate immune response. Published online 2021.doi:10.1101/2021.05.03.21256520351. Wang H, Chen Q, Hu Y, et al. Pathogenic antibodies induced by spike proteins of COVID-19 andSARS-CoV viruses. Published online September 28, 2021. doi:10.21203/ says R to the document-WB. Summary: Covid-19 Vaccine Concerns. Dr. Rich Swier. PublishedSeptember 18, 2021. Accessed September 28, 2021. Commissioner O of the. Coronavirus (COVID-19) Update: July 13, 2021. FDA. Published July 13,2021. Accessed September 28, 2021. Bell’s Palsy After COVID Vaccines Still Very Rare. Published August 16, 2021. AccessedSeptember 28, 2021. Havla J, Schultz Y, Zimmermann H, Hohlfeld R, Danek A, Kümpfel T. First manifestation ofmultiple sclerosis after immunization with the Pfizer-BioNTech COVID-19 vaccine. J Neurol . Publishedonline June 11, 2021. doi:10.1007/s00415-021-10648-w356. Baggen J, Vanstreels E, Jansen S, Daelemans D. Cellular host factors for SARS-CoV-2 infection.Nat Microbiol . 2021;6(10):1219-1232. doi:10.1038/s41564-021-00958-0357. Perez-Miller S, Patek M, Moutal A, et al. Novel Compounds Targeting Neuropilin Receptor 1 withPotential To Interfere with SARS-CoV-2 Virus Entry. ACS Chem Neurosci . 2021;12(8):1299-1312.doi:10.1021/acschemneuro.0c00619358. Daly JL, Simonetti B, Klein K, et al. Neuropilin-1 is a host factor for SARS-CoV-2 infection.Science.2020;370(6518):861-865. doi:10.1126/science.abd3072359. Nader D, Fletcher N, Curley GF, Kerrigan SW. SARS-CoV-2 uses major endothelial integrin αvβ3to cause vascular dysregulation in-vitro during COVID-19.PLOS ONE . 2021;16(6):e0253347.doi:10.1371/journal.pone.0253347360. Petruk G, Puthia M, Petrlova J, et al. SARS-CoV-2 spike protein binds to bacteriallipopolysaccharide and boosts proinflammatory activity. J Mol Cell Biol . 2020;12(12):916-932.doi:10.1093/jmcb/mjaa067361. Suzuki YJ, Gychka SG. SARS-CoV-2 Spike Protein Elicits Cell Signaling in Human Host Cells:Implications for Possible Consequences of COVID-19 Vaccines.Vaccines. 2021;9(1):36.doi:10.3390/vaccines9010036 362. Liu S, Selvaraj P, Lien CZ, et al. The PRRA Insert at the S1/S2 Site Modulates Cellular Tropism ofSARS-CoV-2 and ACE2 Usage by the Closely Related Bat RaTG13. J Virol . 95(11):e01751-20.doi:10.1128/JVI.01751-20363. Johnson BA, Xie X, Kalveram B, et al. Furin Cleavage Site Is Key to SARS-CoV-2 Pathogenesis.bioRxiv . Published online August 26, 2020:2020.08.26.268854. doi:10.1101/2020.08.26.268854364. Deigin Y. Lab-made? CoV2 genealogy through the lens of gain-of-function research. Medium.Published May 3, 2020. Accessed September 28, 2021. Tetz G, Tetz V. SARS-CoV-2 Prion-Like Domains in Spike Proteins Enable Higher Affinity to ACE2.Published online March 29, 2020. doi:10.20944/preprints202003.0422.v1366. Fryer HR, McLean AR. There Is No Safe Dose of Prions.PLOS ONE . 2011;6(8):e23664.doi:10.1371/journal.pone.0023664367. Seneff S, Nigh G. Worse Than the Disease? Reviewing Some Possible Unintended Consequencesof the mRNA Vaccines Against COVID-19.Int J Vaccine Theory Pract Res. 2021;2(1):38-79. AccessedSeptember 28, 2021. Idrees D, Kumar V. SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potentialclues to neurodegeneration.Biochem Biophys Res Commun. 2021;554:94-98.doi:10.1016/j.bbrc.2021.03.100369. Rhea EM, Logsdon AF, Hansen KM, et al. The S1 protein of SARS-CoV-2 crosses the blood–brainbarrier in mice.Nat Neurosci . 2021;24(3):368-378. doi:10.1038/s41593-020-00771-8370. Zhang L, Zhou L, Bao L, et al. SARS-CoV-2 crosses the blood–brain barrier accompanied withbasement membrane disruption without tight junctions alteration.Signal Transduct Target Ther .2021;6(1):1-12. doi:10.1038/s41392-021-00719-9371. Buzhdygan TP, DeOre BJ, Baldwin-Leclair A, et al. The SARS-CoV-2 spike protein alters barrierfunction in 2D static and 3D microfluidic in-vitro models of the human blood-brain barrier.Neurobiol Dis.2020;146:105131. doi:10.1016/j.nbd.2020.105131372. Ricke DO. Two Different Antibody-Dependent Enhancement (ADE) Risks for SARS-CoV-2Antibodies.Front Immunol . 2021;12:640093. doi:10.3389/fimmu.2021.640093373. Halstead SB, Katzelnick L. COVID 19 Vaccines: Should we fear ADE? J Infect Dis. Published onlineAugust 12, 2020:jiaa518. doi:10.1093/infdis/jiaa518374. Yahi N, Chahinian H, Fantini J. Infection-enhancing anti-SARS-CoV-2 antibodies recognize boththe original Wuhan/D614G strain and Delta variants. A potential risk for mass vaccination? J Infect .2021;0(0). doi:10.1016/j.jinf.2021.08.010375. (STUDY) Why so many vaccinated people are getting sick: Antibody Dependent Enhancement(ADE) | Sharyl Attkisson. Accessed September 28, 2021. Lee WS, Wheatley AK, Kent SJ, DeKosky BJ. Antibody-dependent enhancement and SARS-CoV-2vaccines and therapies.Nat Microbiol . 2020;5(10):1185-1191. doi:10.1038/s41564-020-00789-5377. Wen J, Cheng Y, Ling R, et al. Antibody-dependent enhancement of coronavirus.Int J Infect Dis.2020;100:483-489. doi:10.1016/j.ijid.2020.09.015378. Wan Y, Shang J, Sun S, et al. Molecular Mechanism for Antibody-Dependent Enhancement ofCoronavirus Entry. J Virol . 2020;94(5):e02015-19. doi:10.1128/JVI.02015-19379. Liu Y, Arase N, Kishikawa J, et al.The SARS-CoV-2 Delta Variant Is Poised to Acquire CompleteResistance to Wild-Type Spike Vaccines.; 2021:2021.08.22.457114. doi:10.1101/2021.08.22.457114380. Zhang A, Stacey HD, Mullarkey CE, Miller MS. Original Antigenic Sin: How First Exposure ShapesLifelong Anti–Influenza Virus Immune Responses. J Immunol . 2019;202(2):335-340.doi:10.4049/jimmunol.1801149 381. Brown EL, Essigmann HT. Original Antigenic Sin: the Downside of Immunological Memory andImplications for COVID-19.mSphere. 6(2):e00056-21. doi:10.1128/mSphere.00056-21382. Antibody Dependent Enhancement - an overview | ScienceDirect Topics. Accessed September28, 2021. ADE. Accessed September 28, 2021. Shukla R, Ramasamy V, Shanmugam RK, Ahuja R, Khanna N. Antibody-Dependent Enhancement:A Challenge for Developing a Safe Dengue Vaccine.Front Cell Infect Microbiol . 2020;10:597.doi:10.3389/fcimb.2020.572681385. Scientists Discover How Dengue Vaccine Fails to Protect Against Disease. Newsroom. PublishedJune 23, 2021. Accessed September 28, 2021. Mahalingam S, Herring BL, Halstead SB. Call to Action for Dengue Vaccine Failure.Emerg InfectDis. 2013;19(8):1335-1337. doi:10.3201/eid1908.121864387. How the World’s First Dengue Vaccination Drive Ended in Disaster. Scientific American.doi:10.1038/scientificamerican0419-38388. Tseng C-T, Sbrana E, Iwata-Yoshikawa N, et al. Immunization with SARS Coronavirus VaccinesLeads to Pulmonary Immunopathology on Challenge with the SARS Virus.PLOS ONE . 2012;7(4):e35421.doi:10.1371/journal.pone.0035421389. Zhang L, Richards A, Khalil A, et al. SARS-CoV-2 RNA reverse-transcribed and integrated into thehuman genome.BioRxiv Prepr Serv Biol . Published online December 13, 2020:2020.12.12.422516.doi:10.1101/2020.12.12.422516390. MIT & Harvard Study Suggests mRNA Vaccine Might Permanently Alter DNA After All. Rights andFreedoms. Published August 13, 2021. Accessed September 28, 2021. The Injection Fraud – It’s Not a Vaccine – Solari Report. Accessed September 28, 2021. Dec 19 LS| NE| CN|, 2017. Feds lift gain-of-function research pause, offer guidance. CIDRAP.Accessed September 28, 2021. Begley,STAT S. U.S. Lifts Moratorium on Funding Controversial, High-Risk Virus Research.Scientific American. Accessed September 28, 2021. NIH Lifts Funding Pause on Gain-of-Function Research. National Institutes of Health (NIH).Published December 18, 2017. Accessed September 28, 2021. Ralph S. Baric, PhD. UNC Gillings School of Global Public Health. Accessed September 28, 2021. Ralph Baric: On the Front Lines of Coronavirus for Three Decades - UNC General AlumniAssociation. Accessed September 28, 2021. Menachery VD, Yount BL, Debbink K, et al. A SARS-like cluster of circulating bat coronavirusesshows potential for human emergence.Nat Med . 2015;21(12):1508-1513. doi:10.1038/nm.3985398. Inside the risky bat-virus engineering that links America to Wuhan. MIT Technology Review.Accessed September 28, 2021. 399. Suryanarayanan S. Items from coronavirus expert Ralph Baric‘s emails. U.S. Right to Know.Published December 14, 2020. Accessed September 28, 2021. Newsweek Op-Ed: “Congress Must Pursue Answers About the Origin of COVID-19” | SenatorRand Paul. Accessed September 28, 2021. Baker N. The Lab-Leak Hypothesis. Intelligencer. Published January 4, 2021. Accessed September28, 2021. Lerner S, Hvistendahl M, Hibbett M. NIH Documents Provide New Evidence U.S. Funded Gain-of-Function Research in Wuhan. The Intercept. Published September 10, 2021. Accessed September 28,2021. BOMBSHELL: Fauci Kept Funding Peter Daszak’s Wuhan “Gain of Function” Experiments with$7.5 Million after Trump Canceled Grant. National File. Published June 3, 2021. Accessed September 28,2021. miningawareness. USAID (PREDICT) & NIH Gave $ 1.9 Million to the Wuhan (WIV) Lab ThroughDaszak-EcoHealth Alliance; Daszak Talks China Partners’ Work on “Killer” Viruses; Biden BudgetRequests More USAID Money for Similar Projects. Mining Awareness +. Published June 11, 2021.Accessed September 28, 2021. Gallagher: This is Bigger than Dr. Fauci. Congressman Mike Gallagher. Published May 20, 2021.Accessed September 28, 2021. Blog A. EcoHealth Alliance, DARPA Toyed With Infecting Wild Chinese Bats With Covid, LeakedDocs Allege. Algora Blog. Published September 22, 2021. Accessed September 28, 2021. Archive VA, feed G author R. Pentagon gave millions to EcoHealth Alliance for weapons researchprogram. New York Post. Published July 2, 2021. Accessed September 28, 2021. Judicial Watch: New Documents Show Wuhan Lab Asked NIH Official for Information onDisinfectants; Nine Fauci Agency Grants for EcoHealth Bat Coronavirus Research. Judicial Watch.Published July 8, 2021. Accessed September 28, 2021. JW v NIH Wuhan June 2021 00696. Judicial Watch. Accessed September 28, 2021. Opinion | State Department cables warned of safety issues at Wuhan lab studying batcoronaviruses.Washington Post . Accessed September28, 2021.411. Panetta G. US officials were reportedly concerned that safety breaches at a Wuhan lab studyingcoronaviruses in bats could cause a pandemic. Business Insider. Accessed September 28, 2021. (PDF) The possible origins of 2019-nCoV coronavirus. Accessed September 28, 2021. 413. Crist C. 3 Wuhan Lab Workers’ 2019 Illness Raises Concerns. WebMD. Accessed September 28,2021. Williams J. Fauci calls on China to release medical records of Wuhan researchers. TheHill.Published June 4, 2021. Accessed September 28, 2021. Confidential Documents reveal Moderna sent mRNA Coronavirus Vaccine Candidate toUniversity Researchers weeks before emergence of Covid-19. Rights and Freedoms. Published June 26,2021. Accessed September 28, 2021. Confidential Documents reveal Moderna sent mRNA Coronavirus Vaccine Candidate toUniversity Researchers weeks before emergence of Covid-19 – The Expose. Accessed September 28,2021. Jan 11 LS| NE| CN|, 2020. China releases genetic data on new coronavirus, now deadly. CIDRAP.Accessed September 28, 2021. Whole genome of novel coronavirus, 2019-nCoV, sequenced. ScienceDaily. Accessed September28, 2021. Bendix SN Andrew Dunn, Aria. Moderna’s groundbreaking coronavirus vaccine was designed in just 2 days. Business Insider. Accessed September 28, 2021. Moderna designed its coronavirus vaccine in 2 days — here’s how - National | News. Accessed September 28, 2021. Wallace-Wells D. We Had the Vaccine the Whole Time. Intelligencer. Published December 7,2020. Accessed September 28, 2021. The Board of Directors of bioMerieux, chaired by Alain Merieux, has appointed Stephane BancelDirecteur General delegue (Chief Executive Officer) of bioMerieux starting January 1, 2007. bioMérieuxCorporate Website. Accessed September 28, 2021. Stéphane Bancel | HIMSS. Published September 24, 2021. Accessed September 28, 2021. Alain Mérieux receives the prestigious Chinese Reform Friendship Award. Mérieux Foundation.Published September 17, 2013. Accessed September 28, 2021. Beijing JXTWLCI. The Wuhan lab at the core of a virus controversy. Accessed September 28,2021. China Inaugurates the first biocontainment level 4 laboratory in Wuhan --- Wuhan Institute ofVirology. Accessed September 28, 2021. RaTG13 is fake. Nerd Has Power. Accessed September 28, 2021. RaTG13 – the Undeniable Evidence That the Wuhan Coronavirus Is Man-Made. GNEWS.Published May 2, 2020. Accessed September 28, 2021. Scientific history of RaTG13. Peak Prosperity. Accessed September 28, 2021. 430. No one can find the animal that gave people covid-19. MIT Technology Review. AccessedSeptember 28, 2021. How WHO is working to track down the animal reservoir of the SARS-CoV-2 virus. AccessedSeptember 28, 2021. Jewers C. More Lancet letter signatories found to have links to Wuhan. Mail Online. PublishedSeptember 11, 2021. Accessed September 28, 2021. Wang N, Li S-Y, Yang X-L, et al. Serological Evidence of Bat SARS-Related Coronavirus Infection inHumans, China.Virol Sin. 2018;33(1):104-107. doi:10.1007/s12250-018-0012-7434. Daszak and scientists stand by Lancet letter condemning Wuhan lab “conspiracy theories.” MSN.Accessed September 28, 2021. Albaugh G. Journal That Mocked COVID Lab-Leak As “Conspiracy” Recants. Citizens Journal.Published September 22, 2021. Accessed September 28, 2021. Calisher C, Carroll D, Colwell R, et al. Statement in support of the scientists, public healthprofessionals, and medical professionals of China combatting COVID-19.The Lancet .2020;395(10226):e42-e43. doi:10.1016/S0140-6736(20)30418-9437. Lancet’s COVID origins panel disbands over ties to Peter Daszak’s EcoHealth Alliance.swiftheadline. Published September 26, 2021. Accessed September 28, 2021. WHO Covid Expert Peter Daszak’s Alleged China Connection and CCP Money Trail: What’s theTruth? Published February 11, 2021. Accessed September 28, 2021. Rutz D. Media fact-checkers, Facebook cited Wuhan lab-linked scientist to knock down lab leaktheory. Fox News. Published June 3, 2021. Accessed September 28, 2021. Daszak P, Chmura A. A Fall From Grace To… Virulence?Ecohealth. 2008;5(1):96-97.doi:10.1007/s10393-008-0163-3441. Bogich TL, Chunara R, Scales D, et al. Preventing pandemics via international development: asystems approach.PLoS Med . 2012;9(12):e1001354. doi:10.1371/journal.pmed.1001354442. Daszak P, Howard SE, Chmura AA. Rock, paper, scissors; chicken, human, swine.EcoHealth.2009;6(1):159-160. doi:10.1007/s10393-009-0245-x443. Ge X-Y, Li J-L, Yang X-L, et al. Isolation and characterization of a bat SARS-like coronavirus thatuses the ACE2 receptor.Nature. 2013;503(7477):535-538. doi:10.1038/nature12711444. Latinne A, Hu B, Olival KJ, et al. Origin and cross-species transmission of bat coronaviruses inChina.BioRxiv Prepr Serv Biol . Published online May 31, 2020:2020.05.31.116061.doi:10.1101/2020.05.31.116061445. Li H-Y, Zhu G-J, Zhang Y-Z, et al. A qualitative study of zoonotic risk factors among ruralcommunities in southern China.Int Health. 2020;12(2):77-85. doi:10.1093/inthealth/ihaa001446. Li H, Chen Y, Machalaba CC, et al. Wild animal and zoonotic disease risk management andregulation in China: Examining gaps and One Health opportunities in scope, mandates, and monitoringsystems.One Health Amst Neth. 2021;13:100301. doi:10.1016/j.onehlt.2021.100301 447. Nava A, Shimabukuro JS, Chmura AA, Luz SLB. The Impact of Global Environmental Changes onInfectious Disease Emergence with a Focus on Risks for Brazil.ILAR J. 2017;58(3):393-400.doi:10.1093/ilar/ilx034448. Wang N, Li S-Y, Yang X-L, et al. Serological Evidence of Bat SARS-Related Coronavirus Infection inHumans, China.Virol Sin. 2018;33(1):104-107. doi:10.1007/s12250-018-0012-7449. Zeng L-P, Gao Y-T, Ge X-Y, et al. Bat Severe Acute Respiratory Syndrome-Like Coronavirus WIV1Encodes an Extra Accessory Protein, ORFX, Involved in Modulation of the Host Immune Response. JVirol . 2016;90(14):6573-6582. doi:10.1128/JVI.03079-15450. David Martin.The Fauci COVID 19 Dossier .; 2021. Accessed September 28, 2021. 161385360554578. Coronavirus patients WELDED into homes in China as death toll spirals to813. The US Sun. Published February 9, 2020. Accessed September 28, 2021. Archive VA, Author E the, Twitter F on, et al. COVID-19 deaths in NY nursing homes were 50percent higher than claimed: probe. New York Post. Published January 28, 2021. Accessed September28, 2021. Ciavaglia DR and J. Investigations into Northeast nursing homes ongoing as true COVID death tollrises by 16K. The Intelligencer. Accessed September 28, 2021. A and SR. New York health chief, Cuomo defender, resigning. OswegoCounty News Now. Accessed September 28, 2021. Care homes accused of using powerful sedatives to kill corona victims quickly. The Sun.Published July 12, 2020. Accessed September 28, 2021. Wayne Smith, The Man Exposing The Midazolam Mass Murder Care Home Scandal Found Dead -Plandemic. Accessed September 28, 2021. Did the ‘First Wave’ Mean the Mass Murder of the Elderly With Midazolam? – The White Rose.Accessed September 28, 2021. News: Face mask shortage prompts CDC to... (The Washington Post) - Behind the headlines -NLM. NCBI. Accessed September 28, 2021. Evstatieva M. U.S. Companies Shifted To Make N95 Respirators During COVID. Now, They’reStruggling.NPR. Published June 25, 2021. Accessed September 28, 2021.460. Pandemic Market Oddity: N95 Mask Shortage Despite Availability. Verisk. Accessed September28, 2021. In the early days of the pandemic, the U.S. government turned down an offer to manufacturemillions of N95 masks in America.Washington Post . Accessed September 28,2021. 462. Cheong W. The US government turned down an offer to manufacture up to 1.7 million N95masks weekly in January: report. Business Insider. Accessed September 28, 2021. Dugdale CM, Walensky RP. Filtration Efficiency, Effectiveness, and Availability of N95 Face Masksfor COVID-19 Prevention. JAMA Intern Med . 2020;180(12):1612-1613.doi:10.1001/jamainternmed.2020.4218464. What’s a PCR test cycle threshold and why it matters. Full Fact. Published16:47:37.518768+00:00. Accessed September 28, 2021. Rajyalakshmi B, Samavedam S, Reddy PR, Aluru N. Prognostic Value of “Cycle Threshold” inConfirmed COVID-19 Patients.Indian J Crit Care Med Peer-Rev Off Publ Indian Soc Crit Care Med .2021;25(3):322-326. doi:10.5005/jp-journals-10071-23765466. Covid Mandates: Unscientific, Irrational And Fraudulent, Dozens Of Reasons To Stop Them Now| Covid Call To Humanity. Accessed September 28, 2021. The COVID-19 PCR Test Is Key to the Pandemic Fraud | Principia Scientific Intl. Principia ScientificIntl. | A science-based community. Published September 8, 2020. Accessed September 28, 2021. Mandavilli A. Your Coronavirus Test Is Positive. Maybe It Shouldn’t Be.The New York Times. Published August 29, 2020.Accessed September 28, 2021.469. The Fog of COVID-19 Data: How many cases aren’t even cases? John Locke Foundation.Accessed September 28, 2021. Caught Red-Handed: CDC Changes Test Thresholds To Virtually Eliminate New COVID CasesAmong Vaxx’d. Rights and Freedoms. Published May 24, 2021. Accessed September 28, 2021. Trabert D. CDC: maximum 28 CT for post-vaccine COVID PCR tests. The Sentinel. Published May3, 2021. Accessed September 28, 2021. FLCCC-Alliance-MATHplus-Protocol-ENGLISH.pdf. Accessed September 28, 2021. Kashiouris MG, L’Heureux M, Cable CA, Fisher BJ, Leichtle SW, Fowler AA. The Emerging Role ofVitamin C as a Treatment for Sepsis.Nutrients. 2020;12(2):E292. doi:10.3390/nu12020292474. Obi J, Pastores SM, Ramanathan LV, Yang J, Halpern NA. Treating sepsis with vitamin C,thiamine, and hydrocortisone: Exploring the quest for the magic elixir. J Crit Care. 2020;57:231-239.doi:10.1016/j.jcrc.2019.12.011475. Harris R. “Tantalizing” Results For A Test Of Vitamin C For Sepsis.NPR. Published October 1, 2019. Accessed September 28, 2021.476. “Ethically and morally unacceptable”: Reaction to vitamin C for sepsistrial. Accessed September 28, 2021. 477. Research C for DE and. FDA Updates and Press Announcements on NDMA in Zantac (ranitidine).FDA. Published online July 1, 2021. Accessed September 28, 2021. FDA studies: No post-ingestion NDMA from ranitidine. Accessed September 28, 2021. Ahmadi A, Ebrahimzadeh MA, Ahmad-Ashrafi S, Karami M, Mahdavi MR, Saravi SSS.Hepatoprotective, antinociceptive and antioxidant activities of cimetidine, ranitidine and famotidine ashistamine H2 receptor antagonists.Fundam Clin Pharmacol . 2011;25(1):72-79. doi:10.1111/j.1472-8206.2009.00810.x480. Nutrition C for FS and A. LES Labs - 593764 - 07/23/2020. Center for Food Safety and AppliedNutrition. Published July 29, 2020. Accessed September 28, 2021. US senator, NPA press FDA on NAC supplements. Natural Products INSIDER. Published August18, 2021. Accessed September 28, 2021. CRN: ‘This is not the final word on NAC.’ September 28, 2021. Amazon confirms plans on removing NAC supplements. Natural Products INSIDER. PublishedMay 6, 2021. Accessed September 28, 2021. Harvard University Professor and Two Chinese Nationals Charged in Three Separate ChinaRelated Cases. Published January 28, 2020. Accessed September 28, 2021. Research Sponsors - Lieber Research GroupThe Lieber group is focused broadly on science andtechnology at the nanoscale - Lieber Research Group. Accessed September 28, 2021. Shaw J. Virus-Sized Transistors. Harvard Magazine. Published December 16, 2010. AccessedSeptember 28, 2021. Why did a Chinese university hire Charles Lieber to do battery research? Accessed September28, 2021. Writer PRHS. Reading life’s building blocks. Harvard Gazette. Published January 5, 2012.Accessed September 28, 2021. Correspondent CM-MH. Harvard researchers present nanowire devices update. HarvardGazette. Published July 2, 2019. Accessed September 28, 2021. Harvard University Professor Indicted on False Statement Charges. Published June 9, 2020.Accessed September 28, 2021. Barry E, Kolata G. China’s Lavish Funds Lured U.S. Scientists. What Did It Get in Return?The NewYork Times. Published February 6, 2020. Accessed September 28, 2021. 492. Subbaraman N. Harvard chemistry chief’s arrest over China links shocks researchers.Nature.Published online February 3, 2020. doi:10.1038/d41586-020-00291-2493. Portman R, Carper T. Threats to the U.S. Research Enterprise: China’s Talent Recruitment Plans.:109.494. Krige J. Scholars or Spies? U.S.-China Tension in Academic Collaboration. China Research Center.Published October 12, 2020. Accessed September 28, 2021. FBI_Risks_To_Academia.pdf. Accessed September 28, 2021. Zweig D, Kang S. AMERICA CHALLENGES CHINA’S NATIONAL TALENT PROGRAMS. :20.497. Zhang A, Zhao Y, You SS, Lieber CM. Nanowire probes could drive high-resolution brain-machineinterfaces.Nano Today . 2020;31:100821. doi:10.1016/j.nantod.2019.100821498. Hong G, Lieber CM. Novel electrode technologies for neural recordings.Nat Rev Neurosci .2019;20(6):330-345. doi:10.1038/s41583-019-0140-6499. Human Cells Eat Nanowires. IEEE Spectrum. Published December 19, 2016. Accessed September28, 2021. They’ve got the beat. Boston Herald. Published August 29, 2012. Accessed September 28, 2021. Tian B, Liu J, Dvir T, et al. Macroporous nanowire nanoelectronic scaffolds for synthetic tissues.Nat Mater . 2012;11(11):986-994. doi:10.1038/nmat3404502. Board of Directors: Advancing mRNA Science - Moderna. Accessed September 28, 2021. Tognini G. MIT Scientist Bob Langer Becomes A Billionaire Thanks To Moderna Stock Rally.Forbes. Accessed September 28, 2021. Moderna’s Stock Rally Makes Bob Langer a Billionaire. Accessed September 28, 2021. Langer Lab – MIT Department of Chemical Engineering. Accessed September 28, 2021. Nano-Bioelectronics. Lieber Research Group. Accessed September 28, 2021. Durden T. Klaus Schwab: Great Reset Will “Lead To Fusion Of Our Physical, Digital, & BiologicalIdentity.” Invesbrain. Published November 17, 2020. Accessed September 28, 2021. Shaping the Future of the Fourth Industrial Revolution by Klaus Schwab, Nicholas Davis:9781984822611 | Books. Accessed September 28, 2021. Love A. CONFIRMED! Graphene Oxide Main Ingredient In Covid Shots. Ariyana Love. PublishedAugust 9, 2021. Accessed September 28, 2021. Graphene Oxide The Vector For Covid-19 Democide | The Liberty Beacon. Published July 30,2021. Accessed September 28, 2021. 511. ORWELL CITY: Official interim report of Pfizer’s vaccination vial analysis explained by La QuintaColumna. ORWELL CITY. Accessed September 28, 2021. Yi J, Choe G, Park J, Lee JY. Graphene oxide-incorporated hydrogels for biomedical applications.Polym J. 2020;52(8):823-837. doi:10.1038/s41428-020-0350-9513. Kim YH, Jo MS, Kim JK, et al. Short-term inhalation study of graphene oxide nanoplates.Nanotoxicology . 2018;12(3):224-238. doi:10.1080/17435390.2018.1431318514. News · CBC. Potentially toxic masks distributed in schools and daycares in Quebec | CBC News.CBC. Published March 26, 2021. Accessed September 28, 2021. HAF. BOMBSHELL: Disposable Blue Face Masks Found to Contain Toxic, Asbestos-Like Substancethat Destroys Lungs. Accessed September 28, 2021. Reuters. Japan suspends 1.6M doses of Moderna shot after contamination reports. NBC News.Accessed September 28, 2021. Contaminant in Moderna COVID-19 vaccine vials found in Japan was metallic particles: report.FiercePharma. Accessed September 28, 2021. Administrator A. Japan Suspects Contaminant In Moderna Vaccines Is Metallic, ‘Reacts ToMagnets.’ The Burning Platform. Published August 27, 2021. Accessed September 28, 2021. Franceschi Biagioni A, Cellot G, Pati E, et al. Graphene oxide prevents lateral amygdaladysfunctional synaptic plasticity and reverts long lasting anxiety behavior in rats.Biomaterials.2021;271:120749. doi:10.1016/j.biomaterials.2021.120749520. Soothing the symptoms of anxiety with graphene oxide. Graphene Flagship. AccessedSeptember 28, 2021. SARS-CoV-2 Spike Proteins Disrupt the Blood-Brain Barrier, Potentially Raising Risk ofNeurological Damage in COVID-19 Patients. Temple Health. Accessed September 28, 2021. NEUROMODULATORY EFFECTS OF SARS-COV-2 ON THE BLOOD-BRAIN BARRIER. CROIConference. Accessed September 28, 2021. Ohta S, Kikuchi E, Ishijima A, Azuma T, Sakuma I, Ito T. Investigating the optimum size ofnanoparticles for their delivery into the brain assisted by focused ultrasound-induced blood–brainbarrier opening.Sci Rep. 2020;10(1):18220. doi:10.1038/s41598-020-75253-9524. Vu MN, Rajasekhar P, Poole DP, et al. Rapid Assessment of Nanoparticle Extravasation in aMicrofluidic Tumor Model. ACS Appl Nano Mater . 2019;2(4):1844-1856. doi:10.1021/acsanm.8b02056525. Saraiva C, Praça C, Ferreira R, Santos T, Ferreira L, Bernardino L. Nanoparticle-mediated braindrug delivery: Overcoming blood–brain barrier to treat neurodegenerative diseases. J ControlledRelease. 2016;235:34-47. doi:10.1016/j.jconrel.2016.05.044 526. Pappas S. Rare magnetism found in the world’s strongest material. PublishedOctober 14, 2020. Accessed September 28, 2021. Augustyniak-Jabłokow MA, Tadyszak K, Strzelczyk R, Fedaruk R, Carmieli R. Slow spin relaxationof paramagnetic centers in graphene oxide.Carbon. 2019;152:98-105.doi:10.1016/j.carbon.2019.06.024528. Sang M, Shin J, Kim K, Yu KJ. Electronic and Thermal Properties of Graphene and RecentAdvances in Graphene Based Electronics Applications.Nanomaterials. 2019;9(3):374.doi:10.3390/nano9030374529. INBRAIN Neuroelectronics Secures $17 Million in Series A Funding for First AI-PoweredGraphene-Brain Interface. Published March 30, 2021. Accessed September 28, 2021. DARPA and the Brain Initiative. Accessed September 28, 2021. Six Paths to the Nonsurgical Future of Brain-Machine Interfaces. Accessed September 28, 2021. Neuralink and the Brain’s Magical Future. Wait But Why. Published April 20, 2017. AccessedSeptember 28, 2021. Martins NRB, Angelica A, Chakravarthy K, et al. Human Brain/Cloud Interface.Front Neurosci .2019;13:112. doi:10.3389/fnins.2019.00112534. Lee S, Shin Y, Woo S, Lee KK and H-N.Review of Wireless Brain-Computer Interface Systems.IntechOpen; 2013. doi:10.5772/56436535. Researchers demonstrate first human use of high-bandwidth wireless brain-computer interface.Brown University. Accessed September 28, 2021. AI and VR Transform Thoughts to Action with Wireless BCI | Psychology Today. AccessedSeptember 28, 2021. Haselager P. Did I Do That? Brain–Computer Interfacing and the Sense of Agency.Minds Mach.2013;23(3):405-418. doi:10.1007/s11023-012-9298-7538. Mind reading and brain computer interface technology: the future is coming, fast. Privacy SOS.Accessed September 28, 2021. With Magnetic Nanoparticles, Scientists Remotely Control Neurons and Animal Behavior.Accessed September 28, 2021. Brain-machine interfaces may be used to study and regulate mood - Science in the News.Accessed September 28, 2021. Shanechi MM. Brain–machine interfaces from motor to mood.Nat Neurosci . 2019;22(10):1554-1564. doi:10.1038/s41593-019-0488-y542. Opinion / The Last Humans and the Next Brands - Critical Mass - AccessedSeptember 28, 2021. Bonaci T, Herron J, Matlack C, Chizeck HJ. Securing the exocortex: A twenty-first centurycybernetics challenge. In:2014 IEEE Conference on Norbert Wiener in the 21st Century (21CW). ; 2014:1-8. doi:10.1109/NORBERT.2014.6893912544. Can dark triad leaders be a good choice for a leadership position? - Egon Zehnder. Can dark triadleaders be a good choice for a leadership position? - Egon Zehnder. Accessed September 28, 2021. Silver J. The Startling Accuracy of Referring to Politicians as “Psychopaths.” The Atlantic.Published July 31, 2012. Accessed September 28, 2021. Schlesinger T. The Rise of the Psychopath and Sociopath to Political Power. World Issues —Politics, Economics, and More. Published December 1, 2020. Accessed September 28, 2021. Commentary: 12% of corporate leaders are psychopaths. It’s time to take this problem seriously.Fortune. Accessed September 28, 2021. 21 percent of CEOs are psychopaths. Only 21 percent?Washington Post . Accessed September 28, 2021.549. McCullough J. The Psychopathic CEO. Forbes. Accessed September 28, 2021. The brain-computer interface: new rights or new threats to fundamental freedoms? AccessedSeptember 28, 2021.

Millions of books, audiobooks, magazines, documents, sheet music, and more for free.

Bad MedicineCovidDystopiaEducationEvilGeopoliticsVaccines

Omar Zaid

Author, Editor, Physician & Essential Monotheist