Study finds link between COVID-19 deaths and snake venom
University of Arizona researchers find certain enzyme that could be driving COVID deaths.
TUCSON, Ariz. — Snakes are starting to play a big role in COVID-19 research.
According to a study recently published in the Journal of Clinical Investigation, scientists from the University of Arizona have discovered an enzyme similar to one found in rattlesnake venom that could be driving COVID-19 deaths.
"We found evidence that there was an enzyme, a snake-like enzyme, in the blood of people who were in extraordinarily high levels," said Dr. Floyd Chilton, the senior author of the study with the University of Arizona, College of Agriculture and Life Sciences.
Scientists have worked on the study for the past year and a half. The snake-like enzyme is found in healthy people at low levels to prevent bacterial infections. In severe cases of COVID-19, it's doing the opposite.
"These high levels of this enzyme are looking at those tissues in the organs and saying, 'You look like a bacteria, let's shred your membranes. Let's put these organs out of their misery,'" Chilton said.
Chilton said what's even more remarkable is where the study could lead researchers in fighting the pandemic.
"Can we come up with specific therapeutics that will not care which variant is coming toward it?" Chilton said. "Can we come up with specific therapies to address this devastating disease?"
Researchers explain that current clinical trials on snake bites are helping in those efforts. They hope to repurpose some of the treatments being tested, which could one day result in a viable option other than vaccines to prevent death in severe patients.
"That allows us to take a precision medicine approach to the disease," Chilton said. "We can go into clinical trials and choose the people who are at risk of this mechanism and then specifically treat those people."
Researchers say the next step is to develop an international multi-center clinical trial. They are working with global organizations to see how they can make that possible.
Bryan Hughes, a rattlesnake expert and the owner of Rattlesnake Solutions, offered his own take on the study.
"For something that is almost as universally loathed as rattlesnakes, it seems fitting and interesting and ironic that the venom that they have in rattlesnakes might be the key in getting out of this situation," Hughes said.
Like Venom Coursing Through the Body: Researchers Identify Mechanism Driving COVID-19 Mortality
Researchers have identified what may be the key molecular mechanism responsible for COVID-19 mortality – an enzyme related to neurotoxins found in rattlesnake venom.
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By Rosemary Brandt, College of Agriculture and Life Sciences
Aug. 24, 2021
An enzyme with an elusive role in severe inflammation may be a key mechanism driving COVID-19 severity and could provide a new therapeutic target to reduce COVID-19 mortality, according to a study published in the Journal of Clinical Investigation.
Researchers from the University of Arizona, in collaboration with Stony Brook University and Wake Forest School of Medicine, analyzed blood samples from two COVID-19 patient cohorts and found that circulation of the enzyme – secreted phospholipase A2 group IIA, or sPLA2-IIA, – may be the most important factor in predicting which patients with severe COVID-19 eventually succumb to the virus.
The sPLA2-IIA enzyme, which has similarities to an active enzyme in rattlesnake venom, is found in low concentrations in healthy individuals and has long been known to play a critical role in defense against bacterial infections, destroying microbial cell membranes.
When the activated enzyme circulates at high levels, it has the capacity to "shred" the membranes of vital organs, said Floyd (Ski) Chilton, senior author on the paper and director of the UArizona Precision Nutrition and Wellness Initiative in the university's College of Agriculture and Life Sciences.
"It's a bell-shaped curve of disease resistance versus host tolerance," said Chilton, a member of the university's BIO5 Institute. "In other words, this enzyme is trying to kill the virus, but at a certain point it is released in such high amounts that things head in a really bad direction, destroying the patient's cell membranes and thereby contributing to multiple organ failure and death."
Together with available clinically tested sPLA2-IIA inhibitors, "the study supports a new therapeutic target to reduce or even prevent COVID-19 mortality," said study co-author Maurizio Del Poeta, a SUNY distinguished professor in the Department of Microbiology and Immunology in the Renaissance School of Medicine at Stony Brook University.
Collaboration Amid Chaos
"The idea to identify a potential prognostic factor in COVID-19 patients originated from Dr. Chilton," Del Poeta said. "He first contacted us last fall with the idea to analyze lipids and metabolites in blood samples of COVID-19 patients."
Del Poeta and his team collected stored plasma samples and went to work analyzing medical charts and tracking down critical clinical data from 127 patients hospitalized at Stony Brook University Hospital between January and July 2020. A second, independent cohort included a mix of 154 patient samples collected from Stony Brook and Banner University Medical Center in Tucson between January and November 2020.
"These are small cohorts, admittedly, but it was a heroic effort to get them and all associated clinical parameters from each patient under these circumstances," Chilton said. "As opposed to most studies that are well planned out over the course of years, this was happening in real time on the ICU floor."
The research team was able to analyze thousands of patient data points using machine learning algorithms. Beyond traditional risk factors such as age, body mass index and preexisting conditions, the team also focused on biochemical enzymes, as well as patients' levels of lipid metabolites.
"In this study, we were able to identify patterns of metabolites that were present in individuals who succumbed to the disease," said lead study author Justin Snider, an assistant research professor in the UArizona Department of Nutrition. "The metabolites that surfaced revealed cell energy dysfunction and high levels of the sPLA2-IIA enzyme. The former was expected but not the latter."
Using the same machine learning methods, the researchers developed a decision tree to predict COVID-19 mortality. Most healthy individuals have circulating levels of the sPLA2-IIA enzyme hovering around half a nanogram per milliliter. According to the study, COVID-19 was lethal in 63% of patients who had severe COVID-19 and levels of sPLA2-IIA equal to or greater than 10 nanograms per milliliter.
"Many patients who died from COVID-19 had some of the highest levels of this enzyme that have ever been reported," said Chilton, who has been studying the enzyme for over three decades.
An Enzyme with a Bite
The role of the sPLA2-IIA enzyme has been the subject of study for half of a century and it is "possibly the most examined member of the phospholipase family," Chilton explained.
Charles McCall, lead researcher from the Wake Forest School of Medicine on the study, refers to the enzyme as a "shredder" for its known prevalence in severe inflammation events, such as bacterial sepsis, as well as hemorrhagic and cardiac shock.
Previous research has shown how the enzyme destroys microbial cell membranes in bacterial infections, as well as its similar genetic ancestry with a key enzyme found in snake venom.
The protein "shares a high sequence homology to the active enzyme in rattlesnake venom and, like venom coursing through the body, it has the capacity to bind to receptors at neuromuscular junctions and potentially disable the function of these muscles," Chilton said.
"Roughly a third of people develop long COVID, and many of them were active individuals who now can't walk 100 yards," Chilton said. "The question we are investigating now is: If this enzyme is still relatively high and active, could it be responsible for part of the long COVID outcomes that we're seeing?”
Also:
Getting very ill with COVID-19 is like rattlesnake bite: study
Getting very ill with COVID-19 is like getting bitten by a poisonous rattlesnake, according to a new medical study.
Researchers including from Stony Brook University on Long Island have identified an enzyme in the coronavirus that ravages the body like the neurotoxins from rattlesnake venom, according to the analysis published in the Journal of Clinical Investigation.
Targeting the enzyme, which causes severe inflammation, could better treat and save the lives of COVID-19 patients amid the virus’ resurgence with the Delta variant, said the study’s scientists from the SUNY school, the University of Arizona and Wake Forest University.
The coronavirus enzyme, sPLA2-II, has similarities to an active enzyme in rattlesnake venom that is typically found in low concentrations in healthy individuals and has long been known to play a critical role in humans’ defense against bacterial infections, the study says.
But when the same enzyme circulates at high levels, it can “shred” the membranes of vital organs, said University of Arizona’s Floyd “Ski” Chilton, a senior author of the paper.
“The study supports a new therapeutic target to reduce or even prevent COVID-19 mortality,” explained co-author Dr. Maurizio Del Poeta of Stony Brook’s Renaissance School of Medicine.
“Because inhibitors of sPLA2-IIA already exist, our study supports the use of these inhibitors in patients with elevated levels of sPLA2-IIA to reduce, or even prevent, COVID-19 mortality.”
The study says that in high enough concentrations, sPLA2-II can shred the membrane of vital organs.
Del Poeta said Chilton contacted Stony Brook to analyze blood samples in COVID-19 patients to study the snake venom-type enzyme.
Del Poeta and his team, co-led by him and research assistant Jeehyun Karen You, collected stored blood plasma samples and analyzed medical charts from 127 patients hospitalized at Stony Brook University Hospital between January and July 2020.
A collection of 154 patient samples from Stony Brook and Banner University Medical Center in Tucson between January and November 2020 also were examined.
“Our study is especially timely given how the Delta variant is contributing to rising COVID-19 incidence and hospitalization rates both in the US and worldwide,” You said.
As of Friday, 55,453 people have died from COVID-19 in New York state, according to data provided to the federal Centers for Disease Control and Prevention.
“As the Delta variant makes its way through communities across the country, it’s crucial we keep doing everything we can to keep each other safe from the COVID virus,” Gov. Kathy Hochul said in a statement Sunday.
“Wear a mask, and, if you haven’t already, get your vaccine as soon as you can. The vaccine is the best way to protect yourselves and your loved ones.”
Hochul and the state Health Department issued a mandate Friday requiring staff and students in public and private schools to wear masks for the new academic year to prevent the spread of COVID-19.
The DOH last week also approved an emergency rule requiring virtually all 450,000 health care workers in hospitals, nursing homes and other settings to get the coronavirus vaccine — or face disciplinary action including getting fired.
Meanwhile, 634,157 people have been killed by the coronavirus throughout the United States.
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The Snake Venom Hypothesis of Covid – Dr. Bryan Ardis
Monoclonal antibody treatment – the basis
The key finding that Ardis’ case rests on is that an anti-venom treatment administered in a hospital will consist of monoclonal antibodies (MA). He was tipped off to this connection by a colleague. Ardis’ train of thought equates the two, that MAs (all) ARE an anti-venom treatment; so given that MAs work effectively against Covid, Covid itself is caused by some type of venom. So Covid is not a virus and thus is not transmitted by air.
MA treatments have, of course, been attacked by federal health agencies in the US even though they were successful in treating Covid, as are ivermectin, hydroxochloroquine (HCQ) and NAC. Note that HCQ has expressly been forbidden with Remdesivir.
Historically, back in 2020, 3 animals were posited as the source of Covid (bats, pangolins and snakes), but the snake hypothesis would be repeatedly fact-checked and debunked by all the usual sources. Apparently, the genetic sequences of antibodies in sick people in Wuhan back in 2019/2020 were not like those of bats but of protein sequences found in snakes, particularly the Chinese krait and king cobra. In April 2020, a research study in France found that certain receptors in the brain called ‘nicotinic acetylcholinesterase’ receptors bind most tightly to these particular types of snake venom; the spike protein of SARS-CoV-2 is identical (or almost) to these 2 types of venoms.
In May 2020, a young researcher, Dr. Bing LIU at the University of Pittsburgh had been researching the genetic sequencing of spike proteins for 5 months and was going to make a press release on what he and his team had found. Instead, he was found murdered and the results have never been released. (ER: Another young researcher also turned up dead within a calendar month of Dr. Liu – Dr. James Taylor, who was also researching the genetic sequencing of Covid.)
In January 2020, a study was published after research over a 10-year period, which had mapped the genetic sequences of the proteins and peptides of the king cobra venom. The researchers came from a company called Genentech. There are 19 toxic proteins isolated, which specifically target organs in the human body. Funding for this study came from Roche, which put employees in the study in a conflict of interest as they were all shareholders in Roche. Genentech is related to Remdesivir manufacturer, Gilead. Gilead bought 2 facilities that deal with biological studies from Genentech in 2011; 55 of Genentech’s executives were brought into Gilead in 2011 just when the king cobra study started.
Gilead’s Remdesivir is created from synthetic peptides and proteins of king cobra venom. Before and during treatment, the patient’s prothrombin time must be monitored: a high level means the patient’s blood cannot clot. A University of Arizona study in 2021 looked at the tissues of patients who had died of Covid; present were extremely high levels of ‘an enzyme related to neurotoxins found in rattlesnake venom’. The internal organs of these patients had been attacked by this enzyme, leading to multiple organ failure.
Using snake venom in treatment can be an effective way to kill people without the substance administered being suspected. As the venom attacks certain organs (pancreas, heart, liver, spleen, brain, lungs, etc.), people with diseases of these organs will naturally succumb, apparently to their original health problem and not the treatment. Snake venom is thus an effective bioweapon.
Ardis is ‘convinced’ – ‘believes’ – that Covid itself, as well as the vaccines and Remdesivir, all contain some degree of snake venom.
Since 2005, it’s been known that nicotine blocks the receptors in the brain stem that are attacked by cobra venom. These receptors control the diaphragm and thus enable a person to breathe, thereby obtaining sufficient oxygen. The venom ingested will normally reach these brain receptors, paralyzing breathing. However, it was being reported early on that smokers were the least represented demographic among Covid sufferers (less than 5%), which is odd for a respiratory virus that should especially target smokers. In the first 6 months, however, Fauci was telling people to stop smoking; they simply lied about smokers being the most hospitalized group. Nicotine, on the contrary, protects these receptors against poisoning by venom. French researchers in 2020 worked out that the nicotine receptors that control the diaphragm’s ability to breathe were what the spike protein was targeting. So they theorized that people actually need to be given nicotine to prevent Covid.
As a non-smoker, if you go into hospital to be treated for Covid, they give you Remdesivir (based on venom), which attacks the nicotine receptors in the brain stem, paralyzing breathing. Then, in order to put you on a ventilator, they give you one of 5 drugs first (e.g. midazolam, morphine, etc.) which acts to further suppress breathing. So these two drugs, which are worked out in a precise cocktail, are euthanizing patients. Two 5-day back to back treatments are authorized in these circumstances: on average, a person dies on Day 9.
In July of 2021, a Moderna co-founder announced they were using mRNA technology to treat venomous snakebites. The new ‘Opherics’ company, based in San Francisco, would solely produce anti-venom drugs for snake bites, funded by the DoD, Wellcome Trust and the United Nations. How many snake bite victims are there typically in a year? Around 100,000. So why put such effort into creating this technology? mRNA technology was created in 2015 using cobra venom (presumably synthetic form), that was wrapped in nano-particulate dynabeads (made of metal), put in hydrogel to make it very stable. Some vaccinated people are able to attach magnets to their arms.
Canada’s Dr. Charles Hoffa noticed that his (Moderna) vaccinated patients were suffering from elevated D-dimer levels (which indicate clotting). When patients exhibit this, one of the things doctors typically factor in is snake venom poisoning. The classic problem with Remdesivir is kidney failure, which is the number one organ attacked by cobra venom.
Ardis believes that the damage from Covid (SARS-CoV-2), the vaccines, and Remdesivir treatment all correlate with the damage done from snake venom as per the findings of research studies. The disease process put in place by the vaccines, for example, will just continue with the boosters. Further, the sickness going around is not a virus; based on snake venom, it is likely found in water.
Ardis believes this is how the problem was spread. CDC has been tracking waste water on its Covid surveillance site: it has 400 water testing sites in 37 US cities. From January to September, 2020, nobody knew about this water testing. Results are now being released.
Why would you PCR-test water as they have been doing? They test the water to PREDICT viral outbreaks in a given area. Yet this is backwards: if the ‘virus’ is in the water, it assumes that the population has already had the symptoms of infection.
A loss of taste and smell have been signature symptoms of Covid, yet long-term loss of taste and smell are precisely the symptoms people get if they’ve reversed a snake-bite by sucking out the venom from the wound site. This parallels water drinking. Black List, season 4, episode 15, Reddington is poisoned by snake venom from drinking. His symptoms mimic other types of health problems.
Also:
Like venom coursing through the body: Researchers identify mechanism driving COVID-19 mortality
An enzyme with an elusive role in severe inflammation may be a key mechanism driving COVID-19 severity and could provide a new therapeutic target to reduce COVID-19 mortality, according to a study published in the Journal of Clinical Investigation.
Researchers from the University of Arizona, in collaboration with Stony Brook University and Wake Forest University School of Medicine, analyzed blood samples from two COVID-19 patient cohorts and found that circulation of the enzyme -- secreted phospholipase A2 group IIA, or sPLA2-IIA -- may be the most important factor in predicting which patients with severe COVID-19 eventually succumb to the virus.
sPLA2-IIA, which has similarities to an active enzyme in rattlesnake venom, is found in low concentrations in healthy individuals and has long been known to play a critical role in defense against bacterial infections, destroying microbial cell membranes.
When the activated enzyme circulates at high levels, it has the capacity to "shred" the membranes of vital organs, said Floyd (Ski) Chilton, senior author on the paper and director of the UArizona Precision Nutrition and Wellness Initiative housed in the university's College of Agriculture and Life Sciences.
"It's a bell-shaped curve of disease resistance versus host tolerance," Chilton said. "In other words, this enzyme is trying to kill the virus, but at a certain point it is released in such high amounts that things head in a really bad direction, destroying the patient's cell membranes and thereby contributing to multiple organ failure and death."
Together with available clinically tested sPLA2-IIA inhibitors, "the study supports a new therapeutic target to reduce or even prevent COVID-19 mortality," said study co-author Maurizio Del Poeta, a SUNY distinguished professor in the Department of Microbiology and Immunology in the Renaissance School of Medicine at Stony Brook University.
Collaboration Amid Chaos
"The idea to identify a potential prognostic factor in COVID-19 patients originated from Dr. Chilton," Del Poeta said. "He first contacted us last fall with the idea to analyze lipids and metabolites in blood samples of COVID-19 patients."
Del Poeta and his team collected stored plasma samples and went to work analyzing medical charts and tracking down critical clinical data from 127 patients hospitalized at Stony Brook University between January and July 2020. A second independent cohort included a mix of 154 patient samples collected from Stony Brook and Banner University Medical Center in Tucson between January and November 2020.
"These are small cohorts, admittedly, but it was a heroic effort to get them and all associated clinical parameters from each patient under these circumstances," Chilton said. "As opposed to most studies that are well planned out over the course of years, this was happening in real time on the ICU floor."
The research team was able to analyze thousands of patient data points using machine learning algorithms. Beyond traditional risk factors such as age, body mass index and preexisting conditions, the team also focused on biochemical enzymes, as well as patients' levels of lipid metabolites.
"In this study, we were able to identify patterns of metabolites that were present in individuals who succumbed to the disease," said lead study author Justin Snider, an assistant research professor in the UArizona Department of Nutrition. "The metabolites that surfaced revealed cell energy dysfunction and high levels of the sPLA2-IIA enzyme. The former was expected but not the latter."
Using the same machine learning methods, the researchers developed a decision tree to predict COVID-19 mortality. Most healthy individuals have circulating levels of the sPLA2-IIA enzyme hovering around half a nanogram per milliliter. According to the study, COVID-19 was lethal in 63% of patients who had severe COVID-19 and levels of sPLA2-IIA equal to or greater than 10 nanograms per milliliter.
"Many patients who died from COVID-19 had some of the highest levels of this enzyme that have ever been reported," said Chilton, who has been studying the enzyme for over three decades.
An Enzyme with a Bite
The role of the sPLA2-IIA enzyme has been the subject of study for half of a century and it is "possibly the most examined member of the phospholipase family," Chilton explained.
Charles McCall, lead researcher from Wake Forest University on the study, refers to the enzyme as a "shredder" for its known prevalence in severe inflammation events, such as bacterial sepsis, as well as hemorrhagic and cardiac shock.
Previous research has shown how the enzyme destroys microbial cell membranes in bacterial infections, as well as its similar genetic ancestry with a key enzyme found in snake venom.
The protein "shares a high sequence homology to the active enzyme in rattlesnake venom and, like venom coursing through the body, it has the capacity to bind to receptors at neuromuscular junctions and potentially disable the function of these muscles," Chilton said.
"Roughly a third of people develop long COVID, and many of them were active individuals who now can't walk 100 yards. The question we are investigating now is: If this enzyme is still relatively high and active, could it be responsible for part of the long COVID outcomes that we're seeing?"
