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FTR #1117 This program was recorded in one, 60-minute segment.
NB: This description contains material not included in the original broadcast.
Introduction: Researchers found that levels of the Covid-19 virus increased soon after symptoms first appeared, with higher amounts in the nose than in the throats, which is also more consistent with influenza than SARS. Of the 18 patients they examined, one had moderate levels in their nose and throat but no symptoms–people who are asymptomatic can still potentially spread the virus. It’s this combination of airborne transmissions and asymptomatic patients who shed the virus that makes this a particularly infectious disease.
This anomalous new ability to infect the upper respiratory tract, of course, brings up the chilling experiments where researchers modified the H5N1 bird flu virus until it was capable of airborne transmissions between ferrets. That’s the same research that was banned by the NIH following the uproar but has subsequently been reallowed in early 2019. That original 2012 study specifically found that it was mutations that gave the virus the ability to infect the upper respiratory tracts of the ferrets that made it an airborne virus. We have yet to year if the SAR-CoV‑2 virus had the same or similar mutations to those that were induced in the H5N1 bird flu virus experiment but it seems likely.
The infectiousness of the SARS-CoV‑2 coronavirus is unprecedented based on this new study. As one immunologist put it, “This virus is clearly much more capable of spreading between humans than any other novel coronavirus we’ve ever seen. This is more akin to the spread of flu”.
In the context of the Covid-19’s flu-like ability to infect the upper respiratory tract, we explore experiments adapting the lethal H5N1 avian flu to ferrets. These experiments were halted in 2014 but subsequently resumed in 2017.
Might some of this experiment have been adapted to the Covid-19?
We explore additional experiments adapting the lethal H5N1 avian flu to ferrets. These experiments were halted in 2014 but subsequently resumed in 2017.
Might some of this experiment have been adapted to the Covid-19?
These experiments were resumed, shortly before the outbreak of Covid-19. Again, might some of the results of the adaptation of the H5N1 avian flu to ferrets have figured in the Covid-19 phenomenon?
Note that many experts were critical of the process.
A report on the adaptation of the A/H5N1 to ferrets notes that Oseltamivir–marketed under the brand-name Tamiflu–was successful in treating the ferrets. That is one of the anti-virals in a drug cocktail used by Thai doctors to successfully treat a Covid-19 sufferer.
In FTR#55, we noted in 1997 that U.S. Army researchers had successfully recovered genetic material from the 1918 influenza epidemic.
As will be seen in future programs, one of the variants of the Covid-19 does indeed behave like the 1918 flu virus. As we will also see in future programs, that virus was resurrected by researchers in 2005.
In the past, we have heard it alleged by credible sources that Germany was behind the 1918 flu epidemic that killed scores of millions worldwide.
From Germany Watch comes another post reinforcing this line of inquiry.
After maintaining that German agents were sabotaging livestock with anthrax, the post discusses British intelligence distillate indicating that, after discovering the particular strain of virulent flu, German agents began deliberately spreading it in the U.S.
NB: We don’t feel that the information from the book Three Wars with Germany confirms the hypothesis that the flu pandemic was a German bio-warfare weapon gone awry beyond the point of debate. It DOES, however, highlight that possibility.
We then tackle the subject of a cult/church that is at the epicenter of a Covid-19 outbreak in South Korea. The overlap between this organization and the Unification Church is discussed in a Food For Thought post. Might this cult have been a vector for introducing the virus into Wuhan?
The fascistic nature of the cult and some of the rituals and beliefs of the organization would render the group and/or some of its members as viable “useful idiots” for manipulation in connection with this outbreak.
The next two points of discussion concern the fact that the current U.S. Ambassador to South Korea was the former head of the United States Pacific Command. We wonder if he might be ONI and/or CIA, and if he might have any connection to the anti-China blitzkrieg and the Covid-19 outbreak?
As the former Commander of the Guantanamo base in Cuba, Admiral Harris certainly did have operational links with the intelligence community.
1a. Researchers found that levels of the Covid-19 virus increased soon after symptoms first appeared, with higher amounts in the nose than in the throats, which is also more consistent with influenza than SARS. Of the 18 patients they examined, one had moderate levels in their nose and throat but no symptoms–people who are asymptomatic can still potentially spread the virus. It’s this combination of airborne transmissions and asymptomatic patients who shed the virus that makes this a particularly infectious disease.
This anomalous new ability to infect the upper respiratory tract, of course, brings up the chilling experiments where researchers modified the H5N1 bird flu virus until it was capable of airborne transmissions between ferrets. That’s the same research that was banned by the NIH following the uproar but has subsequently been reallowed in early 2019. That original 2012 study specifically found that it was mutations that gave the virus the ability to infect the upper respiratory tracts of the ferrets that made it an airborne virus. We have yet to year if the SAR-CoV‑2 virus had the same or similar mutations to those that were induced in the H5N1 bird flu virus experiment but it seems likely.
The infectiousness of the SARS-CoV‑2 coronavirus is unprecedented based on this new study. As one immunologist put it, “This virus is clearly much more capable of spreading between humans than any other novel coronavirus we’ve ever seen. This is more akin to the spread of flu”:
Scientists in China who studied nose and throat swabs from 18 patients infected with the new coronavirus say it behaves much more like influenza than other closely related viruses, suggesting it may spread even more easily than previously believed.
In at least in one case, the virus was present even though the patient had no symptoms, confirming concerns that asymptomatic patients could also spread the disease.
Although preliminary, the findings published on Wednesday in the New England Journal of Medicine, offer new evidence that this novel coronavirus, which has killed more than 2,000 people mostly in China, is not like its closely-related coronavirus cousins.
“If confirmed, this is very important,” said Dr. Gregory Poland, a virologist and vaccine researcher with the Mayo Clinic in Rochester, Minnesota, who was not involved with the study.
Unlike Severe Acute Respiratory Syndrome (SARS), which causes infections deep in the lower respiratory tract that can result in pneumonia, COVID-19 appears to inhabit both the upper and lower respiratory tracts. That would make it not only capable of causing severe pneumonia, but of spreading easily like flu or the common cold.
Researchers in Guangdong province monitored the amount of coronavirus in the 18 patients. One of them, who had moderate levels of the virus in their nose and throat, never had any disease symptoms.
Among the 17 symptomatic patients, the team found levels of the virus increased soon after symptoms first appeared, with higher amounts of virus present in the nose than in the throats, a pattern more similar to influenza than SARS.
The level of virus in the asymptomatic patient was similar to what was present in patients with symptoms, such as fever.
“What this says is clearly this virus can be shed out of the upper respiratory tract and that people are shedding it asymptomatically,” Poland said.
The findings add to evidence that this new virus, though genetically similar, is not behaving like SARS, said Kristian Andersen, an immunologist at Scripps Research in La Jolla who uses gene sequencing tools to track disease outbreaks.
“This virus is clearly much more capable of spreading between humans than any other novel coronavirus we’ve ever seen. This is more akin to the spread of flu,” said Andersen, who was not involved with the study.
…
———–
1b. We explore experiments adapting the lethal H5N1 avian flu to ferrets. These experiments were halted in 2014 but subsequently resumed in 2017.
Might some of this experiment have been adapted to the Covid-19?
“Mutant Bird-Flu Study Fuels Fears of Airborne H5N1 by Brandon Keim; Wired; 6/21/2012.
After months of anticipation, the second of two controversial experiments to increase the virulence of H5N1 avian influenza has been published.
Many scientific questions are raised by the findings, and the same safety concerns remain that provoked massive public outcry and a temporary halt to the research. But if there were any doubts about H5N1’s ability to become airborne, they’re gone.
In the experiment, researchers made H5N1 strains that passed through the air between ferrets, which are often used as a model for human flu infection. Catching the highly lethal virus typically requires close contact with an infected bird or person.
The resulting virus didn’t kill the animals, and it’s uncertain if a ferret-infecting strain could also infect people. But the fact that just five genetic mutations were needed to produce the airborne strain is troubling.
“One of the next key questions is, ‘How likely is it that such a virus could evolve in nature?’ ” said virologist Derek Smith of the UK’s Cambridge University at a June 20 press conference. The research was led by virologists Sander Herfst and Ron Fouchier of Erasmus University in the Netherlands and published June 21 in Science.
“It’s now clear that we’re living on a fault line,” continued Smith. “It could really do something. What we need to now is how likely that is.”
The researchers started by genetically modifying H5N1 to contain three mutations identified in previous pandemic flu strains as increasing viral transmissibility.
Thus modified, the strain was manually introduced into the noses of ferrets. Once infection was established, the researchers swabbed the ferrets and infected another group. They repeated the cycle multiple times, mimicking a chain of infection between people.
At each stage, some strains became more adapted to surviving and replicating in the ferrets’ upper respiratory tracts, a precursor to making flu spread by cough or sneeze. By the 10th stage’s end, the mutant H5N1 was airborne, passing between ferrets in separate cages.
Ferrets infected by the airborne strains didn’t die, raising the possibility that becoming highly infectious makes H5N1 less lethal. This, however, is far from certain, and perhaps more time would have produced a more-lethal variant.
Making the engineered H5N1 go airborne required a total of five mutations. “Within the first three or four passages, we already see strong adaptations of the virus,” said Fouchier during the press conference. “Only a limited chain of transmission is sufficient in ferrets. We assume that in humans it would take a low number of events for these or similar mutations to accumulate.”
In a study accompanying the findings, researchers led by Smith and microbiologist Colin Russell, also of Cambridge University, looked for the five mutations in naturally circulating strains of H5N1. They found them, though the mutations occurred individually or in pairs, not united simultaneously in single strains.
Whether they could gather in one strain is now a pressing question, as is a more fundamental scientific question: Do the mutations represent a mechanism by which H5N1 could become contagious in humans, or just in ferrets? And if they are directly relevant to human infections, do they represent a primary route, or one of many possible paths?
That’s unknown, but simply being able to see how mutations alter influenza should help researchers, said biomedical informaticist Raul Rabadan of Columbia University, who specializes in analyzing flu genomes.
“Beyond the particular mutations in each paper, these studies point out key necessary elements for mammalian adaptation and transmission,” Rabadan said. “The mutations are important, but more important is what they are telling us about the mechanisms for host adaptation and airborne transmission.”
Smith and Fouchier’s teams hope the findings will guide surveillance efforts, providing researchers who track flu’s natural evolution in humans and other animals. But in a commentary also published in Science, epidemiologists Marc Lipsitch and Barry Bloom of Harvard University said the findings were less useful than advertised.
According to Lipsitch and Bloom, too little is known about flu genetics or its natural evolution to make lab-generated changes a reliable guide for real-world surveillance. “Predictions about how particular influenza strains will behave in humans or, even more important, how they will evolve, remain highly speculative,” they wrote.
Calculating the risks and benefits of these experiments, along with experiments that made H5N1 more virulent by mixing it with the pandemic 2009 flu strain, is a complicated and controversial matter.
Supporters of the research argue that potential benefits outweigh the risks, which are enormous. Beyond giving recipes to would-be bioterrorists, accidental disease exposures at high-security research laboratories are not uncommon, and flu is extraordinarily difficult to control.
Some researchers put H5N1’s human mortality rate at 60 percent, a number likely inflated by epidemiologists overlooking cases that lack severe symptoms. But a mortality rate of just 2.5 percent killed 40 million people in the 1918 pandemic.
Should the findings prove less useful than expected, justification for H5N1 engineering would evaporate. If the findings do prove useful, there’s still powerful disagreement over how the research should be conducted. Many critics say H5N1 experiments should be restrictedto a few highly skilled people in the world’s most secure laboratories.
The National Institutes of Health is currently drafting formal policies to handle this and other potentially dangerous research, a task that should have been completed years ago.
Asked about the study published today, epidemiologist Stephen Morse of Columbia University said, “At least it’s forced us to confront this issue directly, which was never really resolved and badly needs some good policy.”
Correction 6/21: The original wording of the opening paragraphs implied that the new H5N1 strain could infect humans. That is unknown.
1c. A similar adaptation of H5N1 to ferrets also stirred controversy in 2012. That experiment was also resumed following a 2914 moratorium.
Again, was some of this adapted to the Covid-19?
After months of controversy, an experiment describing how H5N1 avian influenza can be modified into potentially human-contagious forms was published today.
The study was originally submitted to the journal Nature in 2011. Concern that its details, along with those in a similar, as-yet-unpublished experiment, could be turned to malevolent ends delayed its publication.
Subsequent public controversy resulted in a temporary moratorium on such research that is still ongoing. The uproar, however, is far from over: Flu researchers and biodefense experts continue to argue over the findings’ safety and scientific value.
“Given the possibility of accidental escape from the lab – a not too uncommon event – the risks seem to me enormous, while the benefits are very small,” said Richard Roberts, a Nobel Prize-winning geneticist who now works at New England Biolabs.
In the study, researchers led by virologist Yoshiro Kawaoka of the University of Wisconsin introduced random genetic mutations to one of the flu virus’ eight genes.
The mutations changed the shape of the protein the gene produced, allowing H5N1 – which until now had great difficulty infecting mammals, including humans – to infect and pass easily between ferrets, an animal commonly used to model human flu pathology. The viruses also attached more easily to human respiratory-tract cells.
The resulting strains were non-lethal to ferrets, and it’s thought they’d be non-lethal to humans as well, though this is obviously untested. Experimental vaccines against naturally occurring H5N1 appeared activated by exposure to the new strains, suggesting a protective effect, though this too remains unproven.
According to the study’s authors and many flu experts, the findings are important in several ways: They prove that it’s indeed possible for H5N1 to evolve to infect humans, they flag several genetic mutations to watch for in naturally evolving strains, and they underscore the need for continued research. The potential hybridization of H5N1 with the H1N1 swine flu of 2009 is especially troubling.
“These findings do not only provide further indication that such a virus may arise naturally; they also pave the way for improved influenza surveillance and pandemic preparedness,” wrote University of Hong Kong virologists Hui-Ling Yen and Malik Peiris, the scientist who first identified SARS, in a commentary accompanying the study.
Over the last several months, objections to the research have frequently been called uninformed or overblown. “Fear needs to be put to rest with solid science and not speculation,” wrote microbiologist Peter Palese of the Mount Sinai School of Medicine in a January commentary in the Proceedings of the National Academy of Sciences.
Hints of that tone remain in an “independent risk assessment” commissioned by Nature, describing how the findings “could be misrepresented by a willful media, in the absence of a knowledgeable public.”
Many experts do, however, remain skeptical of the findings’ value.
The mutations identified are indeed interesting, but thousands of other as-yet-unknown mutations may have the same effect, potentially limiting this work’s relevance. It’s uncertain whether naturally occurring mutations would even behave the same way.
Global flu surveillance is also piecemeal and grossly underfunded, making it unlikely that the identity of these experimental mutations can be put to use in the near future.
“I find it rather unlikely that these experiments would have resulted in the discovery of anything useful other than the knowledge that aerosolic transmission was possible,” said Richard Roberts of New England Biolabs.
Virologist Michael Osterholm of the University of Minnesota expressed a similar sentiment in a January editorial in the journal Science. “The desire to disseminate the entirety of the methods and results of the two H5N1 studies in the general scientific literature will not materially increase our ability to protect the public’s health from a future H5N1 pandemic,” he wrote. Osterholm declined to comment this week.
According to Roberts, many prominent virologists are afraid to criticize the findings publicly for fear of retribution from the National Institutes of Health and other funders that promised the strategy of experimentally making dangerous pathogens more virulent would be safe and valuable.
“That’s certainly not the case,” said Anthony Fauci, director of the National Institutes of Allergy and Infectious Disease, the NIH division that funded the research. “We’re driven by a philosophy of open scientific discourse. Disagreements are one of the fundamental positive aspects of science.”
1d. These experiments were resumed, shortly before the outbreak of Covid-19. Again, might some of the results of the adaptation of the H5N1 avian flu to ferrets have figured in the Covid-19 phenomenon?
Note that many experts were critical of the process.
Controversial lab studies that modify bird flu viruses in ways that could make them more risky to humans will soon resume after being on hold for more than 4 years. ScienceInsider has learned that last year, a U.S. government review panel quietly approved experiments proposed by two labs that were previously considered so dangerous that federal officials had imposed an unusual top-down moratorium on such research.
One of the projects has already received funding from the National Institutes of Health’s (NIH’s) National Institute of Allergy and Infectious Diseases (NIAID) in Bethesda, Maryland, and will start in a few weeks; the other is awaiting funding.
The outcome may not satisfy scientists who believe certain studies that aim to make pathogens more potent or more likely to spread in mammals are so risky they should be limited or even banned. Some are upset because the government’s review will not be made public. “After a deliberative process that cost $1 million for [a consultant’s] external study and consumed countless weeks and months of time for many scientists, we are now being asked to trust a completely opaque process where the outcome is to permit the continuation of dangerous experiments,“ says Harvard University epidemiologist Marc Lipsitch.
One of the investigators leading the studies, however, says he’s happy he can resume his experiments. “We are glad the United States government weighed the risks and benefits … and developed new oversight mechanisms. We know that it does carry risks. We also believe it is important work to protect human health,” says Yoshihiro Kawaoka of the University of Wisconsin in Madison and the University of Tokyo. The other group that got the green light is led by Ron Fouchier at Erasmus University Medical Center in Rotterdam, the Netherlands.
In 2011, Fouchier and Kawaoka alarmed the world by revealing they had separately modified the deadly avian H5N1 influenza virus so that it spread between ferrets. Advocates of such gain of function (GOF) studies say they can help public health experts better understand how viruses might spread and plan for pandemics. But by enabling the bird virus to more easily spread among mammals, the experiments also raised fears that the pathogen could jump to humans. And critics of the work worried that such a souped-up virus could spark a pandemic if it escaped from a lab or was intentionally released by a bioterrorist. After extensive discussion about whether the two studies should even be published (they ultimately were) and a voluntary moratorium by the two labs, the experiments resumed in 2013 under new U.S. oversight rules.
But concerns reignited after more papers and a series of accidents at federal biocontainment labs. In October 2014, U.S. officials announced an unprecedented “pause” on funding for 18 GOF studies involving influenza or the Middle East respiratory syndrome [MERS–D.E.] or severe acute respiratory syndrome viruses [SARS–D.E.]. . . .
. . . . Now, the HHS committee has approved the same type of work in the Kawaoka and Fouchier labs that set off the furor 8 years ago. Last summer, the committee reviewed the projects and made recommendations about risk-benefit analyses, safety measures to avoid exposures, and communications plans, an HHS spokesperson says.
After the investigators revised their plans, the HHS committee recommended that they proceed. Kawaoka learned from NIH on 10 January that his grant has been funded. Fouchier expects the agency may hold off on making a funding decision until after a routine U.S. inspection of his lab in March.
Kawaoka’s grant is the same one on H5N1 that was paused in 2014. It includes identifying mutations in H5N1 that allow it to be transmitted by respiratory droplets in ferrets. . . .
. . . . HHS cannot make the panel’s reviews public because they contain proprietary and grant competition information, says the spokesperson. But critics say that isn’t acceptable. “Details regarding the decision to approve and fund this work should be made transparent,” says Thomas Inglesby, director of Center for Health Security of the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland. The lack of openness “is disturbing. And indefensible,” says microbiologist Richard Ebright of Rutgers University in Piscataway, New Jersey. The critics say the HHS panel should at least publicly explain why it thought the same questions could not be answered using safer alternative methods. . . .
1e. A report on the adaptation of the A/H5N1 to ferrets notes that Oseltamivir–marketed under the brand-name Tamiflu–was successful in treating the ferrets. That is one of the anti-virals in a drug cocktail used by Thai doctors to successfully treat a Covid-19 sufferer.
Highly pathogenic avian influenza A/H5N1 virus can cause morbidity and mortality in humans but thus far has not acquired the ability to be transmitted by aerosol or respiratory droplet (“airborne transmission”) between humans. To address the concern that the virus could acquire this ability under natural conditions, we genetically modified A/H5N1 virus by site-directed mutagenesis and subsequent serial passage in ferrets. The genetically modified A/H5N1 virus acquired mutations during passage in ferrets, ultimately becoming airborne transmissible in ferrets. None of the recipient ferrets died after airborne infection with the mutant A/H5N1 viruses. Four amino acid substitutions in the host receptor-binding protein hemagglutinin, and one in the polymerase complex protein basic polymerase 2, were consistently present in airborne-transmitted viruses. The transmissible viruses were sensitive to the antiviral drug oseltamivir and reacted well with antisera raised against H5 influenza vaccine strains. Thus, avian A/H5N1 influenza viruses can acquire the capacity for airborne transmission between mammals without recombination in an intermediate host and therefore constitute a risk for human pandemic influenza. . . .
1f. In FTR#55, we noted in 1997 that U.S. Army researchers had successfully recovered genetic material from the 1918 influenza epidemic.
As will be seen in future programs, one of the variants of the Covid-19 does indeed behave like the 1918 flu virus. As we will also see in future programs, that virus was resurrected by researchers in 2005.
“Genetic Material from 1918 Flu is Found” by Gina Kolata; The New York Times; 3/21/1997.
A group of Defense Department researchers has found genetic material from the notorious Spanish flu virus that killed at least 20 million people worldwide in the influenza pandemic of 1918.
Fragments of the virus were found lurking in a formaldehyde-soaked scrap of lung tissue from a 21-year-old soldier who died of the flu nearly 80 years ago. And now, medical experts say, investigators at last hope to answer a question that has troubled them for decades: what made this virus so deadly?
One part of the answer is that the Spanish flu virus passed from birds to pigs and then to humans, a mode of transmission that is thought to produce the most dangerous strains of influenza viruses. Indeed, fear of a swine flu epidemic in 1976 caused President Gerald R. Ford to mobilize the nation to immunize against a flu strain that infected soldiers at Fort Dix, N.J. That particular virus, however, turned out not to be a threat.
The search for the 1918 virus is of more than historical interest, said Dr. Jeffrey K. Taubenberger at the Armed Forces Institute of Pathology in Washington, the leader of the team whose report is being published today in the journal Science. Dr. Taubenberger and other researchers hope that understanding the genetic code of the Spanish flu virus might help scientists prepare for the next influenza pandemic, which many scientists think is coming soon.
The Spanish flu epidemic seems to have begun in the United States in late spring and early summer of 1918, when doctors reported scattered outbreaks in military installations where recruits were reporting for training before going to France.
By September, when schools opened, the epidemic was roaring through the entire population and spreading rapidly to every corner of the world, attacking the young and healthy and killing them, often within days.
The flu virus itself is gone, vanished with the epidemic. But scientists have repeatedly tried to find traces of it, studying autopsy specimens and even exhuming bodies buried in Alaska where, they hoped, the virus would have remained preserved.
Even now, an expedition is being proposed to Spitsbergen, a Norwegian archipelago in the Arctic Ocean about 400 miles north of Norway, to exhume the bodies of miners who died of the flu.
An epidemic like that of 1918 ”can come again, and it will,” said Dr. Robert Webster, chairman of viral and molecular biology at St. Jude’s Children’s Research Hospital in Memphis.
Dr. Joshua Lederberg, a geneticist and Nobel laureate who is president emeritus of Rockefeller University in New York, called influenza ”the most urgent, patently visible, acute threat in the world of emerging infections.” And, Dr. Lederberg added, ”the sooner we can learn what to anticipate, the more likely we will be able to blunt the next appearance” of a deadly flu virus.
Dr. Taubenberger studied specimens from Spanish flu victims that are among the millions of autopsy specimens that the pathology institute has been storing in warehouses since the Civil War. But he said he doubted that the study would succeed in light of the dismal history of failed efforts to find the virus.
For example, in the 1950’s, a group of scientists that included Dr. Maurice R. Hilleman, director of the Merck Institute in West Point, Pa., who was then directing viral research at the Walter Reed Army Institute in Washington, traveled to Nome, Alaska, in a secret mission to examine the exhumed bodies of Eskimos who had died of the 1918 flu.
When Eskimo flu victims died, Dr. Hilleman said, they were buried in the middle of winter, in the frozen ground. The Army thought that these bodies, buried in the permafrost, might have remained frozen and preserved. But, Dr. Hilleman said, ”the bodies were in such an advanced state of deterioration that no live virus was found.”
More recently several scientists, including Dr. Webster, examined autopsy tissue from the Armed Forces Institute of Pathology but were unable to find viruses.
Dr. Taubenberger decided to go ahead anyway. Looking in the computerized records, he requested autopsy slides of the lungs of 198 soldiers who died of the Spanish flu.
In examining the slides, he looked for a particular type of pathology. Since the flu virus stops replicating within a couple of days after a person is infected, Dr. Taubenberger and his team wanted lung tissue from someone who died quickly, within a week after becoming ill, so that there might still be virus particles present.
That was possible, Dr. Taubenberger said, because the 1918 influenza strain was so deadly.
”The lungs of some who died in a few days were completely filled with fluids, as if they had drowned,” he said. ”No one has ever seen that before or since. It was a unique pathology.”
Of the 198 cases that Dr. Taubenberger requested, 7 met his criteria. But only one had other features that led the researchers to believe that the flu virus was actively replicating when the man died.
The man was a private from New York State stationed at Fort Jackson, S.C., when he caught the flu.
”He was a healthy 21-year-old male with no medical history until he got this,” Dr. Taubenberger said.
The soldier died within five days of infection, on Sept. 26, 1918, and in October his lung tissue was shipped to Washington, where it was stored, undisturbed, for nearly 80 years.
With the soldier’s lung tissue in hand, the researchers began the tedious process of trying to extract the viral genetic material. The virus carries its genes in eight pieces of RNA that are packaged together in a protein coat. But over the years of storage, the 15,000 nucleotides that make up the viral RNA had broken apart into shards about 200 nucleotides long.
The researchers spent nearly two years amplifying the tiny segments of viral RNA so that they would have enough to analyze and assemble like a jigsaw puzzle. In their paper in Science, they report on the sequences of nine fragments of the virus that include pieces of its major genes.
The group has analyzed only about 7 percent of the virus, Dr. Taubenberger said, although he expects that he will eventually be able to complete the job. Others, like Dr. Webster, agree, but say it is still uncertain whether even that will reveal the secret of the virus’s lethality.
But with his preliminary analysis, Dr. Taubenberger and his colleagues have already ruled out two hypotheses on why the virus was so deadly.
One was based on an analysis of a chicken influenza virus that swept through flocks of chickens in the early 1980’s, killing them overnight.
The chicken virus was peculiar. One of its proteins had three basic amino acids at a spot where the host’s enzymes had to break that protein in order for the virus to infect a cell. Ordinarily, there was only one such amino acid at that spot. So, investigators thought, maybe the three basic amino acids were a clue to lethality, and maybe they were a feature of the Spanish flu virus.
But, Dr. Taubenberger found, that was not the case. There was nothing unusual about the amino acids at that position in the Spanish flu virus.
Another hypothesis was that the flu had gone directly from birds to humans. Ordinarily, human flu viruses spread only in humans, but genetically distinct flu viruses also fester, independently, in birds, which do not become ill when they are infected. Occasionally, viruses from birds infect animals like pigs, and then jump to people. Even worse, some researchers proposed, might be a virus that jumped directly from birds to humans.
Antibodies of survivors of the 1918 epidemic indicated that the virus had lived in pigs before infecting humans. But the antibody evidence was indirect, and some thought it might be incorrect. The genetic analysis, however, indicated that the virus had, indeed, come to humans from pigs.
”I can’t hold up one gene fragment and say, ‘This is the reason,’ ” Dr. Taubenberger said. ”This is the beginning of the story.”
But it raises additional questions, the most immediate of which is whether the planned expedition to Norway should go forward.
The trip was proposed by Dr. Kirsty Duncan, who studies medicine and geography at the University of Windsor in Ontario. Dr. Duncan learned that seven miners who were digging coal in Spitsbergen died of the flu in 1918 and were buried there. She and her colleagues have been working with Dr. Nancy Cox, the chief of the influenza branch at the Centers for Disease Control and Prevention in Atlanta, to plan the trip to Norway.
Dr. Duncan said the team would meet in Atlanta. ”We’ll be debating how to proceed,” she said.
Dr. Cox said the study of viral RNA from autopsy specimens might reveal all of the virus’s secrets.
The question, of course, is whether it is worthwhile to risk unleashing live viruses that might still be in the frozen tissue of the miners.
2. In the past, we have heard it alleged by credible sources that Germany was behind the 1918 flu epidemic that killed scores of millions worldwide.
From Germany Watch comes another post reinforcing this line of inquiry.
After maintaining that German agents were sabotaging livestock with anthrax, the post discusses British intelligence distillate indicating that, after discovering the particular strain of virulent flu, German agents began deliberately spreading it in the U.S.
NB: We don’t feel that the information from the book Three Wars with Germany confirms the hypothesis that the flu pandemic was a German bio-warfare weapon gone awry beyond the point of debate. It DOES, however, highlight that possibility.
“150 Million Deaths?”; Germany Watch; 9/5/2012.
Was Germany behind the 1918 Flu virus that killed 50–150 million people?
Admiral Hall, Chief of British Naval Intelligence during WW1, supplied information to an American legal claim against German sabotage within the USA.
The claim was originally meant for compensation for the Germans blowing up a chunk of Manhattan in the biggest terror attack in US history pre‑9/11.
But when Major Peaslee, heading the US investigation, read copies of the British intercepts of German traffic and ciphers, he discovered that the Germans were not just blowing up US munitions depots (before a declaration of war); they were using biological warfare on a large scale.
It is quiet public knowledge that Germany was using Anthrax and other biologicals on cattle, with 1000s of animals heading for the Allied war effort infected by German agents at various ports. But in 1916 the Germans had discovered a flu variant that killed by over-stimulation of the immune system, therefore perfectly targeting the healthiest of men; Soldiers.The links will show you that a German agent was in the US releasing their new Bio-weapon in January 1918. The same month the first recorded case of 1918 flu turned up in Maryland barracks.
Germany fought the legal case not in normal terms, but tried bribery, pressure, everything they could, to not be found guilty of the sabotage of the Manhattan munitions depot, despite the US only asking for $20m damages. They could have even settled outside of an offical ‘guilty’, but they didn’t.
WHY? Because they knew the evidence could point to them releasing the 1918 flu.
They underestimated the effectiveness of the weapon, as it of course eventually spread to Germans via the battlefield anyway.
But they did everything they could in desperation to conceal it during legal proceedings. The US eventually won damages for the sabotage after 15 years of litigation, by which point it was 1939. So there were then other immediate things to worry about, and this has largely been forgotten. The Criminals running Germany at this point, were so confident they were about to win the next war, that they undoubtedly thought they could bury the evidence of their WW1 crimes after taking out Britain and the US, as a bonus.
3a. We then tackle the subject of a cult/church that is at the epicenter of a Covid-19 outbreak in South Korea. The overlap between this organization and the Unification Church is discussed in a Food For Thought post. Might this cult have been a vector for introducing the virus into Wuhan?
. . . . Now, health officials are zeroing in on the church’s practices as they seek to contain South Korea’s alarming coronavirus outbreak, in which members of Shincheonji and their relatives account for more than two-thirds of the confirmed infections. On Friday, the number of cases in the country soared above 200 — second only to mainland China, if the outbreak on the Diamond Princess cruise ship is excluded from Japan’s count. . . .
. . . . As of Friday, more than 340 members of Shincheonji, which mainstream South Korean churches consider a cult, still could not be reached, according to health officials, who were frantically hoping to screen them for signs of infection. . . .
. . . . Jung Eun-kyeong, director of the Korea Centers for Disease Control and Prevention, said the authorities were investigating reports that Shincheonji had operations in Hubei, the Chinese province that includes Wuhan, where the virus emerged. The South Korean news agency Newsis reported on Friday that Shincheonji had opened a church in Wuhan last year, and that references to it had been removed from the church’s website. Church officials could not immediately be reached for comment. . . .
3b. The fascistic nature of the cult and some of the rituals and beliefs of the organization would render the group and/or some of its members as viable “useful idiots” for manipulation in connection with this outbreak.
“Shincheonji”; Truthbuildersonline.com
. . . . Lee Man-Hee has a very exalted view of himself. He teaches that just as the Old Testament pointed to Jesus and was full of prophecies about him, so the New Testament points to Lee and has many prophecies about him. For example, in John’s Gospel Christ repeatedly referred to the “Comforter” or “Counselor” who was to come. Lee states clearly that he is the “second advocate,” and the “spirit of truth.” For this reason only Lee has the right to speak on behalf of Jesus—for he is the “spirit of truth.” Essentially when Lee had his vision and answered God’s call to be the last days’ messenger, he fulfilled the prophecies of the Second Coming. Jesus has spiritually returned to earth through the words and ministry of Lee Man-Hee. Lee says he is the very embodiment of Jesus Christ, as well as the embodiment of the Holy Spirit also.
One of the most common designations for Lee as God’s messenger is “the promised pastor.” He is supposed to be the shepherd and leader of God’s people for these end times. The promised pastor is the leader of God’s church. The time will come when God and Christ will rule over the nations through the promised pastor. In addition to “promised pastor” another common title for Lee is “Teacher.” In Korean this is Seon Saeng Nim; so Lee is often called simply “SSN.”
As God’s anointed messenger, it is rumored that Lee is immortal, and cannot die. Lee is reluctant to declare this publicly. However, it is commonly accepted as true by his followers. . . .
. . . . Here is a summary of the doctrine taught by Lee and the SCJ:
- There is no Trinity. This is a false and devilish belief.
- Jesus is not God.
- The Holy Spirit is just one of many spirits in heaven. All angels are holy spirits.
- The SCJ is the only the true church. All other churches are corrupt and evil.
- Since they see everything as symbolic in Scripture, then they naturally see the new heaven and new earth as something spiritual. The church, SCJ, is the new heaven and new earth.
- Salvation does not consist in just believing in Jesus. Salvation is in following the promised pastor and in obedience to God’s commands. Lee says, “It is only when a person believes in the promised pastor and keeps the words of his testimony that he or she can attain salvation”
- Understanding the SCJ’s teaching on Revelation is especially necessary for salvation.
- Jesus’s world has ended. There is now a new heaven which is the SCJ. Lee calls for all people, all religions, to come to this new heaven. They must become part of the 12 Tribes (SCJ) in order to achieve salvation. They must learn the “new song,” which is SCJ doctrine. Those who refuse will be destroyed.
- Anyone who opposes SCJ is a Satan and the antichrist. Whoever listens to the teaching of ministers other than the promised pastor has received the mark of the Beast.
- Sometime in the future, before the Millennium, the souls of martyrs and other believers will come back to earth with Jesus. The souls of the dead believers will merge with living members of the SCJ and indwell them. They will be united together. This is what the Bible means by the first resurrection of Revelation 20:4–6.
- Throughout history God has sent different messengers for each age. Noah, Moses and Jesus were God’s messengers for their time. Lee (SSN) is the messenger for this new age. This is the plan that God has been working on for the 6000 years of human history.
- The 144,000 spoken of in Revelation 7 and 14 refer to the SCJ. It is believed that within the 144,000 there are 12 spiritual tribes. The completion of the 144,000 will result in the end of all things, and a new heaven and new earth.
- The 144,000 will rule over the earth. Earth’s inhabitants will have an opportunity to accept the heavenly state and become part of the kingdom. Anyone who rejects the heavenly state will be cast into hell.
- Individual churches are organized into 12 Tribes. Each tribe is named after an Apostle. So each member of the SCJ is identified as being a member of the one of the 12 Tribes.
It is a Cult!
- Even secular sources recognize the cultic nature of this group. They use typical cultic techniques of manipulation and mind control to enlist and maintain their members. Some of these controlling techniques include sleep deprivation, fatigue due to excessive meetings and events, intense indoctrination, and military style exercise programs. The church keeps close watch over its members, with little outside contact. There is controlled isolation from family, friends and anyone outside the group. When joining the SCJ, followers typically give all their money to the SCJ. They work for the cult for free. The cult is all consuming. If there ever is a time when they are allowed to meet with family, SCJ members are present.
- The church at large needs to be aware of the SCJ and wary of contact with them. They are extremely deceptive in their recruiting. They are infamous for inviting people to social events under one of their various front organizations. They also are known for encouraging people to a Bible study (often through the internet, e.g., by Skype), without any reference to the SCJ or Lee. People often are seduced by their aberrant doctrine before they even realize what group they have become involved with. As with other cults, knowledge and awareness of their teaching is a frontline defense against “seducing spirits and doctrines of demons”
4a. The next two points of discussion concern the fact that the current U.S. Ambassador to South Korea was the former head of the United States Pacific Command. We wonder if he might be ONI and/or CIA, and if he might have any connection to the anti-China blitzkrieg and the Covid-19 outbreak.
“The American Moustache Ruffling Feathers in South Korea” by Choe Sang-Hun; The New York Times; 1/16/2020.
. . . . In an interview with The Korea Times last month, Mr. Harris noted that throughout his career, his ethnic background had come into play only twice — by the Chinese and now by South Koreans. When he [retired Admiral Harry B. Harris, Jr.] was head of the United States Pacific Command, he was outspoken about China’s aggressive moves in the East and South China Seas, and China’s state-run news media often cited his ethnic background when attacking him. . . . .
4b. As the former Commander of the Guantanamo base in Cuba, he certainly did have operational links with the intelligence community.
Harry B. Harris, Jr.; Wikipedia.com
Director, Current Operations and Anti-Terrorism/Force Protection Division (OPNAV N31/34)[edit]
In August 2004, in his first Flag assignment, he reported to the staff of the Chief of Naval Operations, where he was responsible for Navy current operations, the Navy Command Center, and anti-terrorism/force protection policy.
Commander, Joint Task Force Guantanamo[edit]
In March 2006, he assumed command of Joint Task Force Guantanamo in Cuba. His service was notable as he was in charge when three prisoners, Mani Shaman Turki al-Habardi Al-Utaybi, Salah Ali Abdullah Ahmed al-Salami and Yasser Talal Al Zahrani, died in the custody of US forces. Defense reported the deaths as suicides. Harris said at the time,
I believe this was not an act of desperation, but an act of asymmetrical warfare waged against us.[20]
Harris ordered a full investigation by the Naval Criminal Investigative Service (NCIS), which published its report in a heavily redacted version in August 2008.
Main article: Guantanamo Bay homicide accusations
Main article: Guantanamo Bay detention camp suicide attempts
A report, Death in Camp Delta, was published in December 2009 by the Center for Policy & Research of Seton Hall University School of Law, under the supervision of its director, Professor Mark Denbeaux, attorney for two Guantanamo detainees, criticizing numerous inconsistencies in the official accounts of these deaths.[21][22][23] The report suggested there had either been gross negligence or an attempt to cover up homicides of the men, perhaps due to torture under interrogation.
On 18 January 2010, Scott Horton of Harper’s Magazine published a story suggesting that al-Salami, Al-Utaybi and Al-Zahrani had died as a result of accidental manslaughter during a torture session, and that the official account was a cover-up.[20] Horton had undertaken a joint investigation with NBC News, based on an account by four former guards at Guantanamo Bay detention camp. They suggested that the men had died at a black site, informally called “Camp No,” used for interrogation including torture. It was located about a mile outside the regular camp boundaries.[20]
5. We note the foreshadowing of the Covid-19 outbreak in an October, 2019 exercise–“Event 201” in New York City.
Dr. Mercola noted that:” . . . . As mentioned, a number of reports raise questions about the source of the 2019-nCoV [The Chinese coronavirus–D.E.]. For starters, a 2014 NPR article32 was rather prophetic. It discusses the October 2014 U.S. moratorium on experiments on coronaviruses like SARS and MERS, as well as influenza virus, that might make the viruses more pathogenic and/or easy to spread among humans. The ban came on the heels of ‘high-profile lab mishaps’ at the CDC and ‘extremely controversial flu experiments’ in which the bird flu virus was engineered to become more lethal and contagious between ferrets. The goal was to see if it could mutate and become more lethal and contagious between humans, causing future pandemics. . . . However, for the past decade there have been red flags raised in the scientific community about biosecurity breaches in high containment biological labs in the U.S. . . . The federal moratorium on lethal virus experiments in the U.S. was lifted at the end of December 2017,38 even though researchers announced in 2015 they had created a lab-created hybrid coronavirus similar to that of SARS that was capable of infecting both human airway cells and mice. . . .
” . . . . Equally curious is the fact that Johns Hopkins Center for Health Security, the World Economic Forum and the Bill and Melinda Gates Foundation sponsored a novel coronavirus pandemic preparedness exercise October 18, 2019, in New York called ‘Event 201.‘46 The simulation predicted a global death toll of 65 million people within a span of 18 months.47 As reported by Forbes December 12, 2019:48
‘The experts ran through a carefully designed, detailed simulation of a new (fictional) viral illness called CAPS or coronavirus acute pulmonary syndrome. This was modeled after previous epidemics like SARS and MERS.’
Sounds exactly like NCIP, doesn’t it? Yet the new coronavirus responsible for NCIP had not yet been identified at the time of the simulation, and the first case wasn’t reported until two months later.
Forbes also refers to the fictional pandemic as ‘Disease X’ — the same designation used by The Telegraph in its January 24, 2020, video report, “Could This Coronavirus be Disease X?“49 which suggests that media outlets were briefed and there was coordination ahead of time with regard to use of certain keywords and catchphrases in news reports and opinion articles.
Johns Hopkins University (JHU) is the biggest recipient of research grants from federal agencies, including the National Institutes of Health, National Science Foundation and Department of Defense and has received millions of dollars in research grants from the Gates Foundation.50 In 2016, Johns Hopkins spent more than $2 billion on research projects, leading all U.S. universities in research spending for the 38th year in a row.51
If research funded by federal agencies, such as the DOD or HHS is classified as being performed ‘in the interest of national security,’ it is exempt from Freedom of Information Act (FOIA) requests.52
Research conducted under the Biomedical Advanced Research and Development Authority (BARDA) is completely shielded from FOIA requests by the public.53 Additionally, agencies may deny FOIA requests and withhold information if government officials conclude that shielding it from public view ‘protects trade secrets and commercial or financial information which could harm the competitive posture or business interests of a company.’ . . . .”
“Novel Coronavirus–The Latest Pandemic Scare” by Dr. Joseph Mercola; Mercola; 2/4/2020.
. . . . Moratorium on SARS/MERS Experiments Lifted in 2017
As mentioned, a number of reports raise questions about the source of the 2019-nCoV [The Chinese coronavirus–D.E.]. For starters, a 2014 NPR article32 was rather prophetic. It discusses the October 2014 U.S. moratorium on experiments on coronaviruses like SARS and MERS, as well as influenza virus, that might make the viruses more pathogenic and/or easy to spread among humans.
The ban came on the heels of “high-profile lab mishaps” at the CDC and “extremely controversial flu experiments” in which the bird flu virus was engineered to become more lethal and contagious between ferrets. The goal was to see if it could mutate and become more lethal and contagious between humans, causing future pandemics.
However, for the past decade there have been red flags raised in the scientific community about biosecurity breaches in high containment biological labs in the U.S. and globally.33 There were legitimate fears that a lab-created superflu pathogen might escape the confines of biosecurity labs where researchers are conducting experiments. It’s a reasonable fear, certainly, considering that there have been many safety breaches at biolabs in the U.S. and other countries.34,35,36,37
The federal moratorium on lethal virus experiments in the U.S. was lifted at the end of December 2017,38 even though researchers announced in 2015 they had created a lab-created hybrid coronavirus similar to that of SARS that was capable of infecting both human airway cells and mice.
The NIH had allowed the controversial research to proceed because it had begun before the moratorium was put in place — a decision criticized by Simon Wain-Hobson, a virologist at Pasteur Institute in Paris, who pointed out that “If the [new] virus escaped, nobody could predict the trajectory.“39
Others, such as Richard Ebright, a molecular biologist and biodefence expert at Rutgers University, agreed, saying “The only impact of this work is the creation, in a lab, of a new, non-natural risk.“40
Wuhan is Home to Lab Studying World’s Latest PathogensIn January 2018, China’s first maximum security virology laboratory (biosecurity level 4) designed for the study of the world’s most dangerous pathogens opened its doors — in Wuhan.41,42 Is it pure coincidence that Wuhan City is now the epicenter of this novel coronavirus infection?
The year before, Tim Trevan, a Maryland biosafety consultant, expressed concern about viral threats potentially escaping the Wuhan National Biosafety Laboratory,43 which happens to be located just 20 miles from the Wuhan market identified as ground zero for the current NCIP outbreak.44 As reported by the Daily Mail:45
“The Wuhan lab is also equipped for animal research,” and “Regulations for animal research — especially that conducted on primates — are much looser in China than in the U.S. and other Western countries … But that was also cause for concern for Trevan.
Studying the behavior of a virus like 209-nCoV and developing treatments or vaccines for it requires infecting these research monkeys, an important step before human testing.
Monkeys are unpredictable though, warned [Rutgers University microbiologist Dr. Richard] Ebright. ‘They can run, they can scratch they can bite,’ he said, and the viruses they carry would go where their feet, nails and teeth do.’ ”
Coronavirus Outbreak Simulation Took Place in October 2019
Equally curious is the fact that Johns Hopkins Center for Health Security, the World Economic Forum and the Bill and Melinda Gates Foundation sponsored a novel coronavirus pandemic preparedness exercise October 18, 2019, in New York called “Event 201.“46 The simulation predicted a global death toll of 65 million people within a span of 18 months.47 As reported by Forbes December 12, 2019:48
“The experts ran through a carefully designed, detailed simulation of a new (fictional) viral illness called CAPS or coronavirus acute pulmonary syndrome. This was modeled after previous epidemics like SARS and MERS.”
Sounds exactly like NCIP, doesn’t it? Yet the new coronavirus responsible for NCIP had not yet been identified at the time of the simulation, and the first case wasn’t reported until two months later.
Forbes also refers to the fictional pandemic as “Disease X” — the same designation used by The Telegraph in its January 24, 2020, video report, “Could This Coronavirus be Disease X?“49 which suggests that media outlets were briefed and there was coordination ahead of time with regard to use of certain keywords and catchphrases in news reports and opinion articles.
Johns Hopkins University (JHU) is the biggest recipient of research grants from federal agencies, including the National Institutes of Health, National Science Foundation and Department of Defense and has received millions of dollars in research grants from the Gates Foundation.50 In 2016, Johns Hopkins spent more than $2 billion on research projects, leading all U.S. universities in research spending for the 38th year in a row.51
If research funded by federal agencies, such as the DOD or HHS is classified as being performed “in the interest of national security,” it is exempt from Freedom of Information Act (FOIA) requests.52
Research conducted under the Biomedical Advanced Research and Development Authority (BARDA) is completely shielded from FOIA requests by the public.53 Additionally, agencies may deny FOIA requests and withhold information if government officials conclude that shielding it from public view “protects trade secrets and commercial or financial information which could harm the competitive posture or business interests of a company.“54
The U.S. Centers for Disease Control and Prevention under the U.S. Department of Health and Human Services states that its mission is “to protect America from health, safety and security threats, both foreign and in the U.S.“55 Clearly, it will be difficult to obtain information about government-funded biomedical research on microbes like coronavirus conducted at major universities or by pharmaceutical corporations in biohazard labs.
How likely is it, then, that the coronavirus outbreak making people so sick today “suddenly” emerged simply because people ate bats and snakes in a Wuhan market? It looks more like a biosecurity accident but, until more is known, inevitably there will be more questions than answers about whether this latest global public health emergency is a more ambitious tactical “sand table exercise,” echoing unanswered questions about the 2009 swine flu pandemic fiasco.
This time, there could be a lot more bodies left on the field, although some statisticians conducting benefit cost analyses may consider 65 million casualties in a global human population of 7.8 billion people56 to be relatively small when advancing medical research conducted in the name of “the greater good.”
Hi Dave, can’t recall you mentioning this, but I came across an interesting link between Yoshiro Kawaoka of the University of Wisconsin, discussed above, and Antony Fauci. This NY Times article describes $605,206 as having been provided to Kawaoka by Fauci’s NIAID after gain of function research was restarted:
https://www.nytimes.com/2019/03/01/health/bird-flu-pandemic.html
Also wondering, have you ever considered publishing a book, or series of books, that could serve as a companion to the Spitfire List website? Just brainstorming here: a 100 page book, 10 chapters, 10 pages each. Each chapter presents a synopsis of i.e. the end of denazification, with citations to books and articles, as well as relevant broadcasts you have done.