>>18508167

>>18507981 (lb)

>>18508068 (lb)

>microscopic camels

Anybody want to dig on the AC? If trump was engineering 'microscopic camels', was he in fact engineering gain of function for MERS SARS? Someone was...

And in 2012 and 2016 he was not in gov't, so how did or would he have access to crispr and level 4 biolab facilities?

https://pubmed.ncbi.nlm.nih.gov/27255185/

Review Virol J

. 2016 Jun 3;13:87. doi: 10.1186/s12985-016-0544-0.

Middle East Respiratory Syndrome Coronavirus (MERS-CoV) origin and animal reservoir

Abstract

Middle East Respiratory Syndrome-Coronavirus (MERS-CoV) is a novel coronavirus discovered in 2012 and is responsible for acute respiratory syndrome in humans. Though not confirmed yet, multiple surveillance and phylogenetic studies suggest a bat origin. The disease isheavily endemic in dromedary camel populationsof East Africa and the Middle East. It is unclear as to when the virus was introduced to dromedary camels, but data from studies that investigated stored dromedary camel sera and geographical distribution of involved dromedary camel populations suggested that the virus was present in dromedary camels several decades ago. Though bats and alpacas can serve as potential reservoirs for MERS-CoV, dromedarycamels seem to be the only animal host responsible for the spill over human infections.

passing microscopic camels through the eye of a needle...

virus of bat origin.

https://www.islamweb.net/en/fatwa/185279/the-hadeeth-camels-were-created-from-devils

>>18508802

>was he in fact engineering gain of function for MERS SARS

Meant MERS-CoV

>>18508802

Ecohealth Alliance Conducted Risky Experiments on the MERS Virus in China Was Gain of Function

Documents released under FOIA by the NIH contradict the seriousness of research that EcoHealth Alliance was conducting about its experiments on bat coronaviruses in Wuhan. Instead, they were working on the gain of function research.

https://theintercept.com/2021/10/21/virus-mers-wuhan-experiments/

A summary of the group's work includes a description of the EcoHealth Alliance's experiment involving infectious clones of MERS-CoV. This virus caused a deadly Middle East respiratory syndrome outbreak in 2012. MERS has a case-fatality rate as high as 35 percent, much higher than Covid-19's.

EcoHealth Alliance's collaborator was the Wuhan Laboratory.

Here's what they did to this virus, which sounds much like what they did to COVID-19 by constructing a "full-length infectious clone."

According to the report, the scientists swapped out the virus's receptor-binding domain, or RBD, a part of the spike protein that enables it to enter a host's cells. "We constructed the full-length infectious clone of MERS-CoV and replaced the RBD of MERS-CoV with the RBDs of various strains of HKU4-related coronaviruses previously identified in bats from different provinces in southern China," the scientists wrote.

"Changing the receptor binding site on MERS is sort of crazy," wrote Jack Nunberg, a virologist, and director of the Montana Biotechnology Center at the University of Montana, in an email to The Intercept after reviewing the documents. "Although these new chimeric viruses may retain properties of the MERS-CoV genetic backbone, engineering a known human pathogen raises new and unpredictable risks beyond those posed by their previously reported studies using a non-pathogenic bat virus backbone." The researchers' intent, which some scientists consider integral to defining gain-of-function, remains unclear

Sound familiar…?

This research was in China, and the Wuhan Laboratory was the primary collaborator.

This was hazardous research, definitely Gain of Function research.

This is the Brave New World we live in.

https://www.reddit.com/r/conspiracy/comments/11kkq7w/ecohealth_alliance_conducted_risky_experiments_on/

>>18508917

https://www.science.org/content/article/was-nih-funded-work-mers-virus-china-too-risky-science-examines-controversy

Was NIH-funded work on MERS virus in China too risky? Science examines the controversy

Questions related to the frustrating search for the origin of the COVID-19 pandemic keep creating commotion. Last week, the U.S. National Institutes of Health (NIH) placed one of its grantees, and itself, in the hot seat when it told Congress in a letter that the EcoHealth Alliance in New York City had failed to promptly report potentially worrisome results from a virology experiment done by a collaborator in China. In a progress report for one of its grants, EcoHealth had mentioned an altered bat coronavirus made mice sicker than expected, a discovery it should have notified the agency of immediately, NIH asserted in a letter to Congress.

EcoHealth, which has directed some of its NIH money to researchers at the Wuhan Institute of Virology (WIV), was already under attack. Some scientists, politicians, and journalists espouse the idea that the ongoing pandemic was likely sparked by a virus that escaped from WIV.

There is no concrete evidence for that. But to detractors of NIH and EcoHealth, the letter and the progress report show NIH supported what’s often called gain-of-function (GOF) virus research in China, the type of studies that can make pathogens more dangerous to humans and that some think may have spawned SARS-CoV-2. (“In Major Shift, NIH Admits Funding Risky Virus Research in Wuhan,” Vanity Fair declared, for example.)

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NIH has consistently denied that it has funded risky GOF research in China, and still does. EcoHealth’s work didn’t meet the bar, the agency says, because the more pathogenic bat coronavirus was created from one not known to infect humans. Still, NIH demanded that EcoHealth provide by this week any unpublished data beyond its last progress report, which covered year five of the grant.

Peter Daszak, EcoHealth’s founder and president, tells ScienceInsider the group has submitted a response and defends its efforts as transparent and legitimate. Echoing what an EcoHealth spokesperson said last week, Daszak also challenges NIH’s claim that EcoHealth has violated any grant conditions with the mouse results, saying it notified them of the data and NIH failed to request follow-up action. “This is spelled out in detail in a letter we sent to NIH yesterday, with detailed documentary evidence, strongly refuting that we were out of compliance with our reporting requirements,” he wrote to ScienceInsider today.

But to some scientists, another part of EcoHealth’s year five grant progress report was also troubling: results from studies that manipulated a different coronavirus, the one that causes Middle East respiratory syndrome (MERS). That virus, MERS-CoV, which originated in bats before spreading to camels and then people, is lethal in roughly 35% of diagnosed human cases.

Concerns about risky studies with MERS-CoV, SARS-CoV—the virus that caused the 2003 severe acute respiratory syndrome (SARS) outbreak—and H5N1 avian influenza led to a 2017 U.S. policy requiring a special review to weigh potential benefits and risks for certain work with specific pathogens. Some virologists and biosecurity experts say EcoHealth’s studies with MERS-CoV should have warranted that type of review, and expressed dismay that EcoHealth backed such work in China.

But NIH says EcoHealth’s MERS-CoV experiments didn’t fit the Department of Health and Human Services’s (HHS’s) definition of research requiring special review because “the research was not reasonably anticipated to result in an ePPP,” or an enhanced pathogen of pandemic potential. (NIH has recently asked media to avoid the term “gain of function,” saying it is confusing for the public—it even scrubbed the term from a web page URL and header in favor of ePPP last week, a move that was quickly spotted.)

The letter has reignited the debate about the benefits and risks of engineering pathogens that could spark a pandemic. A recent draft directive from a Senate appropriations committee may force NIH and the virology community to revisit that contentious topic in depth.

Here’s a closer look at the issues, including Daszak’s defense of EcoHealth’s work with MERS-CoV.

What experiments were done with the MERS virus and why?

p1

>>18508933

EcoHealth and WIV researchers had collected novel bat viruses dubbed HKU4 in several provinces in southern China, found they were closely related to the MERS virus, and wanted to study their ability to transmit and cause disease in other species, to see whether they posed a pandemic risk. Some of their work focused on the spike surface protein that coronaviruses use to infect cells, specifically a portion called the receptor-binding domain (RBD).

Researchers frequently can genetically sequence coronaviruses found when sampling bats in the wild, but they rarely can grow those viruses in culture. So they create chimeric viruses with ones that do grow in culture, which in this case was MERS-CoV.

Specifically, the scientists isolated the genetic code for the RBD from various HKU4 strains and swapped it into the genetic “backbone” of the MERS virus, a June 2018–May 2019 progress report states. The researchers showed these chimeric viruses could infect human tissues, and that they replicated well in cells that had a receptor named DPP4 that MERS-CoV uses to enter human cells. “The results suggest potential risk of the bat HKU4r-CoVs for cross-species infection in humans,” the report concludes.

Are such studies justified and necessary?

That’s where scientists disagree. To put RBDs from some of the novel HKU4 viruses into MERS-CoV, already a lethal human pathogen, is “sort of crazy” and “unjustified,” says University of Montana, Missoula, virologist Jack Nunberg.

Tulane University virologist Robert Garry has a more charitable take. “They are trying to determine if the HKU4 viruses have pathogenic potential,” or whether these viruses could jump to humans if they acquire certain mutations, he says. “That’s legitimate.” Another lab that has collaborated with WIV, Ralph Baric’s group at the University of North Carolina, Chapel Hill, has done similar, albeit controversial chimeric virus studies with SARS-CoV, the virus that caused the global SARS outbreak of 2003. “I don’t think [this Wuhan work] is that different,” says virologist Stephen Goldstein, a postdoc at the University of Utah.

Another reason to modify MERS-CoV and SARS-CoV is to be able to infect mice with these viruses, which makes other types of studies possible, Goldstein notes. For example, Baric has developed a mouse model to test drugs and vaccines against viruses related to MERS-CoV.

Yet the EcoHealth studies may not have been necessary because Baric’s lab had already done studies with HKU4 “pseudoviruses,” which are designed to bind and enter cells but can’t replicate, Garry says. Virologist Stanley Perlman of the University of Iowa says he’s not convinced the chimeric viruses tell scientists anything more about pathogenicity than pseudoviruses. “I think that this is not the best way to answer the question,” Perlman says.

But Daszak argues that the chimeric viruses added crucial information beyond infectivity. “Pseudoviruses will demonstrate capacity to bind cells, recombinant viruses allow measures of things like viral genome copy per gram–clues as to the potential importance of these viruses for public health,” he wrote in an email to ScienceInsider.

The MERS-CoV studies are modifying a dangerous human virus. So why didn’t the work qualify as ePPP (or GOF, the term NIH now wants to abandon), which would have triggered an extra layer of review?

p2

>>18508935

NIH says the work did not qualify as ePPP because the researchers did not anticipate that the modified MERS viruses would be more infectious to people than the original virus. (Here’s an EcoHealth letter from 2016 where it and NIH are discussing the MERS work.) Virologist Michael Imperiale of the University of Michigan, Ann Arbor, says that makes sense. “MERS-CoV already infects humans,” he says; if the same virus but with a bit of bat virus RNA stitched in does the same, that isn’t GOF research, Imperiale says.

Garry does not see a problem either. “The odds of combining any random bat virus with MERS-CoV and getting a more pathogenic virus than MERS-CoV is vanishingly small,” he says. And it did not happen: In the EcoHealth-backed cell experiments, one chimeric virus replicated equally as well as MERS-CoV in cells expressing DPP4, and three others did not grow as well.

Why did EcoHealth deny it was doing MERS-CoV studies?

EcoHealth did not keep the MERS-CoV studies secret from NIH. It included the MERS-CoV plans in its 2014 grant proposal that NIH approved, and also noted the intended studies in its fourth year progress report. Yet The Intercept, which recently obtained these documents with a public records lawsuit, reported that in September, EcoHealth spokesperson Robert Kessler had said the group did not conduct the MERS-CoV studies described in the grant proposal.

Daszak calls that a straightforward “mistake,” adding: “The actual permission for us to do this work was requested in a letter to NIH at the end of year 3 of the grant. NIH allowed the work to move forwards. Robert Kessler didn’t have access to that letter at the time – he’s a spokesperson, not a scientist.”

Daszak also told ScienceInsider the MERS-CoV chimeric studies were conducted in WIV’s biosafety level-3 labs, the same level of biosafety required in the United States for such research.

What will happen next?

Daszak told ScienceInsider that EcoHealth submitted a response on 26 October. The last progress report, dated in August but covering work in 2018–19, noted plans to test MERS-CoV chimeric viruses in live mice, so there may be some data on that in EcoHealth’s response.

The debate over the MERS virus experiments may give more impetus to revisiting the HHS policy on potentially risky pathogen research. A Senate report accompanying a bill funding NIH’s 2022 budget calls for such a review by the National Science Advisory Board for Biosecurity (NSABB), a panel of outside advisers that helped develop the current policy. NSABB last met in late January 2020 to discuss whether federal decisions about ePPP research should be more transparent—just as COVID-19 had begun its global spread.

The Senate demand will have to survive the budget reconciliation process, which may not be done until the end of the year. NIH Director Francis Collins and Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, told The Wall Street Journal in September they’re open to reviewing the policies.

With reporting by Jon Cohen.

Update, 29 October, 2:15 p.m.: This story has been updated with a PDF of EcoHealth’s 26 October response to NIH and another document it sent. The Wall Street Journal was the first to make the letter public, on 28 October, although Science independently obtained it and EcoHealth’s other submissions to NIH on the same day.

3 of 3

>>18508802

>>18508917

MERS-Cov genetic sequence is patented

byFOUCHIER

https://en.wikipedia.org/wiki/MERS-related_coronavirus

Research and patent[edit]

Saudi officials had not given permission for Dr. Zaki, the first isolator of the human strain, to send a sample of the virus to Fouchier and were angered when Fouchier claimed the patent on the full genetic sequence of MERS-CoV.[54]

The editor of The Economist observed, "Concern over security must not slow urgent work. Studying a deadly virus is risky. Not studying it is riskier."[54] Dr. Zaki was fired from his job at the hospital as a result of bypassing the Saudi Ministry of Health in his announcement and sharing his sample and findings.[55][56][57][58]

At their annual meeting of the World Health Assembly in May 2013, WHO chief Margaret Chan declared that intellectual property, or patents on strains of new virus, should not impede nations from protecting their citizens by limiting scientific investigations. Deputy Health Minister Ziad Memish raised concerns that scientists who held the patent for MERS-CoV would not allow other scientists to use patented material and were therefore delaying the development of diagnostic tests.[59] Erasmus MC responded that the patent application did not restrict public health research into MERS and MERS-CoV,[60] and that the virus and diagnostic tests were shipped—free of charge—to all that requested such reagents.

Fouchier study reveals changes enabling airborne spread of H5N1

Robert Roos June 21, 2012

Jun 21, 2012 (CIDRAP News) – A study showing that it takes as few as five mutations to turn the H5N1 avian influenza virus into an airborne spreader in mammals—and that launched a historic debate on scientific accountability and transparency—was released today in Science, spilling the full experimental details that many experts had sought to suppress out of concern that publishing them could lead to the unleashing of a dangerous virus.

In the lengthy report, Ron Fouchier, PhD, of Erasmus Medical Center in the Netherlands and colleagues describe how they used a combination of genetic engineering and serial infection of ferrets to create a mutant H5N1 virus that can spread among ferrets without direct contact.

They say their findings show that H5N1 viruses have the potential to evolve in mammals to gain airborne transmissibility, without having to mix with other flu viruses in intermediate hosts such as pigs, and thus pose a risk of launching a pandemic.

The Fouchier study is paired with another in which an international team used mathematical modeling to reach the conclusion that, given how few mutations it took to yield an airborne transmissible virus, such a virus probably could evolve in nature, though it's not possible to quantify the risk. They noted that two of the five mutations in the airborne virus already are common in natural H5N1viruses.

"We now know that we're living on a fault line," said Derek J. Smith, PhD, of the University of Cambridge, senior author of the modeling study, at a Science press conference yesterday. "It could do something. What we need to know is how likely is that."

Second of two controversial studies

Fouchier's study is one of two H5N1 transmissibility experiments that sparked a fierce controversy beginning late last fall, and is the second to see print. The first study, led by Yoshihiro Kawaoka, DVM, PhD, of the University of Wisconsin and the University of Tokyo, was published in Nature in early May.

Kawaoka's team used a somewhat different approach to achieve the same goal as Fouchier. Kawaoka and colleagues introduced mutations in the hemagglutinin (HA) gene from an H5N1 virus and then combined it with seven genes from a 2009 H1N1 virus, creating a hybrid virus that was able to spread by air between ferrets. They said the study demonstrated that a flu virus with H5 HA can spread among mammals—something that natural H5N1 viruses have done extremely rarely, if at all.

When word of the Fouchier and Kawaoka studies got out last fall, it sparked concern about the potential for creation and intentional or unintentional release of a pandemic virus. This led to a review by the US National Science Advisory Board for Biosecurity (NSABB), which advises the Department of Health and Human Services.

After long deliberations, the board recommended in December that both studies be stripped of key details before publication, but that the details be shared with selected scientists and officials on a need-to-know basis.

But after the authors—especially Fouchier—provided some additional information and clarifications, the board recommended on Mar 30 that the full versions of both studies be published, and federal health officials endorsed the recommendation. The NSABB voted unanimously in favor of publication for Kawaoka's paper, but it split 12-6 on Fouchier's.

The heated controversy over publication of the studies prompted a group of 39 leading flu researchers, including Fouchier and Kawaoka, to impose a voluntary moratorium on research designed to increase the transmissibility of H5N1 viruses in mammals. The moratorium remains in effect, awaiting the further development of government policies on biosafety and biosecurity for such research (see related CIDRAP News story).

The controversy also prompted the US government in March to outline a new general policy on the handling of "dual use research of concern," or DURC, meaning research that could be used for either good or ill. US officials said this week that further details on that policy will be released soon in the form of draft guidance for institutional biosafety committees.

p1

>>18508971

In a question-and-answer sheet released with Fouchier's study, Erasmus officials said the paper was revised to better explain the research goals and the benefits to public health, and "display items" were added to explain the virulence and transmission properties of the airborne virus, but the methods and results were not changed. Also, the manuscript was revised to improve clarity, since it was expected to draw a broader readership than such reports usually do.

As for safety, the experiments were conducted in an Animal Biosafety Level 3 (ABSL3+) lab at Erasmus, the report says. Inspectors from the Dutch government and the US Centers for Disease Control and Prevention approved the facilities and procedures before and during the research. Researchers wore protective equipment and were offered seasonal and H5N1 flu vaccines.

Indonesian H5N1 strain used

Fouchier's team started with an H5N1 virus collected in Indonesia and used reverse genetics to introduce mutations that have been shown in previous research to make H5N1 viruses more human-like in how they bind to airway cells or in other ways. Avian flu viruses prefer to bind to alpha2,3-linked sialic acid receptors on cells, whereas human flu viruses prefer alpha2,6-linked receptors. In both humans and ferrets, alpha2,6 receptors are predominant in the upper respiratory tract, while alpha 2,6 receptors are found mainly in the lower respiratory tract.

The amino acid changes the team chose included N182K, Q222L, and G224S, the numbers referring to positions in the virus's HA protein, the viral surface molecule that attaches to host cells. Q222L and G224S together change the binding preference of H2 and H3 subtype flu viruses, changes that contributed to the 1957 and 1968 flu pandemics, according to the report. And N182K was found in a human H5N1 case.

The scientists created three mutant H5N1 virus strains to launch their experiment: one containing N182K, one with Q222L and G2242, and one with all three changes, the report explains. They then launched their lengthy series of ferret experiments by inoculating groups of six ferrets with one of these three mutants or the wild-type H5N1 virus. Analysis of samples during the 7-day experiment showed that ferrets infected with the wild-type virus shed far more virus than those infected with the mutants.

In a second step, the team used a mutation in a different viral gene, PB2, the polymerase complex protein. The mutation E627K in PB2 is linked to the acquisition by avian flu viruses of the ability to grow in the human respiratory tract, which is cooler than the intestinal tract of birds, where the viruses usually reside, according to the report.

The researchers found that this mutation, when added to two of the HA mutations (Q224L and G224S), did not produce a virus that grew more vigorously in ferrets, and the virus did not spread through the air from infected ferrets to uninfected ones.

The passaging step

Seeing that the this mutant failed to achieve airborne transmission, the researchers decided to "passage" this strain through a series of ferrets in an effort to force it to adapt to the mammalian respiratory tract—the move that Fouchier called "really, really stupid," according to a report of his initial description of the research at a European meeting last September.

They inoculated one ferret with the three-mutation strain and another with the wild-type virus and took daily samples until they euthanized the animals on day 4 and took tissue samples (nasal turbinates and lungs). Material from the tissue samples was then used to inoculate another pair of ferrets, and this step was carried out six times. For the last four passages, the scientists used nasal-wash samples instead of tissue samples, in an effort to harvest viruses that were secreted from the upper respiratory tract.

p2

>>18508975

The amount of mutant virus found in the nasal turbinate and nose swab samples increased with the number of passages, signaling that the virus was increasing its capacity to grow in the ferret upper airway. In contrast, viral titers in the samples from ferrets infected with the wild-type virus stayed the same.

The next step was to test whether the viruses produced through passaging could achieve airborne transmission. Four ferrets were inoculated with samples of the "passage-10" mutant virus, and two ferrets were inoculated with the passage-10 wild strain. Uninfected ferrets were placed in cages next to the infected ones but not close enough for direct contact.

The ferrets exposed to those with the wild virus remained uninfected, but three of the four ferrets placed near those harboring the mutant virus did get infected, the researchers found. Further, they took a sample from one of the "recipient" ferrets and used it to inoculate another ferret, which then transmitted the virus to two more ferrets that were placed near it.

Thus, a total of six ferrets became infected with the mutant virus via airborne transmission. However, the level of viral shedding indicated the airborne virus didn't transmit as efficiently as the 2009 H1N1 virus does.

In the course of the airborne transmission experiments, the ferrets showed signs of illness, including lethargy, loss of appetite, and ruffled fur. One of the directly inoculated ferrets died, but all those infected via airborne viruses survived.

When the scientists sequenced the genomes of the viruses that spread through the air, they found only two amino acid switches, both in HA, that occurred in all six viruses: H103Y and T156A. They noted several other mutations, but none that occurred in all six airborne viruses.

"Together, these results suggest that as few as five amino acid substitutions (four in HA and one in PB2) may be sufficient to confer airborne transmission of [highly pathogenic avian flu] H5N1 virus," the researchers wrote.

In further steps, the researchers inoculated six ferrets with high doses of the airborne-transmissible virus; after 3 days, the ferrets were either dead or "moribund." "Intratracheal inoculations at such high doses do not represent the natural route of infection and are generally used only to test the ability of viruses to cause pneumonia," the report notes.

Mutant virus sensitive to antiviral

The team also determined that the airborne-transmissible virus was sensitive to the antiviral drug oseltamivir (Tamiflu), just as natural H5N1 viruses usually are.

In addition, they assessed whether an existing H5N1 vaccine would be likely to offer any protection against the virus. They generated a hybrid virus consisting of the mutant HA and PB2 genes combined with six genes from a mouse-adapted virus called PR8. This hybrid reacted well with antibodies generated by several existing H5N1 vaccines, suggesting that the vaccines could provide some protection.

p3

>>18508978

Finally, the team tested whether antibodies in elderly people (over 70) could recognize the PR8/H5 hybrid virus. The answer was no, suggesting they would have little immunity to it or to the airborne-transmissible mutant.

The scientists note that substitutions Q222L and G224S, which are linked to changes in binding preference, have been found in avian H2 and H3 viruses in nature, though not in H5N1 viruses.

The other three mutations that were found consistently in the airborne-transmissible mutant have all been found in natural H5N1 viruses, which suggests that they don't impair viral "fitness." H103Y has been identified only once, but E627K in PB2 has been found in about 27% of avian H5N1 sequences and about 29% of human H5N1 sequences, the report says. Also, Q222L is one of the four key mutations identified in the Kawaoka study.

"Given the large numbers of HPAI A/H5N1 virus-infected hosts globally, the high viral mutation rate, and the apparent lack of detrimental effects on fitness of the mutations that confer airborne transmission, it may simply be a matter of chance and time before a human-to-human transmissible A/H5N1 virus emerges," the scientists state.

Modeling study suggests possible threat

In the accompanying modeling study, Cambridge researchers sought to estimate the risk that an airborne-transmissible virus like Fouchier's could evolve naturally. Analyzing surveillance data for the past 15 years, they noted that two of the mutations involved (T156A and E627K) are common in natural H5N1 isolates, and a number of isolates had both changes.

The researchers developed a mathematical model of how viruses replicate and evolve in a mammal and assessed the chances that the three additional needed mutations could evolve in a single host or a short chain of transmission. Among the factors they included were random mutation, prolonged infections, transmission, immune response, and deleterious mutations.

"With the information we have, it is impossible to say what the exact risk is of the virus becoming airborne transmissible among humans," senior author Smith said in a Cambridge press release. "However, the results suggest that the remaining three mutations could evolve in a single human host, making a virus evolving in nature a potentially serious threat."

The authors recommend several strategies for further research, starting with increased surveillance in regions where airborne-transmission-enabling mutations have been identified.

Debate continues

Early indications are that the release of Fouchier's study will not end the controversy over its publication and the broader problem of dealing with dual-use research.

At yesterday's press conference, Anthony Fauci, MD, director of the US National institute of Allergy and Infectious Diseases, defended publishing the full details. "I think the benefits that will come out of the Fouchier paper in stimulating thought and pursuing ways to understand better the transmissibility, adaptation, pathogenicity [of H5N1] in my mind far outweigh the risk of nefarious use of this information," he said in response to questions.

p4

>>18508979

"When you get something out in the general literature, you stimulate thought and input from people who at first glance you wouldn't think would have an interest in it," he added. He said publication can trigger involvement by people in a wide range of disciplines, which can pay benefits.

Some biosecurity experts, though, voiced misgivings today.

Eric S. Toner, MD, senior associate in the Center for Biosecurity at the University of Pittsburgh Medical Center, commented by e-mail, "I think that the publication does increase the probability that others will want to replicate the experiments and pursue this line of research further. The more labs that are doing this research, the more likely an accidental escape becomes.

"Clearly if all the lab workers were effectively vaccinated against the virus, the risk of accidental escape would decrease. The paper says the lab workers were offered H5N1 vaccination. It would be nice to know if it was required and that the workers had good antibody titers as well as that the specific H5N1 vaccine had demonstrated efficacy against the research strain."

Toner also said the findings strongly support the concern that a naturally occurring H5N1 pandemic is possible. But he called the findings "only modestly useful" for flu surveillance.

"Many of the mutations they reported were previously known to be ones of concern," he said. "For the other mutations that had not previously been suspected to be associated with mammalian transmission, the paper suggest that it may not be individual mutations that are important but rather various combinations of mutations that produce a similar result. Knowing the significance of all the possible combinations of a nearly infinite number of possible mutations is beyond our current capabilities."

He added that the study underlines "the pressing need for a much more robust global surveillance effort, including much more sequencing and much more timely reporting of sequencing data. It also underscores the need to have a global action plan based on the surveillance. In other words, what do we do that we are not doing now if we find increasing evidence of worrisome mutations?"

An NSABB member who opposed publishing the full version of Fouchier's paper maintained that position today and expressed concern about the bosafety risks if other labs around the world use the findings to launch similar studies.

Michael T. Osterholm, PhD, MPH, director of the University of Minnesota's Center for Infectious Disease Research and Policy, publisher of CIDRAP News, said he supports the type of research done by Fouchier and Kawaoka and thinks it should continue, but not in labs all over the world.

He said the Fouchier and Kawaoka studies mark the first time humans have ever broken the barrier between nontransmissibility and transmissibility of a pathogen in animals. The heart of the issue is transmissibility, not the virulence of the lab-derived viruses, he asserted.

What a ferret-transmissible H5N1 virus would do in humans is unknown, he commented. "But if it started to circulate, such as in swine, all bets are off. Once you break that transmissibility barrier, this virus is open for serious mischief."

The details of Fouchier's study "should've been disseminated on a need-to-know basis," Osterholm said. "I think we punted on this, we didn't exhaust every possibility for disseminating it." He was referring to the conclusion of most officials and scientists involved that it was not possible to quickly devise a way to share the details only with a select group.

"We're making it much easier for everyone to do this," he said. "What if some vaccine manufacturing company in a developing country decides they want to work with this and it gets out?"

He commented that the release of a dangerous flu virus through a lab accident has already happened once, with the re-emergence of the H1N1 virus in 1977: "That was a clear case of a virus that leaked out of work that the Russians were doing."

Osterholm also warned that the issues raised by the Fouchier paper won't go away, saying research papers now in the pipeline will raise even greater concerns about possible misuse and biosafety.

"I think the federal government and the NSABB are very poorly position to deal with the future manuscripts that are already in the pipeline," he said.

Another NSABB member, David A. Relman, MD, of Stanford University, expressed the view that the Fouchier study shouldn't have been done in the first place, let alone published.

p5

>>18508984

"When you get something out in the general literature, you stimulate thought and input from people who at first glance you wouldn't think would have an interest in it," he added. He said publication can trigger involvement by people in a wide range of disciplines, which can pay benefits.

Some biosecurity experts, though, voiced misgivings today.

Eric S. Toner, MD, senior associate in the Center for Biosecurity at the University of Pittsburgh Medical Center, commented by e-mail, "I think that the publication does increase the probability that others will want to replicate the experiments and pursue this line of research further. The more labs that are doing this research, the more likely an accidental escape becomes.

"Clearly if all the lab workers were effectively vaccinated against the virus, the risk of accidental escape would decrease. The paper says the lab workers were offered H5N1 vaccination. It would be nice to know if it was required and that the workers had good antibody titers as well as that the specific H5N1 vaccine had demonstrated efficacy against the research strain."

Toner also said the findings strongly support the concern that a naturally occurring H5N1 pandemic is possible. But he called the findings "only modestly useful" for flu surveillance.

"Many of the mutations they reported were previously known to be ones of concern," he said. "For the other mutations that had not previously been suspected to be associated with mammalian transmission, the paper suggest that it may not be individual mutations that are important but rather various combinations of mutations that produce a similar result. Knowing the significance of all the possible combinations of a nearly infinite number of possible mutations is beyond our current capabilities."

He added that the study underlines "the pressing need for a much more robust global surveillance effort, including much more sequencing and much more timely reporting of sequencing data. It also underscores the need to have a global action plan based on the surveillance. In other words, what do we do that we are not doing now if we find increasing evidence of worrisome mutations?"

An NSABB member who opposed publishing the full version of Fouchier's paper maintained that position today and expressed concern about the bosafety risks if other labs around the world use the findings to launch similar studies.

Michael T. Osterholm, PhD, MPH, director of the University of Minnesota's Center for Infectious Disease Research and Policy, publisher of CIDRAP News, said he supports the type of research done by Fouchier and Kawaoka and thinks it should continue, but not in labs all over the world.

He said the Fouchier and Kawaoka studies mark the first time humans have ever broken the barrier between nontransmissibility and transmissibility of a pathogen in animals. The heart of the issue is transmissibility, not the virulence of the lab-derived viruses, he asserted.

What a ferret-transmissible H5N1 virus would do in humans is unknown, he commented. "But if it started to circulate, such as in swine, all bets are off. Once you break that transmissibility barrier, this virus is open for serious mischief."

The details of Fouchier's study "should've been disseminated on a need-to-know basis," Osterholm said. "I think we punted on this, we didn't exhaust every possibility for disseminating it." He was referring to the conclusion of most officials and scientists involved that it was not possible to quickly devise a way to share the details only with a select group.

"We're making it much easier for everyone to do this," he said. "What if some vaccine manufacturing company in a developing country decides they want to work with this and it gets out?"

He commented that the release of a dangerous flu virus through a lab accident has already happened once, with the re-emergence of the H1N1 virus in 1977: "That was a clear case of a virus that leaked out of work that the Russians were doing."

Osterholm also warned that the issues raised by the Fouchier paper won't go away, saying research papers now in the pipeline will raise even greater concerns about possible misuse and biosafety.

"I think the federal government and the NSABB are very poorly position to deal with the future manuscripts that are already in the pipeline," he said.

Another NSABB member, David A. Relman, MD, of Stanford University, expressed the view that the Fouchier study shouldn't have been done in the first place, let alone published.

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Fouchier

https://www.newyorker.com/magazine/2012/03/12/the-deadliest-virus

The Deadliest Virus

Did a scientist put millions of lives at risk—and was he right to do it?

(2012)

On May 21, 1997, a three-year-old boy died in Hong Kong from a viral infection that turned out to be influenza. The death was not unusual: flu viruses kill hundreds of thousands of people every year. Hong Kong is among the world’s most densely populated cities, and pandemics have a long history of first appearing there or in nearby regions of southern China, and then spreading rapidly around the globe.

This strain, however, was unusual, and it took an international team of virologists three months to identify it as H5N1—“bird flu,” as it has come to be called. Avian influenza had been responsible for the deaths of hundreds of millions of chickens, but there had never been a report of an infected person, even among poultry workers.

By the end of the year, eighteen people in Hong Kong had become sick, and six had died. That’s a remarkably high mortality rate: if seasonal flu were as virulent, it would kill twenty million Americans a year. Hong Kong health officials, fearing that the virus was on the verge of becoming extremely contagious, acted forcefully to build a moat around the outbreak: during the last week of December, they destroyed every chicken in the city.

The tactic worked. Bird flu disappeared, at least for a while. “We felt we had dodged a bullet,” Keiji Fukuda told me earlier this year, when I visited him in his office at the World Health Organization’s headquarters, in Geneva. Fukuda, as the assistant director-general for health, security, and environment, oversees influenza planning. At the end of 1997, when he was the chief influenza epidemiologist at the Centers for Disease Control and Prevention, in Atlanta, he spent a few tense weeks in Hong Kong, searching for clues to how the virus was transmitted from chickens to humans and whether it would set off a global pandemic. “It was a very scary time,” he said, “and we were bracing ourselves for the worst. But by the end of the month nobody else got sick, so we crossed our fingers and went back to Atlanta.”

Then, in 2003, the virus reëmerged, in Thailand; it has since killed three hundred and forty-six of the five hundred and eighty-seven people it is known to have infected—nearly sixty per cent. The true percentage is undoubtedly lower, since many cases go unreported. Even so, the Spanish-flu epidemic of 1918, which killed at least fifty million people, had a mortality rate of between two and three per cent. Influenza normally kills far fewer than one-tenth of one per cent of those infected. This makes H5N1 one of the deadliest microbes known to medical science.

To ignite a pandemic, even the most lethal virus would need to meet three conditions: it would have to be one that humans hadn’t confronted before, so that they lacked antibodies; it would have to kill them; and it would have to spread easily—through a cough, for instance, or a handshake. Bird flu meets the first two criteria but not the third. Virologists regard cyclical pandemics as inevitable; as with earthquakes, though, it is impossible to predict when they will occur. Flu viruses mutate rapidly, but over time they tend to weaken, and researchers hoped that this would be the case with H5N1. Nonetheless, for the past decade the threat of an airborne bird flu lingered ominously in the dark imaginings of scientists around the world. Then, last September, the threat became real.

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>>18509007

At the annual meeting of the European Scientific Working Group on Influenza, in Malta, several hundred astonished scientists sat in silence as Ron Fouchier, a Dutch virologist at the Erasmus Medical Center, in Rotterdam, reported that simply transferring avian influenza from one ferret to another had made it highly contagious. Fouchier explained that he and his colleagues “mutated the hell out of H5N1”—meaning that they had altered the genetic sequence of the virus in a variety of ways. That had no effect. Then, as Fouchier later put it, “someone finally convinced me to do something really, really stupid.” He spread the virus the old-fashioned way, by squirting the mutated H5N1 into the nose of a ferret and then implanting nasal fluid from that ferret into the nose of another. After ten such manipulations, the virus began to spread around the ferret cages in his lab. Ferrets that received high doses of H5N1 died within days, but several survived exposure to lower doses.

When Fouchier examined the flu cells closely, however, he became alarmed. There were only five genetic changes in two of the viruses’ eight genes. But each mutation had already been found circulating naturally in influenza viruses. Fouchier’s achievement was to place all five mutations together in one virus, which meant that nature could do precisely what he had done in the lab. Another team of researchers, led by Yoshihiro Kawaoka, at the University of Wisconsin, created a slightly different form of the virus, which, while not as virulent, was also highly contagious. One of the world’s most persistent horror fantasies, expressed everywhere from Mary Shelley’s “Frankenstein” to “Jurassic Park,” had suddenly come to pass: a dangerous form of life, manipulated and enhanced by man, had become lethal.

Fouchier’s report caused a sensation. Scientists harbored new fears of a natural pandemic, and biological-weapons experts maintained that Fouchier’s bird flu posed a threat to hundreds of millions of people. The most important question about the continued use of the virus, and the hardest to answer, is how likely it is to escape the laboratory. “I am not nearly as worried about terrorists as I am about an incredibly smart, smug kid at Harvard, or a lone crazy employee with access to these sequences,” Michael T. Osterholm, the director of the Center for Infectious Disease Research and Policy at the University of Minnesota Health Center, told me. Osterholm is one of the nation’s leading experts on influenza and bioterrorism. “We have seen many times that accidental releases of dangerous microbes are not rare,” he said.

Osterholm’s anxiety was based in recent history. The last person known to have died of smallpox, in 1978, was a medical photographer in England named Janet Parker, who worked in the anatomy department of the University of Birmingham Medical School. Parker became fatally ill after she was accidentally exposed to smallpox grown in a research lab on the floor below her office. In the late nineteen-seventies, a strain of H1N1—“swine flu”—was isolated in northern China, near the Russian border, and it later spread throughout the world. Most virologists familiar with the outbreak are convinced that it came from a sample that was frozen in a lab and then released accidentally. In 2003, several laboratory technicians in Hong Kong were infected with the SARS virus. The following year, a Russian scientist died after mistakenly infecting herself with the Ebola virus.

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>>18509008

Biological labs are given four possible biosafety-level security grades, ranging from BSL-1 to BSL-4. Research on the most lethal and contagious organisms is carried out at BSL-4 laboratories. Under U.S. guidelines, BSL-3 facilities contain microbes that cause “serious or potentially lethal diseases” but do not easily pass among people, or for which there are easily accessible preventives. BSL-4 laboratories house agents that have no preventives or treatments. The labs in Rotterdam and in Wisconsin where the H5N1 ferret work was conducted were both BSL-3 facilities that had been enhanced with additional security measures. In such laboratories, scientists are typically subjected to security checks; they wear spacesuits and breathe through special respirators. Although no safeguards are absolute, negative air filters attempt to insure that no particles accidentally escape from the lab.

“I feel terrible—I took it from a job creator.”

Link copied

Last December, the National Science Advisory Board for Biosecurity, a panel of science, defense, and public-health experts, was asked by the Department of Health and Human Services to evaluate Fouchier’s research. The panel recommended that the two principal scientific journals, Science and Nature, reconsider plans to publish information about the methods used to create the H5N1 virus. It was the first time that the Advisory Board, which was formed after the anthrax attacks of 2001 to provide guidance on “dual use” scientific research, which could both harm and protect the public, had issued such a request. “We are in the midst of a revolutionary period in the life sciences,” the advisers wrote. “With this has come unprecedented potential for better control of infectious diseases and significant societal benefit. However, there is also a growing risk that the same science will be deliberately misused and that the consequences could be catastrophic.” The Times published an editorial that echoed the Advisory Board’s concern, and even questioned the purpose of the experiments: “We believe in robust research and almost always oppose censorship. But in this case the risks—of doing the work and publishing the results—far outweigh the benefits.” The journal New Scientist agreed: “ONE MISTAKE AWAY FROM A WORLDWIDE FLU PANDEMIC.” Television talk shows and the Internet pulsated with anxiety.

The widespread alarm led Science and Nature to agree to postpone publication. Fouchier’s virus, which now sits in a vault within his securely guarded underground laboratory in Rotterdam, has fundamentally altered the scope of the biological sciences. Like the research that led to splitting the atom and the creation of nuclear energy, the knowledge that his experiment has provided could be used to attack the public as well as to protect it.

“Terror is not an unjustified reaction to knowing this virus exists,” Osterholm, who serves on the Advisory Board, told me. “We have no room to be wrong about this. None. We can be wrong about other things. If smallpox got out, it would be unfortunate, but it has a fourteen-day incubation period, it’s easy to recognize, and we would stop it. Much the same is true with SARS. But with flu you are infectious before you even know you are sick. And when it gets out it is gone. Those researchers have all of our lives at the ends of their fingers.”

Fouchier, a lanky forty-five-year old man with intense blue eyes, works at one of the most highly regarded virological laboratories in Europe. “I have spent many years and this institution has paid millions of dollars to insure that this research was carried out in the safest possible manner,” he told me when we met in a conference room in the grim research facility that houses his laboratories at the Erasmus Medical Center. The center devoted several years to constructing a special lab for Fouchier’s research. From the windows, one can see barges and hulking gray cranes; Rotterdam is Europe’s busiest port. It is an industrial cityscape whose bleakness, on the day I visited, seemed to match Fouchier’s mood. As he spoke, he stared at his hands, which he clenched nervously. “People are acting like I am some mad scientist,” he said.

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>>18509010

Fouchier spent much of his career working on the structure of the AIDS virus. In 1997, he abruptly turned to bird flu, both because he was fascinated by its molecular structure and because he quickly grasped its pandemic potential. He has published scores of scientific articles on how influenza viruses move between species. Since December, however, when the Advisory Board recommended postponing publication of the bird-flu research, and some of his colleagues called for stopping it entirely, he has felt, he says, like the focus of “an international witch hunt.” He was incensed. “To attempt to prevent this research from reaching the largest number of scientists is bullshit,” he told me. “The more people who have access to it, the more likely we are to get answers to the many questions we still need to ask. Everyone who knows anything about virology can get hold of the recipe.” There were nearly a thousand people at the Malta meeting where he first announced his findings. “This moratorium serves some fake sense of security,” he said. “It does not serve the public health.”

Fouchier, as well as Kawaoka and other researchers, had been trying for years to learn whether H5N1 could trigger a worldwide pandemic. He wondered why the virus has destroyed so many poultry flocks in the United States, Europe, and Asia but infected so few people. Fouchier hoped to characterize the properties that make the virus so much deadlier than others. The only way to answer these questions was to create a variant that would cling to human cells in the nose and throat. Fouchier’s research was hardly the work of a furtive renegade. Several international review committees oversaw his experiments, and he received funding from the National Institutes of Health. Despite the risks, most people in his field believed that the experiments were necessary. Moreover, they were not without precedent. In 2002, Eckard Wimmer, at Stony Brook University, stitched together hundreds of DNA fragments, mostly acquired via the Internet, then used them to create a fully functional polio virus. In the fall of 2005, several published academic papers described the genomic sequence of the 1918 Spanish flu, which caused the world’s deadliest influenza pandemic. In each case, the publications were initially denounced but were eventually accepted as valuable.

“In this profession, you always do it wrong,” Ab Osterhaus, a leading infectious-disease expert who runs the virology department at Erasmus, said. “Either you give too much warning or not enough. Either you take things too seriously or not seriously enough. Fouchier’s work is essential, and the questions it raises must be addressed.”

There have been many hypotheses about how bird flu could become epidemic. Most researchers had believed that the avian virus would have to combine with human genes in pigs. Pigs usually serve as a mixing vessel for influenza viruses that make the transition from poultry to humans. (This is how the global pandemic starts in Steven Soderbergh’s recent film “Contagion”: Gwyneth Paltrow is exposed to a pig that’s been infected by a bat, and soon much of the world is dead or dying.) Other scientists believed that the H5 protein, because of its molecular structure, could not easily infect human cells. (Strains of influenza are named for two proteins on their surface that latch on to respiratory cells and make it possible for them to invade our lungs.) “There has been a lot of speculation that this virus cannot be transmitted easily or through the air,” Fouchier told me. “That speculation has been wrong.”

Although no animal study can predict with certainty what will happen in humans, ferrets get flu pretty much the way we do. Their lung physiology is similar to humans’, and avian-influenza viruses bind to the same receptor cells in their respiratory tracts. Still, there has been sharp debate among scientists about whether results in ferrets can predict how humans will react to similar infections, with some researchers discounting the data entirely.

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>>18509015

“The mutations . . . could cause the viruses to be more transmissible between humans,” Peter Palese, a prominent microbiologist at Mount Sinai School of Medicine, wrote recently. “But this is simply unknowable from available data.” Palese argues that the virus may be better adapted to ferrets than to other mammals.

“You cannot say, ‘Just forget about it, because it happened in a ferret,’ ” Fouchier said. “This is our best model. But you also can’t say, ‘Because it happened in a ferret, it will happen in a human.’ So it becomes a question of whether it’s worth the risk of finding out. This is one of the most dangerous viruses you can imagine. It’s not my virus—it’s our virus. And it’s out there. We need to deal with that. And, if we focus on what matters, we can.”

Once you create a virus that could kill millions of people, what should you do with it? And how should you handle the knowledge that made it possible?

There have been angry calls for Fouchier’s virus to be destroyed, for it to be transferred to a military-level bioweapons facility, and for research to be stopped entirely. “It’s just a bad idea for scientists to turn a lethal virus into a lethal and highly contagious virus,” Dr. Thomas Inglesby, a bioterrorism expert and the director of the Center for Biosecurity, at the University of Pittsburgh Medical Center, said. “And it’s a second bad idea for them to publish how they did it, so others can copy it.”

Still, most scientists who work with viruses insist that the value of this research outweighs the risks. Anthony S. Fauci, the longtime chief of the Institute of Allergy and Infectious Diseases, told me, “Those data could help scientists determine rapidly whether existing vaccines or drugs are effective against such a virus, as well as help in the development of new medications. It’s hard to stop something if you don’t know what it’s made of. Naturally, if epidemiologists in countries where pandemics most often arise know what they are looking for, they will be able to move with greater urgency to contain the spread.”

“It’s a magic potion that makes everything you say interesting.”

Link copied

How likely is it that publishing the genetic sequence could help a terrorist, a rogue, or a legitimate researcher who might develop a novel vaccine or drug? “Most of us are unequivocal about the value of the research,” Fauci said. “But deciding what to do with these types of studies is complicated. At the moment, there are no official governing bodies to regulate such decisions. They rely on the good will of researchers.” Fauci and others have noted that, precisely because flu is so hard to control, the virus would be difficult to use as a weapon.

In this case, as in most other cases, the work was supported heavily by the National Institutes of Health, and it seems unlikely to proceed without U.S. government support. Scientists bicker as vigorously as any other group, but rarely about the right to share and publish the data on which their research depends. Even the National Science Advisory Board for Biosecurity has made clear its general support for open investigation and full publication. The scientific method and the entire edifice of institutional research depend on such openness; without it, progress would slow dramatically. As biology has become more accessible, the balance between freedom and protection has become harder to maintain. This is certainly not the last time that preventing wide dissemination of information may seem necessary. But who should make those decisions, and how? Scientists fear that any regulatory body will stifle research. In 1975, when biologists met at Asilomar, California, to discuss the potential hazards of the new field of recombinant DNA technology, the group drew up voluntary guidelines to govern their research. Those guidelines have worked well, and that meeting is often regarded as a model of coöperative regulation.

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>>18509017

We live in a very different world now. Secretary of State Hillary Clinton recently gave a speech at a biological-weapons conference in Geneva in which she stressed that the threat of biological terror can no longer be ignored. “There are warning signs,” Clinton said, including “evidence in Afghanistan that . . . Al Qaeda in the Arabian Peninsula made a call to arms for—and I quote—‘brothers with degrees in microbiology or chemistry to develop a weapon of mass destruction.’ ”

While scientists disagree sharply about whether it would be easy to replicate such a virus in a laboratory, and whether it would be worth the effort, there is no question that we are moving toward a time when work like this, and even more complex biology, will be accessible to anyone with the will to use it, a few basic chemicals, and a relatively small amount of money.

Those realities have compelled many scientists to reconsider their unilateral support of the principle of open research. “I can tell you that when I began this journey I was certainly of the view that everything should be out and science should not be interfered with,” Arturo Casadevall, the chief of infectious disease at the Albert Einstein College of Medicine and a member of the Advisory Board, said at a recent forum on the issue sponsored by the New York Academy of Sciences. “And as the result of hundreds of hours of the deliberative process I changed my mind.” Others are even more emphatic, arguing that although the information is bound to become available, any delay is better than none. Many countries lack proper surveillance capacities, and existing vaccines are not good enough to stop influenza viruses from taking hold in the human population. By the time that public-health officials were fully aware of the swine-flu virus that originated in Mexico in 2009, for instance, it had spread across the globe.

In January, a few days before we met in Rotterdam, Fouchier had agreed to a sixty-day moratorium on the project, but only after he received a long, late-night phone call from Fauci, who convinced him that a worldwide time-out—the first since the beginning of the era of molecular biology—would allow people to cool off and enable them to explain the value of such research to the public. In mid-February, a committee of specialists, including Fouchier, met in Geneva at the W.H.O. headquarters and announced that the papers would eventually be published in full, but that a sixty-day moratorium was probably not long enough. It is not clear when or where the research will continue.

Attempts to control information or to prohibit research rarely succeed for long. As the physicist and synthetic biologist Rob Carlson has written, most notably in his 2010 book, “Biology Is Technology,” in the case of crystal methamphetamine both prohibition and efforts by the federal government to shut down production labs have failed, and in similar ways. In each case, success in cracking down on small-time dealers led to failure on a larger scale. Carlson believes that cutting the flow of H5N1 data will have the same effect. “Any attempt to secure the data would have to start with an assessment of how widely it is already distributed,” he wrote recently on his blog, Synthesis. “I have yet to meet an academic who regularly encrypts e-mail, and my suspicion is that few avail themselves of the built-in encryption on their laptops.” Carlson noted that, in addition to university computers and e-mail servers in facilities where the science originated, the information is probably stored in the computers of reviewers, on servers at Nature and Science, at the Advisory Board, and, depending on how the papers were distributed and discussed by the board’s members, possibly on their various e-mail servers and individual computers as well. “And,” Carlson wrote, “let’s not forget the various unencrypted phones and tablets all of those reviewers now carry around.”

Carlson and others argue that restricting publication would retard the progress of the research without increasing safety. With influenza viruses, speed matters. Vaccine-production methods have not changed substantially in sixty years, and it was months before a useful vaccine was widely available for the H1N1 pandemic of 2009. That virus infected more than a billion people. Future bird-flu research could help scientists learn how it is transmitted through the air, why it makes the leap from animal to man, and how specifically it binds to human cell receptors. By placing the virus into tissue culture, scientists could discover more about how it destroys cells and make a better assessment of whether current vaccines would protect us—and, if they wouldn’t, the research could guide us toward making more effective vaccines. None of these experiments are without risk, but one must also consider the risk of not carrying them out.

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>>18509021

“We can learn a great deal about transmission of influenza virus through the air from this work, and it’s something we know very little about,” Ab Osterhaus, the leader of the Erasmus team, said. “Nobody was going to make this virus in his garage. There are so many better ways to create terror. You have to compare the risk posed by nature with the theoretical risk that a human might use this virus for harm. I take the bioterror threat very seriously. But we have to address the problems logically. And nature is much more sophisticated than anyone in any lab. Nature is going to manufacture this virus or something like it. We know that. Bioterrorists might, but nature will. Look at the past century: the 1918 flu, H.I.V., Ebola, and H1N1. The Spanish flu took months. SARS maybe a couple of weeks. This is happening all the time, and we have ways to fight it. So where is the greatest risk? Is it in someone’s garage or in nature? Because you cannot prevent scientists from getting the information they need to address that risk. I understand politics and publicity. But I also understand that viruses do not care about any of that.” ♦

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ECOHEALTH ALLIANCE CONDUCTED RISKY EXPERIMENTS ON MERS VIRUS IN CHINA

Documents released by the NIH contradict previous assertions by EcoHealth Alliance about its experiments on bat coronaviruses in Wuhan.

https://theintercept.com/2021/10/21/virus-mers-wuhan-experiments/

Documents released by the National Institutes of Health yesterday raise new questions about government-funded research on viruses conducted in China. The annual grant reports from EcoHealth Alliance, which the NIH sent to The Intercept in response to a lawsuit, provided additional evidence that the U.S. nonprofit — which studies emerging infectious diseases — and its sub-awardee, the Wuhan Institute of Virology, were engaged in risky experiments and that the NIH may not have been fully aware of these activities.

In September, The Intercept received two grant proposals by EcoHealth Alliance that were submitted to the NIH. One of the proposals, “Understanding the Risk of Bat Coronavirus Emergence,” detailed troubling and potentially dangerous research conducted with bat coronaviruses in Wuhan, China. But the first release of the documents, which The Intercept received more than a year after it requested them, did not include the progress report for the grant’s fifth and final funding year.

Yesterday, the NIH provided that missing report for the period ending May 2019, which was inexplicably dated August 2021. That summary of the group’s work includes a description of an experiment the EcoHealth Alliance conducted involving infectious clones of MERS-CoV, the virus that caused a deadly outbreak of Middle East respiratory syndrome in 2012. MERS has a case-fatality rate as high as 35 percent, much higher than Covid-19’s. The scientists swapped out the virus’s receptor-binding domain, or RBD, a part of the spike protein that enables it to enter a host’s cells, according to the report. “We constructed the full-length infectious clone of MERS-CoV, and replaced the RBD of MERS-CoV with the RBDs of various strains of HKU4-related coronaviruses previously identified in bats from different provinces in southern China,” the scientists wrote.

“Changing the receptor binding site on MERS is sort of crazy,” wrote Jack Nunberg, a virologist and director of the Montana Biotechnology Center at the University of Montana, in an email to The Intercept after reviewing the documents. “Although these new chimeric viruses may retain properties of the MERS-CoV genetic backbone, engineering of a known human pathogen raises new and unpredictable risks beyond those posed by their previously reported studies using a non-pathogenic bat virus backbone.” The researchers’ intent, which some scientists consider integral to defining gain-of-function, remains unclear.

“In the very same report, they showed data that one of their chimeric SARS-like viruses caused more severe disease in a humanized animal model than the original virus,” said Alina Chan, a Boston-based molecular biologist and co-author of the upcoming book “Viral: The Search for the Origin of Covid-19.” “After seeing that result, why did they do similar work using the MERS human pathogen?”

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>>18509046

>>18509046

The Intercept previously asked EcoHealth Alliance about work on MERS-CoV referenced in sections of the grant that NIH released in September. At the time, EcoHealth spokesperson Robert Kessler insisted that the group had not conducted the work. “The MERS work proposed in the grant is suggested as an alternative and was not undertaken,” Kessler wrote in an email in September. Kessler did not respond to a query The Intercept sent yesterday about the apparent falsity of his previous statement.

The work with the MERS virus complicates EcoHealth Alliance’s previous claims that the research covered in the grant had not involved work with “potential pandemic pathogens,” or viruses, bacteria, and microorganisms that carry a likely risk of uncontrollable spread between humans. Kessler had previously told The Intercept that “All the other viruses studied under this grant are bat viruses, not human viruses.” But MERS is known to infect and spread in humans, and was specifically designated under the NIH’s former pause on funding gain-of-function research of concern.

Other questions arise from the group’s experiments with bat coronaviruses. As The Intercept previously reported, the EcoHealth Alliance grant proposals released in September contained descriptions of an experiment on mice that had been genetically engineered to contain an enzyme receptor found in human cells. These “humanized mice” were infected with bat coronaviruses containing parts of other viruses. At certain times during the experiment, the mutant viruses reproduced far more quickly in the mice than the original bat virus on which they were based and were also somewhat more pathogenic, leading several experts to conclude that they fit the NIH’s definition of gain-of-function research.

The federal government temporarily paused such gain-of-function research involving potential pandemic pathogens in 2014, though it was resumed in 2017, when the Department of Health and Human Services introduced guidelines known as P3CO, which were meant to safeguard against the risk of disease outbreak.

In September, The Intercept asked the NIH whether anyone at the agency was aware of the humanized mouse experiments and whether, after they resulted in evidence of enhanced virus growth greater than 1 log over the parental backbone strain, the grantees were made to “stop all experiments with these viruses and provide the NIAID Program Officer and Grants Management Specialist, and Wuhan Institute of Virology Institutional Biosafety Committee with the relevant data and information related to these unanticipated outcomes,” as the grant had specifically required. We also asked why that research was not subject to either the temporary pause or the P3CO guidelines.

In response, NIH spokesperson Elizabeth Deatrick wrote, “The PI [principal investigator] reported these results in the year 4 progress report and grant renewal application. The research described was reviewed, and was determined not subject to the 2014-2017 Gain-of-Function Research Funding Pause or to the P3CO Framework.”

Yet in a letter sent to Rep. James Comer, R-Ky., yesterday, NIH Principal Deputy Director Lawrence Tabak seemed to suggest that the agency had not been aware of the problematic research. “EcoHealth failed to report this finding right away, as was required by the terms of the grant,” Tabak wrote to Comer, the ranking member of the House Committee on Oversight and Reform, which also received a copy of the annual progress report from the bat coronavirus grant yesterday.

While critical of EcoHealth Alliance, Tabak also seemed to suggest that there was nothing alarming about the research, which he referred to as “limited experiments.” After acknowledging that some of the humanized mice that were infected with the mutant viruses became sicker than those infected with the original viruses, he said the scientists had not been intent on that outcome. “As sometimes occurs in science, this was an unexpected result of the research, rather than something the researchers set out to do.”

Tabak also emphasized, as The Intercept has previously reported, that the viruses studied in the mouse experiments were so evolutionarily distant from SARS-CoV-2 that they could not have mutated into the virus that caused the Covid-19 pandemic. That view was echoed in a brief analysis of the research that NIH posted to its website yesterday.

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>>18509048

Also among the documents NIH released to The Intercept yesterday was the original version of an annual report from the fourth year of the bat coronavirus grant. The version released to The Intercept in September indicated that it had been submitted in 2020, after the pandemic began and more than two years after it was due. The two versions appear to be almost identical, though they include different reference publications. NIH has not yet released communications around the grant that may explain why the document was updated.

According to Tabak’s letter, the NIH has demanded additional information from EcoHealth Alliance. “EcoHealth is being notified that they have five days from today to submit to NIH any and all unpublished data from the experiments and work conducted under this award,” he wrote. “Additional compliance efforts continue.”

“This is a pattern of dishonesty,” said Chan, the molecular biologist and “Viral” author. “It should be clear now that we cannot take the word of conflicted parties in the search for the origin of Covid-19,” she added. “It is urgently important that the public and investigators gain full access to all EcoHealth documents relating to research conducted in Wuhan.”

Update: October 21, 2021, 2:33 p.m. ET

This story has been updated to clarify a statement by Jack Nunberg and include an additional comment from Alina Chan.

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Fouchier

Ronaldus (Ron) Adrianus Maria Fouchier (born 13 October 1966) is a Dutch virologist who is Deputy head of the Erasmus MC Department of Viroscience, headed by Prof. Marion Koopmans.

Notability

Fouchier is notable for his research on respiratory viruses of humans and animals, antigenic drift, and influenza virus zoonoses, transmission and pandemics. His team contributed substantially to the identification and characterization of various “new” viruses, such as human metapneumovirus, human coronavirus NL63, SARS coronavirus, MERS coronavirus, and influenza A virus subtype H16.

Fouchier is elected member of the Royal Dutch Academy of Sciences (KNAW), the Royal Holland Society of Sciences and Humanities (KHMW) and Academia Europaea. In 2006 he received the Heine-Medin award of the European Society for Clinical Virology and in 2013 the Huibregtsen award for top innovative science with societal impact. He is a member of the CEIRR Center coordinated at the Icahn School of Medicine at Mount Sinai in New York City. Fouchier is a web-of-science Highly Cited author.

Awards and honours

2006 - Heine Medin award of the European Society for Clinical Virology [1]

2013 - Huibregtsen award for top innovative science with societal impact [2]

Selected publications

Human metapneumovirus: A newly discovered human pneumovirus isolated from young children with respiratory tract disease van den Hoogen BG, de Jong JC, Groen J, Kuiken T, de Groot R, Fouchier RA, Osterhaus AD. Nat Med. 2001 Jun;7(6):719-24. doi: 10.1038/89098. PMID: 11385510

Human coronavirus NL63: A previously undescribed coronavirus associated with respiratory disease in humans Fouchier RA, Hartwig NG, Bestebroer TM, Niemeyer B, de Jong JC, Simon JH, Osterhaus AD. Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6212-6. doi: 10.1073/pnas.0400762101. Epub 2004 Apr 8. PMID: 15073334

SARS coronavirus: Aetiology: Koch's postulates fulfilled for SARS virus Fouchier RA, Kuiken T, Schutten M, van Amerongen G, van Doornum GJ, van den Hoogen BG, Peiris M, Lim W, Stöhr K, Osterhaus AD. Nature. 2003 May 15;423(6937):240. doi: 10.1038/423240a. PMID: 12748632

MERS coronavirus: Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia Zaki AM, van Boheemen S, Bestebroer TM, Osterhaus AD, Fouchier RA. N Engl J Med. 2012 Nov 8;367(19):1814-20. doi: 10.1056/NEJMoa1211721. Epub 2012 Oct 17. PMID: 23075143

Influenza virus H16: Characterization of a novel influenza A virus hemagglutinin subtype (H16) obtained from black-headed gulls Fouchier RA, Munster V, Wallensten A, Bestebroer TM, Herfst S, Smith D, Rimmelzwaan GF, Olsen B, Osterhaus AD. J Virol. 2005 Mar;79(5):2814-22. doi: 10.1128/JVI.79.5.2814-2822.2005. PMID: 15709000

External links

Prof. Ron Fouchier is member of the Royal Dutch Academy of Sciences (KNAW) KNAW / Ron Fouchier

Prof. Ron Fouchier is member of the Royal Holland Society of Sciences (KHMW) [3]

Prof. Ron Fouchier is member of the Academia Europaea [4]

Google Scholar Profile

Scopus Profile

The Mind of the Universe (in Dutch)

Interview with virologist Ron Fouchier (in Dutch)

Collaborating investigator of the CRIPT centre in CEIRR [5]

Heine Medin award [6]

Huibregtsenprijs [7]

Podcast of the Royal Dutch Academy of Sciences (KNAW) about Planetary Health (in Dutch) [8]

Chances of Fauci and Fouchier being key players in world effecting gain of function viruses?

>>18508936

CBDC incoming worldwide.

>>18509185

https://off-guardian.org/2023/03/07/central-bank-digital-currency-is-the-endgame-part-1/

Mar 7, 2023

Central Bank Digital Currency Is the Endgame – Part 1

Iain Davis

>>18509196

>hell bound

Pretty much.

>>18509222

UBI will be the welcomed 'carrot'

Who speaks in such a manner?

Christ like or ANTI-Christ like?

Do not be deceived.