Sunday, April 11, 2021

Remember Where You Heard It First (Last March-April)


Seriously - Am I The Only Cat Fixated On This LOW HANGING SARS-CoV2 FRUIT?!?!?!

thescientist |  Ralph Baric, an infectious-disease researcher at the University of North Carolina at Chapel Hill, last week (November 9) published a study on his team’s efforts to engineer a virus with the surface protein of the SHC014 coronavirus, found in horseshoe bats in China, and the backbone of one that causes human-like severe acute respiratory syndrome (SARS) in mice. The hybrid virus could infect human airway cells and caused disease in mice, according to the team’s results, which were published in Nature Medicine.

The results demonstrate the ability of the SHC014 surface protein to bind and infect human cells, validating concerns that this virus—or other coronaviruses found in bat species—may be capable of making the leap to people without first evolving in an intermediate host, Nature reported. They also reignite a debate about whether that information justifies the risk of such work, known as gain-of-function research. “If the [new] virus escaped, nobody could predict the trajectory,” Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris, told Nature.

In October 2013, the US government put a stop to all federal funding for gain-of-function studies, with particular concern rising about influenza, SARS, and Middle East respiratory syndrome (MERS). “NIH [National Institutes of Health] has funded such studies because they help define the fundamental nature of human-pathogen interactions, enable the assessment of the pandemic potential of emerging infectious agents, and inform public health and preparedness efforts,” NIH Director Francis Collins said in a statement at the time. “These studies, however, also entail biosafety and biosecurity risks, which need to be understood better.”

Baric’s study on the SHC014-chimeric coronavirus began before the moratorium was announced, and the NIH allowed it to proceed during a review process, which eventually led to the conclusion that the work did not fall under the new restrictions, Baric told Nature. But some researchers, like Wain-Hobson, disagree with that decision.

The debate comes down to how informative the results are. “The only impact of this work is the creation, in a lab, of a new, non-natural risk,” Richard Ebright, a molecular biologist and biodefence expert at Rutgers University, told Nature.

But Baric and others argued the study’s importance. “[The results] move this virus from a candidate emerging pathogen to a clear and present danger,” Peter Daszak, president of the EcoHealth Alliance, which samples viruses from animals and people in emerging-diseases hotspots across the globe, told Nature.
We Built a Chimeric Virus Encoding a Novel, Zoonotic CoV Spike Protein

I'm not a virologist and don't pretend to be. But I can read a fugging manual with the best of them, and understand what I've read. That said, slowly reread the nature paper from 2015 yourself. 

Therefore, to examine the emergence potential (that is, the potential to infect humans) of circulating bat CoVs, we built a chimeric virus encoding a novel, zoonotic CoV spike protein—from the RsSHC014-CoV sequence that was isolated from Chinese horseshoe bats1—in the context of the SARS-CoV mouse-adapted backbone. The hybrid virus allowed us to evaluate the ability of the novel spike protein to cause disease independently of other necessary adaptive mutations in its natural backbone. Using this approach, we characterized CoV infection mediated by the SHC014 spike protein in primary human airway cells and in vivo, and tested the efficacy of available immune therapeutics against SHC014-CoV. Together, the strategy translates metagenomics data to help predict and prepare for future emergent viruses.

Shi Zhengli - you know you done f'd up...., 

Mebbe what I'm watching from other "gain of function" virologists is a poster-child instance of the Weinstein's Distributed Information Suppression Complex?

The Proximal Origin of SARS-C0V2

virological |   Since the first reports of a novel pneumonia (COVID-19) in Wuhan city, Hubei province, China there has been considerable discussion and uncertainty over the origin of the causative virus, SARS-CoV-2. Infections with SARS-CoV-2 are now widespread in China, with cases in every province. As of 14 February 2020, 64,473 such cases have been confirmed, with 1,384 deaths attributed to the virus. These official case numbers are likely an underestimate because of limited reporting of mild and asymptomatic cases, and the virus is clearly capable of efficient human-to-human transmission. Based on the possibility of spread to countries with weaker healthcare systems, the World Health Organization has declared the COVID-19 outbreak a Public Health Emergency of International Concern (PHEIC). There are currently neither vaccines nor specific treatments for this disease.

SARS-CoV-2 is the seventh member of the Coronaviridae known to infect humans. Three of these viruses, SARS CoV-1, MERS, and SARS-CoV-2, can cause severe disease; four, HKU1, NL63, OC43 and 229E, are associated with mild respiratory symptoms. Herein, we review what can be deduced about the origin and early evolution of SARS-CoV-2 from the comparative analysis of available genome sequence data. In particular, we offer a perspective on the notable features in the SARS-CoV-2 genome and discuss scenarios by which these features could have arisen. Importantly, this analysis provides evidence that SARS-CoV-2 is not a laboratory construct nor a purposefully manipulated virus.

Say What?

The genomic comparison of both alpha- and betacoronaviruses (family Coronaviridae ) described below identifies two notable features of the SARS-CoV-2 genome: (i) based on structural modelling and early biochemical experiments, SARS-CoV-2 appears to be optimized for binding to the human ACE2 receptor; (ii) the highly variable spike (S) protein of SARS-CoV-2 has a polybasic (furin) cleavage site at the S1 and S2 boundary via the insertion of twelve nucleotides. Additionally, this event led to the acquisition of three predicted O-linked glycans around the polybasic cleavage site.

Controlaspecies: Gain Of Function Research And The Blame Game

harvardtothebighouse |  we have Peter Daszak.  His company, EcoHealth Alliance, which is a non-profit that depends largely on multi-million dollar government grants to function, has been partnering with Chinese researcher for years in an attempt to secure funding for more and more research into coronaviruses. At least they’re not really even pretending to be philanthropic.

And in one of the more transparent attempts at blatant PR-spin, Daszak was featured alongside one of the researchers who learned how to create hyper-virulent bat coronaviruses at UNC back in 2015, Zhengli Shi. Their article insists we should take Zhengli at her word when she claims to have not found a match after she checked COVID-19’s genome against everything in her lab. As if someone responsible for releasing the most virulent pathogen to hit humanity in modern history, one that’s already killed thousands and is projected to kill millions and millions more all across the globe, would simply fess-up to it, torpedoing her career and the years of research performed by her and her colleagues? And possibly opening all of them up to legal and other repercussions?

If you still aren’t sure whether the scientists involved with kind of research are being forthright, there’s Dr. Ralph Baric. It was in his lab at UNC that a hyper-virulent bat Franken-virus was created by splicing a new protein-spike on an existing coronavirus, creating a monster so vicious that a virologist with the Louis Pasteur Institute of Paris warned: If the [new] virus escaped, nobody could predict the trajectory.” It should also be noted that several years prior to tinkering directly with bat coronavirus spike-proteins, Baric orchestrated research that involved isolating a coronavirus from civets and then passing it through mammalian ACE2 receptor cells that were grown in the lab from kidney and brain samples – serial passage through host cell lines instead of entire hosts, which imparted a strong affinity for ACE2, and presumably created an airborne strain of coronavirus. And if cells derived from kidneys and brains were used for the serial passage development of COVID-19, that might help explain its affinity for attacking the kidneys and brains of its human hosts.

So if he was being honest, you might expect him to warn the public about the lethal potential coronaviruses pose during our current outbreak. However, when he was asked if the public should be worried about COVID-19 he said that people should be more worried about the seasonal flu. Pretty bizarre statement from a scientist who knew full well how dangerous coronaviruses could be, especially given the fact that not only was Zhengli Shi working in his lab on that project in 2015, but Xing-Yi Ge was too. Both of whom returned to Wuhan where they’ve continued their work for years.

Xing-Yi Ge is especially notable since in 2013 he became the very first scientist to isolate a bat coronavirus from nature that uses the ACE2 receptor, which is found in human, tree shrew, and ferret lungs and allows coronaviruses to become airborne. And as you might have learned by now, that’s the exact receptor used by COVID-19 to enter human cells – if anyone would know how to finagle that part of the coronavirus genome, it’d be him. So both Xing-Yi Ge and Zhengli Shi were part of the research team that created this hybridized hyper-virulent bat coronavirus under Baric, who’s actively downplayed the risk posed by COVID-19, and then returned to work in Wuhan, where funding provided in part by Daszak’s company allowed them to continue their work on coronaviruses with plenty of research to cut-and-paste into their work at the Wuhan Institute of Virology’s Disease Engineering Technical Research Center.

And as Dr. Ian Malcolm puts it in Jurassic Park, it is never a good idea to futz around with science and research when you don’t fully understand it, nor its possible implications.

However it wasn’t just Daszak funding their work, Zhengli also secured millions of dollars in grant money from various American institutions including our Department of Defense as well as the U.S. Biological Defense Research Directorate, and millions more from other foreign governments.
So although the Chinese Communist Party deserves its share of the blame for attempting to cover the outbreak up, arresting the heroic scientists trying to warn us and issuing gag-orders and the destruction of evidence, this research likely wouldn’t have occurred at all if the NIH hadn’t lifted the ban on gain-of-function research in the first place. And it was funded directly by American tax dollars, by government officials willing to let others play god at their behest.

But now that the virus is out of the lab, are the private entities responsible for its creation going to bear any of the blame at all? Or will America and China continue to point fingers at each other until the worst happens?

“Mars will accuse Earth of using a bio-weapon. Earth will claim it was Mars. The Belt will blame the other two. It’s a good way to start a war and cover it up.”

One last spoiler warning… okay, so in The Expanse the central plot device pushing things forward is the discovery of a mysterious substance dubbed the protomolecule, which seems to have a mind of its own and seek out radiation as sustenance before then beginning “the Work,” a mysterious intergalactic goal that isn’t revealed until later seasons.

And its not individual nations who first attempt to harness the protomolecule, but their Peter Daszak, the aforementioned scientist and CEO named Jules-Pierre Mao, who attempts to weave it into the genomes of immuno-compromised children to create hybridized super-soldiers. Not for his own private army, but as a game-changing bio-weapon he’ll sell to whichever government is willing to pay the most for it. So in The Expanse, it takes amoral scientists as well as the collusion of officials affiliated with both governments for this research to happen and be hidden, and when these Hybrids are eventually dropped between both armies the carnage is immense.

Luckily, we haven’t gotten that far on earth yet, but the rhetoric between America and China has been heading in that direction – it’s been growing increasingly hostile as each blames the other for starting the pandemic and covering it up, with China even going so far as to threaten to cut off our supply of antibiotics and other life-saving medical goods.  Meanwhile Daszak, Baric, Zhengli, and others sit back counting their lucky stars and their money, since both governments and the public at large seem to have bought their story that there’s no way this virus leaked out of one of their labs, and every government on earth now wants to harness their research to help create vaccines and treatments.
And these researchers have been assisted by scientifically spurious and journalistically vacuous articles which mindlessly regurgitate claims from the Chinese government, and its scientific propaganda arm, the WHO, about how bad the outbreak was in the past and how contained it is now. As the Chinese government arrested whistle-blowers and sent agents out into the street in bio-hazard gear while carrying automatic weapons to detain anyone suspected of breaking quarantine, while literally welding apartments buildings shut, the American media fawned over China’s “decisive and heroic” actions.
Please take a moment to consider the fact that almost everyone reading the news to you on television was selected due to their connections or how photogenic they are, not because of any actual journalistic chops or ability to think critically.

So as two superpowers are pushed closer and closer to conflict, the research that’s almost certainly the source of COVID-19 not only continues unabated, but if anything talk of more funding to stop this sort of supposedly natural pandemic from happening again is pouring into the pockets of the people who, if they weren’t directly responsible, should certainly have been at the forefront of warning the world about the risks posed by lab-altered coronaviruses, and been disclosing the existence of this sort of research in the first place.

Oddly, each and everyone one of them is pretending that viral dual-use gain-of-function research has never occurred at all. Or not so oddly, when you stop and think about how much they have to lose if their role in this pandemic is revealed.

“The hardest part of this game is figuring out who the enemy really is.”

Other than the fact it doesn’t bear the direct marks of genetic tampering, just like the engineered hyper-virulent H5N1 Bird Flu, there’s literally nothing natural about COVID-19’s behavior or clinical presentation. And hauntingly, peer-reviewed research has noted that a crucial region of its genome “may provide a gain-of-function… for efficient spreading in the human population.”

Not only is it so distant from any other coronavirus that it forms its own clade, but there isn’t even a natural path for it to have emerged through – assertions about pangolins have always been dubious at best, but were even further debunked when analysis of COVID-19’s genome at the regions that most accurately show heritage made it “very unlikely” that pangolins had ever been involved at all.

Beyond that is the fact that its affinity for the ACE2 receptor is somewhere between 10 and 20 times higher than SARS, and it also creates viral loads thousands of times higher than SARS. These two characteristics point towards COVID-19 using antibody-dependent enhancement, or ADE, to enter human cells. This is when the virus is able to hijack white blood cells to more easily enter into the rest of our body’s cells, allowing it to seep deep into its hosts’ nervous systems, creating permanent neurological damage in the hosts it doesn’t kill outright. ADE could also explain why between 5% and 10% of once “recovered” patients in Wuhan have been showing up with fresh infections, since that phenomenon allows a virus to hijack the antibodies created by a previous infection to re-attack an old host. And curiously Zhengli Shi, of UNC and Wuhan fame, co-authored a 2019 paper which used inert viral shells to figure out exactly how SARS, with its affinity to the ACE2 receptor just like COVID-19, was able to harness ADE to hijack white blood cells for enhanced cell entry. A gain-of-function extension of this research would be exactly the kind of experiment that could’ve given birth to COVID-19, especially considering that 2019 paper managed to fine-tune the exact concentration of antibodies that would best facilitate ADE.

Both HIV and Dengue Fever use antibody-dependent enhancement to boost their virulence, however its generally a phenomenon that takes a long time to occur when it happens in nature. However COVID-19 looks like it may have had its ADE jacked into hyper-drive as it was passed between a series of animal hosts, since it has the aforementioned much stronger ability to bind to host cells and creates viral loads orders of magnitude higher, and also appears to immediately to be able to enter its hosts nervous systems, killing many of its victims by attacking the region of the brain that controls breathing, drastically lowering white blood cell counts early on in infections, and apparently re-infecting individuals who had already appeared to clear their infection.

Further increasing the possibility that COVID-19’s unique clinical presentation may be due to its ADE being juiced by laboratory engineering are the observations from an ER doctor who’s stated that I have seen things that I have never seen before… I have witnessed medical phenomenon that just don’t make sense in the context of treating a disease that is supposed to be viral pneumonia. In an interview with Medscape, Dr. Cameron Kyle-Sidell went on to say that the closest thing to the symptoms he was witnessing in his emergency room.
Fauci Transferred Gain Of Function Research To Wuhan In 2015 After Obama Banned It

newsweek |   The NIH research consisted of two parts. The first part began in 2014 and involved surveillance of bat coronaviruses, and had a budget of $3.7 million. The program funded Shi Zheng-Li, a virologist at the Wuhan lab, and other researchers to investigate and catalogue bat coronaviruses in the wild. This part of the project was completed in 2019.

A second phase of the project, beginning that year, included additional surveillance work but also gain-of-function research for the purpose of understanding how bat coronaviruses could mutate to attack humans. The project was run by EcoHealth Alliance, a non-profit research group, under the direction of President Peter Daszak, an expert on disease ecology. NIH canceled the project just this past Friday, April 24th, Politico reported. Daszak did not immediately respond to Newsweek requests for comment.

The project proposal states: "We will use S protein sequence data, infectious clone technology, in vitro and in vivo infection experiments and analysis of receptor binding to test the hypothesis that % divergence thresholds in S protein sequences predict spillover potential."

In layman's terms, "spillover potential" refers to the ability of a virus to jump from animals to humans, which requires that the virus be able to receptors in the cells of humans. SARS-CoV-2, for instance, is adept at binding to the ACE2 receptor in human lungs and other organs.

According to Richard Ebright, an infectious disease expert at Rutgers University, the project description refers to experiments that would enhance the ability of bat coronavirus to infect human cells and laboratory animals using techniques of genetic engineering. In the wake of the pandemic, that is a noteworthy detail.

Ebright, along with many other scientists, has been a vocal opponent of gain-of-function research because of the risk it presents of creating a pandemic through accidental release from a lab.

 Dr. Fauci is renowned for his work on the HIV/AIDS crisis in the 1990s. Born in Brooklyn, he graduated first in his class from Cornell University Medical College in 1966. As head of NIAID since 1984, he has served as an adviser to every U.S. president since Ronald Reagan.

A decade ago, during a controversy over gain-of-function research on bird-flu viruses, Dr. Fauci played an important role in promoting the work. He argued that the research was worth the risk it entailed because it enables scientists to make preparations, such as investigating possible anti-viral medications, that could be useful if and when a pandemic occurred.

The work in question was a type of gain-of-function research that involved taking wild viruses and passing them through live animals until they mutate into a form that could pose a pandemic threat. Scientists used it to take a virus that was poorly transmitted among humans and make it into one that was highly transmissible—a hallmark of a pandemic virus. This work was done by infecting a series of ferrets, allowing the virus to mutate until a ferret that hadn't been deliberately infected contracted the disease.