Showing posts sorted by relevance for query shi. Sort by date Show all posts
Showing posts sorted by relevance for query shi. Sort by date Show all posts

Thursday, April 30, 2020

DAYYUM! There Go Those Virus Reparations Lawsuits - Er, Uh, You See What Happened Wuz...,



washingtontimes |  Meanwhile, a number of suspicious actions and a paper trail suggest that the virus escaped from one of the labs, though China is clamping down on the ability to pursue those leads.

 “The most logical place to investigate the virus origin has been completely sealed off from outside inquiry by the CCP,” said the document, referring to the Chinese Communist Party.

The party has taken draconian steps to control information about the virus since January.
“A gag order to both places was issued on Jan. 1, 2020, and a major general from the PLA who is China’s top military microbiologist essentially took over the [Wuhan Institute of Virology] since mid-January.”

Labs face scrutiny
Both of the labs under scrutiny in the report have conducted extensive research on bat coronaviruses, including those that have close molecular similarities to SARS-Cov-2, the full designation of the new pathogen.

Among the most significant circumstantial evidence identified in the report are the activities of Shi Zhengli, a leader in bat coronavirus research with the Wuhan Institute of Virology, China’s only high-security, level four research laboratory.

Ms. Shi has been involved in bioengineering bat coronaviruses, and a medical doctor named Wu Xiaohua launched an online campaign to expose Ms. Shi’s work. Dr. Wu said she believes the coronavirus at the root of the pandemic is one of 50 viruses in a database Ms. Shi manages.

The document also points to a 2015 academic report in Nature Medicine by Ms. Shi and 14 other scientists who said that while researching the potential for bat coronaviruses to infect humans, “we built a chimeric virus encoding a novel, zoonotic [animal-origin] spike protein … that was isolated from Chinese horseshoe bats.”

The scientists said the “hybrid virus” allowed researchers to study the ability of the virus to “cause disease.”

Dr. Wu stated in an internet posting that Ms. Shi used laboratory animals to test the human-infecting virus, and one of those animals may have been the origin of the pandemic.

Dr. Wu also asserted that the institute’s virus-carrying animals had been sold as pets, dead laboratory animals were not properly disposed of, and lab workers were known to boil and eat laboratory-used eggs.

“Wu’s charges of WIV management negligence are specific and have not been convincingly rebutted by WIV,” the analysis said.

Ms. Shi has worked closely with several U.S. virologists, and some American scientists have defended her and the institute from critics who point to her work with bat viruses as a needed focus of an investigation, the analysis says. Ms. Shi, in response to Dr. Wu’s assertions, said in March on her social media account: “I promise with my life that the virus has nothing to do with the lab.”

Tuesday, March 03, 2020

We Made The Coronavirus Epidemic: NYTimes Called Out Shi Zhengli A Month Ago


NYTimes |  Despite the new virus’s name, though, and as the people who christened it well know, nCoV-2019 isn’t as novel as you might think.

Something very much like it was found several years ago in a cave in Yunnan, a province roughly a thousand miles southwest of Wuhan, by a team of perspicacious researchers, who noted its existence with concern. The fast spread of nCoV-2019 — more than 4,500 confirmed cases, including at least 106 deaths, as of Tuesday morning, and the figures will have risen by the time you read this — is startling but not unforeseeable. That the virus emerged from a nonhuman animal, probably a bat, and possibly after passing through another creature, may seem spooky, yet it is utterly unsurprising to scientists who study these things.

One such scientist is Zheng-Li Shi, of the Wuhan Institute of Virology, a senior author of the draft paper (not yet peer reviewed and so far available only in preprint) that gave nCoV-2019 its identity and name. It was Ms. Shi and her collaborators who, back in 2005, showed that the SARS pathogen was a bat virus that had spilled over into people. Ms. Shi and colleagues have been tracing coronaviruses in bats since then, warning that some of them are uniquely suited to cause human pandemics.

In a 2017 paper, they set out how, after nearly five years of collecting fecal samples from bats in the Yunnan cave, they had found coronaviruses in multiple individuals of four different species of bats, including one called the intermediate horseshoe bat, because of the half-oval flap of skin protruding like a saucer around its nostrils. The genome of that virus, Ms. Shi and her colleagues have now announced, is 96 percent identical to the Wuhan virus that has recently been found in humans. And those two constitute a pair distinct from all other known coronaviruses, including the one that causes SARS. In this sense, nCoV-2019 is novel — and possibly even more dangerous to humans than the other coronaviruses.


Tuesday, September 20, 2011

what is entosis?

TheScientist | Though the mechanisms of engulfment may differ among cell and cancer types, the end result is nearly indistinguishable—a whole, living cell is housed within a large vacuole inside a tumor cell. Internalized cells usually follow one of three paths. They can continue living, at least temporarily, within the host cell, even dividing within their vacuole homes. Occasionally, they escape from the host cell to once again become a single, individual cell in the extracellular space. By and large, however, death is the most common fate for cells engulfed by tumor cells. Wang and colleagues demonstrated evidence of the apoptotic death of NK cells following their uptake by tumor cells. Nearly 90 percent of the internalized lymphocytes underwent traditional, programmed cell death, as evidenced by the activation of caspase 3. Work by Overholtzer’s group, on the other hand, suggests that cell engulfment between tumor cells represents a different type of cell death altogether—one mediated by lysosomes. The vacuoles housing the internalized tumor cells, his group observed, became acidic and surrounded by lysosomal membranes, indicative of fusion with lysosomes. Furthermore, when the researchers overexpressed B-cell lymphoma 2 (Bcl-2) to inhibit apoptosis, it had little effect on the death of internalized cells. On the other hand, inhibiting lysosomal acidification of the vacuoles could rescue the captured cells, when it was combined with apoptotic inhibitors. Interestingly, when only the lysosomal inhibitors were introduced, more cells appeared to undergo an apoptotic death, suggesting that apoptosis serves as a backup mechanism to the more common lysosomal death of the internalized cells.

Fais suggests it is simply the acidic environment of the tumor-cell vacuoles in metastatic melanoma cells that kills the internalized lymphocytes, though lytic enzymes may help to further digest the cell, he says. He argues that the engulfment and subsequent killing of cells such as lymphocytes is cell cannibalism in the most literal sense—one cell eating another. Once the victim is digested, the tumor cell can theoretically derive nutrients from it, promoting cancer survival and growth.

“We know that nutritional stress is a common feature of tumors,” says Eileen White, a cancer biologist at The Cancer Institute of New Jersey and Rutgers University. “We know they’ll undergo this process of autophagy where they’ll eat themselves. If they have the capability of eating each other or other cells—that would open a whole new door for tumors to sustain themselves.”

As evidence for this hypothesis, Fais showed in vitro that cell cannibalism increased under starvation conditions, and that the ingestion of T cells promoted the survival of melanoma cells. “The T cell is great because it has all these wonderful complex carbohydrates on the surface,” says cancer biologist Thomas Seyfried of Boston College. “They can all be degraded to glucose and other fuels [that tumor cells] could be using.”

But even if cells are deriving nourishment from their cannibalistic activities, it’s likely not the only benefit of the behavior, says immunologist Yufang Shi, who studies apoptosis at the Chinese Academy of Sciences and the Child Health Institute of New Jersey. “For one cell to digest another cell and to get energy . . . this is very uneconomical,” Shi explains. “You have to really make the cell into amino acids and polysaccharides. It’s very hard to use that as energy.” The fact that cell cannibalism increased when the cells were starving may simply be due to the fact that nutrient deprivation can cause cells to become detached from the extracellular matrix, Shi added—an event that Overholtzer’s group suggests could promote cell engulfment as a result of imbalanced cell-cell adhesion forces.

Another possibility is that the engulfed cells are driving the process. Internalized immune cells, for example, may have the potential to suppress tumor growth. During his initial graduate studies in the 1980s and again when he resumed this work more recently, Wang observed that some NK cells internalized by tumor cells can actually kill their host cells from the inside out. “After they enter into the tumor cells, they make the tumor cells erupt,” Wang says. “When [these NK cells] die, they also release a lot of enzymes,” Shi explains. “They are cytotoxic cells, so they can kill by releasing directly into the target cell, like the suicide bombers.”

But whether the internalized NK cells are initiating the engulfment is still unclear. If, on the other hand, the tumor cells are actively consuming the lymphocytes, it could provide a way for cancer to evade attack by the immune system. “I have a suspicion that maybe tumor [cells] in some conditions can kill the NK cells as a way to escape the surveillance of the immune system,” Wang says. This may become particularly important as the cancer metastasizes, Yao adds. “One of the physical challenges for those tumor cells will be how to survive in the new sites. One way is by taking [up] those NK cells and other immune cells to damage the immune response of cancer [patients].”

The bizarre phenomenon may also contribute to the genetic instability of cells, perhaps contributing to the formation of cancer early on. This March, Overholtzer and colleagues published the finding that cell-in-cell structures can act as cleavage barriers that disrupt cell division, leading to changes in ploidy—the number of sets of chromosomes in the cell—which are known to drive tumor progression.5 Conversely, cell engulfment may act to suppress tumor growth, such as when tumor cells eat other tumor cells. “Entosis has a dual nature,” says Overholtzer. “It clearly can kill [tumor] cells, but also, it can disrupt ploidy—one is predicted to be tumor suppressive, one is tumor promoting.”

For now, the question of function remains “a puzzle,” Fais says, and “I don’t have all the pieces.” But with evidence growing for significance of cell engulfment in tumor pathogenesis, researchers are now considering whether the phenomenon could serve to aid in diagnosis or in the development of new cancer treatments. “I think in the next few years this will be a very active field,” Shi says.

Friday, May 07, 2021

The Bulletin Of The Atomic Scientists DESTROYS Any Further Doubt About Covid's Origin

This is School For You!!!

Accept No MuthaPhukkin Substitutes...,

thebulletin |  Why would anyone want to create a novel virus capable of causing a pandemic? Ever since virologists gained the tools for manipulating a virus’s genes, they have argued they could get ahead of a potential pandemic by exploring how close a given animal virus might be to making the jump to humans. And that justified lab experiments in enhancing the ability of dangerous animal viruses to infect people, virologists asserted.

With this rationale, they have recreated the 1918 flu virus, shown how the almost extinct polio virus can be synthesized from its published DNA sequence, and introduced a smallpox gene into a related virus.

These enhancements of viral capabilities are known blandly as gain-of-function experiments. With coronaviruses, there was particular interest in the spike proteins, which jut out all around the spherical surface of the virus and pretty much determine which species of animal it will target. In 2000 Dutch researchers, for instance, earned the gratitude of rodents everywhere by genetically engineering the spike protein of a mouse coronavirus so that it would attack only cats.

Virologists started studying bat coronaviruses in earnest after these turned out to be the source of both the SARS1 and MERS epidemics. In particular, researchers wanted to understand what changes needed to occur in a bat virus’s spike proteins before it could infect people.

Researchers at the Wuhan Institute of Virology, led by China’s leading expert on bat viruses, Shi Zheng-li or “Bat Lady,” mounted frequent expeditions to the bat-infested caves of Yunnan in southern China and collected around a hundred different bat coronaviruses.

Shi then teamed up with Ralph S. Baric, an eminent coronavirus researcher at the University of North Carolina. Their work focused on enhancing the ability of bat viruses to attack humans so as to “examine the emergence potential (that is, the potential to infect humans) of circulating bat CoVs [coronaviruses].” In pursuit of this aim, in November 2015 they created a novel virus by taking the backbone of the SARS1 virus and replacing its spike protein with one from a bat virus (known as SHC014-CoV). This manufactured virus was able to infect the cells of the human airway, at least when tested against a lab culture of such cells.

The SHC014-CoV/SARS1 virus is known as a chimera because its genome contains genetic material from two strains of virus. If the SARS2 virus were to have been cooked up in Shi’s lab, then its direct prototype would have been the SHC014-CoV/SARS1 chimera, the potential danger of which concerned many observers and prompted intense discussion.

“If the virus escaped, nobody could predict the trajectory,” said Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris.

Baric and Shi referred to the obvious risks in their paper but argued they should be weighed against the benefit of foreshadowing future spillovers. Scientific review panels, they wrote, “may deem similar studies building chimeric viruses based on circulating strains too risky to pursue.” Given various restrictions being placed on gain-of function (GOF) research, matters had arrived in their view at “a crossroads of GOF research concerns; the potential to prepare for and mitigate future outbreaks must be weighed against the risk of creating more dangerous pathogens. In developing policies moving forward, it is important to consider the value of the data generated by these studies and whether these types of chimeric virus studies warrant further investigation versus the inherent risks involved.”

That statement was made in 2015. From the hindsight of 2021, one can say that the value of gain-of-function studies in preventing the SARS2 epidemic was zero. The risk was catastrophic, if indeed the SARS2 virus was generated in a gain-of-function experiment.

Tuesday, April 14, 2020

WaPo Throwing Shade On Shi Zhengli And The Wuhan Virological Institute


WaPo |  Two years before the novel coronavirus pandemic upended the world, U.S. Embassy officials visited a Chinese research facility in the city of Wuhan several times and sent two official warnings back to Washington about inadequate safety at the lab, which was conducting risky studies on coronaviruses from bats. The cables have fueled discussions inside the U.S. government about whether this or another Wuhan lab was the source of the virus — even though conclusive proof has yet to emerge.

In January 2018, the U.S. Embassy in Beijing took the unusual step of repeatedly sending U.S. science diplomats to the Wuhan Institute of Virology (WIV), which had in 2015 become China’s first laboratory to achieve the highest level of international bioresearch safety (known as BSL-4). WIV issued a news release in English about the last of these visits, which occurred on March 27, 2018. The U.S. delegation was led by Jamison Fouss, the consul general in Wuhan, and Rick Switzer, the embassy’s counselor of environment, science, technology and health. Last week, WIV erased that statement from its website, though it remains archived on the Internet.

What the U.S. officials learned during their visits concerned them so much that they dispatched two diplomatic cables categorized as Sensitive But Unclassified back to Washington. The cables warned about safety and management weaknesses at the WIV lab and proposed more attention and help. The first cable, which I obtained, also warns that the lab’s work on bat coronaviruses and their potential human transmission represented a risk of a new SARS-like pandemic.

“During interactions with scientists at the WIV laboratory, they noted the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory,” states the Jan. 19, 2018, cable, which was drafted by two officials from the embassy’s environment, science and health sections who met with the WIV scientists. (The State Department declined to comment on this and other details of the story.)

The Chinese researchers at WIV were receiving assistance from the Galveston National Laboratory at the University of Texas Medical Branch and other U.S. organizations, but the Chinese requested additional help. The cables argued that the United States should give the Wuhan lab further support, mainly because its research on bat coronaviruses was important but also dangerous.

As the cable noted, the U.S. visitors met with Shi Zhengli, the head of the research project, who had been publishing studies related to bat coronaviruses for many years. In November 2017, just before the U.S. officials’ visit, Shi’s team had published research showing that horseshoe bats they had collected from a cave in Yunnan province were very likely from the same bat population that spawned the SARS coronavirus in 2003.

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.

Sunday, April 12, 2020

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.

Tuesday, March 03, 2020

Wuhan Institute of Virology: HATERS HURT'N MY FEELINGS! I DINDU NUFFIN!!!


SCMP |  A Chinese research institute in the city of Wuhan – ground zero of the coronavirus outbreak
– has again dismissed rumours suggesting it is linked to the public health crisis, saying it has been “badly hurt” by conspiracy theories circulating online.
 
“The rumours … have caused severe damage to our researchers who have been dedicated to working on the front line, and seriously interrupted the emergency research we are doing during the epidemic,” the Wuhan Institute of Virology (WIV), which is affiliated with the Chinese Academy of Sciences, said in a statement.

Those rumours included that the new virus strain was “man-made”, “leaked from the WIV lab”, that “the WIV was taken over by the military”, “a WIV researcher died from the leaked virus”, “a WIV student is patient zero”, and “a WIV researcher reported to authorities that the WIV chief was responsible” for the epidemic, the statement posted on its website on Wednesday said.

The institute runs the Wuhan National Biosafety Laboratory, the only facility in China equipped to diagnose and research easily transmitted pathogens at the highest biosafety level of four.

“Looking back on our hard work over the past month, we have nothing to be ashamed of or to regret,” the statement said.

A prominent virologist with the institute has also been targeted by the rumours. Shi Zhengli’s exploration of caves in Yunnan province discovered that another deadly coronavirus – which caused the severe acute respiratory syndrome, or Sars, epidemic in 2002-03 – had originated in bats. Her database of viruses found in bats provided evidence for the theory that the coronavirus at the centre of the ongoing epidemic was also linked to bats. The new virus strain was found to be 96 per cent identical to one found in bats.

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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.


 

Tuesday, June 08, 2021

Believe The Science: SARS-CoV2 Was Lab Synthesized

WSJ  |  A genome is a blueprint for the factory of a cell to make proteins. The language is made up of three-letter “words,” 64 in total, that represent the 20 different amino acids. For example, there are six different words for the amino acid arginine, the one that is often used in supercharging viruses. Every cell has a different preference for which word it likes to use most.

In the case of the gain-of-function supercharge, other sequences could have been spliced into this same site. Instead of a CGG-CGG (known as “double CGG”) that tells the protein factory to make two arginine amino acids in a row, you’ll obtain equal lethality by splicing any one of 35 of the other two-word combinations for double arginine. If the insertion takes place naturally, say through recombination, then one of those 35 other sequences is far more likely to appear; CGG is rarely used in the class of coronaviruses that can recombine with CoV-2.

In fact, in the entire class of coronaviruses that includes CoV-2, the CGG-CGG combination has never been found naturally. That means the common method of viruses picking up new skills, called recombination, cannot operate here. A virus simply cannot pick up a sequence from another virus if that sequence isn’t present in any other virus.

Although the double CGG is suppressed naturally, the opposite is true in laboratory work. The insertion sequence of choice is the double CGG. That’s because it is readily available and convenient, and scientists have a great deal of experience inserting it. An additional advantage of the double CGG sequence compared with the other 35 possible choices: It creates a useful beacon that permits the scientists to track the insertion in the laboratory.

Now the damning fact. It was this exact sequence that appears in CoV-2. Proponents of zoonotic origin must explain why the novel coronavirus, when it mutated or recombined, happened to pick its least favorite combination, the double CGG. Why did it replicate the choice the lab’s gain-of-function researchers would have made?

Yes, it could have happened randomly, through mutations. But do you believe that? At the minimum, this fact—that the coronavirus, with all its random possibilities, took the rare and unnatural combination used by human researchers—implies that the leading theory for the origin of the coronavirus must be laboratory escape.

When the lab’s Shi Zhengli and colleagues published a paper in February 2020 with the virus’s partial genome, they omitted any mention of the special sequence that supercharges the virus or the rare double CGG section. Yet the fingerprint is easily identified in the data that accompanied the paper. Was it omitted in the hope that nobody would notice this evidence of the gain-of-function origin?

Tuesday, May 11, 2021

Sen. Rand Paul Goes In On Lil'Fauci's Gain Of Function Culpability

NYMag  |  Take, for instance, this paper from 1995: “High Recombination and Mutation Rates in Mouse Hepatitis Viruses Suggest That Coronaviruses May Be Potentially Important Emerging Viruses.” It was written by Dr. Ralph Baric and his bench scientist, Boyd Yount, at the University of North Carolina. Baric, a gravelly voiced former swim champion, described in this early paper how his lab was able to train a coronavirus, MHV, which causes hepatitis in mice, to jump species, so that it could reliably infect BHK (baby-hamster kidney) cell cultures. They did it using serial passaging: repeatedly dosing a mixed solution of mouse cells and hamster cells with mouse-hepatitis virus, while each time decreasing the number of mouse cells and upping the concentration of hamster cells. At first, predictably, the mouse-hepatitis virus couldn’t do much with the hamster cells, which were left almost free of infection, floating in their world of fetal-calf serum. But by the end of the experiment, after dozens of passages through cell cultures, the virus had mutated: It had mastered the trick of parasitizing an unfamiliar rodent. A scourge of mice was transformed into a scourge of hamsters. And there was more: “It is clear that MHV can rapidly alter its species specificity and infect rats and primates,” Baric said. “The resulting virus variants are associated with demyelinating diseases in these alternative species.” (A demyelinating disease is a disease that damages nerve sheaths.) With steady prodding from laboratory science, along with some rhetorical exaggeration, a lowly mouse ailment was morphed into an emergent threat that might potentially cause nerve damage in primates. That is, nerve damage in us.

A few years later, in a further round of “interspecies transfer” experimentation, Baric’s scientists introduced their mouse coronavirus into flasks that held a suspension of African-green-monkey cells, human cells, and pig-testicle cells. Then, in 2002, they announced something even more impressive: They’d found a way to create a full-length infectious clone of the entire mouse-hepatitis genome. Their “infectious construct” replicated itself just like the real thing, they wrote.

Not only that, but they’d figured out how to perform their assembly seamlessly, without any signs of human handiwork. Nobody would know if the virus had been fabricated in a laboratory or grown in nature. Baric called this the “no-see’m method,” and he asserted that it had “broad and largely unappreciated molecular biology applications.” The method was named, he wrote, after a “very small biting insect that is occasionally found on North Carolina beaches.”

In 2006, Baric, Yount, and two other scientists were granted a patent for their invisible method of fabricating a full-length infectious clone using the seamless, no-see’m method. But this time, it wasn’t a clone of the mouse-hepatitis virus — it was a clone of the entire deadly human SARS virus, the one that had emerged from Chinese bats, via civets, in 2002. The Baric Lab came to be known by some scientists as “the Wild Wild West.” In 2007, Baric said that we had entered “the golden age of coronavirus genetics.”

“I would be afraid to look in their freezers,” one virologist told me.

Baric and Shi Zhengli of the Wuhan Institute of Virology, the two top experts on the genetic interplay between bat and human coronaviruses, began collaborating in 2015.

Saturday, March 06, 2021

"We" Don't Know Bupkis Beyond Whatever You Tell "Us" - And You Ain't Told The Truth Yet!!!

bloomberg  |  More than a year after Covid-19 touched off the worst pandemic in more than a century, scientists have yet to determine its origins. The closest related viruses to SARS-CoV-2 were found in bats more than 1,000 miles from the central Chinese city of Wuhan, where the disease erupted in late 2019. Initially, cases were tied to a fresh food market and possibly the wildlife sold there. Other theories allege the virus accidentally escaped from a nearby research laboratory, or entered China via imported frozen food. Amid all the posturing and finger-pointing, governments and scientists agree that deciphering the creation story is key to reducing the risk of future pandemics.

1. Why don’t we know where it came from?

Where, when and how a pathogen crosses the species barrier and begins spreading in humans can be difficult, if not impossible, to pinpoint. Although SARS-CoV-2 is genetically similar to coronaviruses collected from a type of bat, it may have followed a long and convoluted path to Wuhan, a city of 11 million people. Scientists are tracing the earliest known cases to try to establish how they were infected, but the trail backward largely goes cold in early December 2019. Where a new disease starts spreading isn’t necessarily where it spilled over from the animal kingdom to infect the first human. HIV, for instance, is thought to have originated in chimpanzees in southeastern Cameroon, but didn’t begin spreading readily in people until the 1920s, when it reached the city of Kinshasa, hundreds of miles away. Scientists reported that finding in 2014, some three decades after the AIDS pandemic was recognized.

2. Who’s looking?

The World Health Organization was asked in May to help with the research, and a team of 17 international scientists, including one based in the U.S., concluded a four-week joint mission with 17 researchers from China in early February. Their findings are slated to be released in March. Other groups, including an expert panel convened by the medical journal The Lancet called the Covid-19 Commission, are also

3. What do we know so far?

Not much. Bats are the source of two coronaviruses that caused lethal outbreaks in people during the past two decades -- severe acute respiratory syndrome (SARS) and Middle Eastern respiratory syndrome (MERS) -- and the flying mammals are considered the reservoir host for SARS-CoV-2 as well as a plethora of other viruses. (A reservoir host is an animal that harbors a pathogen but isn’t sickened by it.) After SARS-CoV-2 emerged, Shi Zhengli, a virologist who heads a group that studies bat-borne coronaviruses at the Wuhan Institute of Virology, identified three closely related viruses collected during the previous 15 years. The closest, which is about 96% identical to SARS-CoV-2, was isolated from swabs and fecal material from Rhinolophus affinis, a species of horseshoe bat, in the southern Chinese province of Yunnan in 2013. Some researchers have linked that particular virus to a mineshaft in Mojiang county in Yunnan, where six men contracted a pneumonia-like disease in 2012 that killed three of them. Although SARS-CoV-2 and the virus from Yunnan may share a common ancestor, they’re not sufficiently similar to indicate SARS-CoV-2 was derived from the Yunnan virus. Sampling of bats in Hubei, the province of which Wuhan is the capital, haven’t found any positive for the pandemic strain. Coronaviruses sharing certain genetic features with SARS-CoV-2 have been found in other Rhinolophus bat species and pangolins, a scaly, ant-eating mammal, elsewhere in Asia, highlighting the broad distribution of related coronaviruses that may have contributed to SARS-CoV-2’s evolution. That’s led to multiple hypotheses for how and where it emerged.

probing the virus’s origins.

Thursday, July 23, 2020

Zheng-Li Shi..., Gurrl We Coming For Your Dome-Piece


counterpunch |  Our proposal is consistent with all the principal undisputed facts concerning SARS-CoV-2 and its origin. The MMP proposal has the additional benefit of reconciling many observations concerning SARS-CoV-2 that have proven difficult to reconcile with any natural zoonotic hypothesis.

For instance, using different approaches, numerous researchers have concluded that the SARS-CoV-2 spike protein has a very high affinity for the human ACE2 receptor (Walls et al., 2020; Piplani et al., 2020; Shang and Ye et al., 2020; Wrapp et al., 2020). Such exceptional affinities, ten to twenty times as great as that of the original SARS virus, do not arise at random, making it very hard to explain in any other way than for the virus to have been strongly selected in the presence of a human ACE2 receptor (Piplani et al., 2020).

In addition to this, a recent report found that the spike of RaTG13 binds the human ACE2 receptor (Shang and Ye et al., 2020). We proposed above that the virus in the mine directly infected humans lung cells. The main determinant of cell infection and species specificity of coronaviruses is initial receptor binding (Perlman and Netland, 2009). Thus RaTG13, unlike most bat coronaviruses, probably can enter and infect human cells, providing biological plausibility to the idea that the miners became infected with a coronavirus resembling RaTG13.

Moreover, the receptor binding domain (RBD) of SARS-CoV-2, which is the region of the spike that physically contacts the human ACE2 receptor, has recently been crystallised to reveal its spatial structure (Shang and Ye et al., 2020). These authors found close structural similarities between the spikes of SARS-CoV-2 and RaTG13 in how they bound the human ACE2 receptor:

“Second, as with SARS-CoV-2, bat RaTG13 RBM [a region of the RBD] contains a similar four-residue motif in the ACE2 binding ridge, supporting the notion that SARS-CoV-2 may have evolved from RaTG13 or a RaTG13-related bat coronavirus (Extended Data Table 3 and Extended Data Fig. 7). Third, the L486F, Y493Q and D501N residue changes from RaTG13 to SARS CoV-2 enhance ACE2 recognition and may have facilitated the bat-to-human transmission of SARS-CoV-2 (Extended Data Table 3 and Extended Data Fig. 7). A lysine-to-asparagine mutation at the 479 position in the SARS-CoV-2 RBD (corresponding to the 493 position in the SARS-CoV-2 RBD) enabled SARS-CoV to infect humans. Fourth, Leu455 contributes favourably to ACE2 recognition, and it is conserved between RaTG13 and SARS CoV-2; its presence in the SARS CoV-2 RBM may be important for the bat-to-human transmission of SARS-CoV-2″ (Shang and Ye et al., 2020). (italics added)

The significance of this molecular similarity is very great. Coronaviruses have evolved a diverse set of molecular solutions to solve the problem of binding ACE2 (Perlman and Netland, 2009; Forni et al., 2017). The fact that RaTG13 and SARS CoV-2 share the same solution makes RaTG13 a highly likely direct ancestor of Sars-CoV-2.

A further widely noted feature of SARS-CoV-2 is its furin site (Coutard et al., 2020). This site is absent from RaTG13 and other closely related coronaviruses. The most closely related virus with such a site is the highly lethal MERS (which broke out in 2012). Possession of a furin site enables SARS-CoV-2 (like MERS) to infect lungs and many other body tissues (such as the gastrointestinal tract and neurons), explaining much of its lethality (Hoffman et al., 2020; Lamers et al., 2020). However, no convincing explanation for how SARS-CoV-2 acquired this site has yet been offered. Our suggestion is that it arose due to the high selection pressure which existed in the miner’s lungs and which in general worked to ensure that the virus became highly adapted to the lungs. This explanation, which encompasses how SARS-CoV-2 came to target lung tissues in general, is an important aspect of our proposal.

The implication is therefore that the furin site was not acquired by recombination with another coronavirus and simply represents convergent evolution (as suggested by Andersen et al., 2020).
An intriguing alternative possibility is that SARS-CoV-2 acquired its furin site directly from the miner’s lungs. Humans possess an epithelial sodium channel protein called ENaC-a whose furin cleavage site is identical over eight amino acids to SARS-CoV-2 (Anand et al., 2020). ENaC-a protein is present in the same airway epithelial and lung tissues infected by SARS-CoV-2. It is known from plants that positive-stranded RNA viruses recombine readily with host mRNAs (Greene and Allison, 1994; Greene and Allison, 1996; Lommel and Xiong, 1991; Borja et al., 2007). The same evidence base is not available for positive-stranded animal RNA viruses, (though see Gorbalenya, 1992) but if plant viruses are a guide then acquisition of its furin site via recombination with the mRNA which encodes ENaC-a by SARS-CoV-2 is a strong possibility.

A further feature of SARS-CoV-2 has been the very limited adaptive evolution of its genome since the pandemic began (Zhan et al., 2020; van Dorp et al., 2020; Starr et al., 2020). It is a well-established principle that viruses that jump species undergo accelerated evolutionary change in their new host (e.g. Baric et al., 1997). Thus, SARS and MERS (both coronaviruses) underwent rapid and readily detectable adaptation to their new human hosts (Forni et al., 2017; Dudas and Rambaut, 2016). Such an adaptation period has not been observed for SARS-CoV-2 even though it has now infected many more individuals than SARS or MERS did. This has even led to suggestions that the SARS-CoV-2 virus had a period of cryptic circulation in humans infections that predated the pandemic (Chaw et al., 2020). The sole mutation consistently observed to accumulate across multiple studies is a D614G substitution in the spike protein (e.g. Korber et al., 2020). The numerically largest analysis of SARS-CoV-2 genomes, however, found no evidence at all for adaptive evolution, even for D614G (van Dorp et al., 2020).

The general observation is therefore that Sars-CoV-2 has remained functionally unchanged or virtually so (except for inconsequential genetic changes) since the pandemic began. This is a very important observation. It implies that SARS-CoV-2 is highly adapted across its whole set of component proteins and not just at the spike (Zhan et al., 2020). That is to say, its evolutionary leap to humans was completed before the 2019 pandemic began.

It is hard to imagine an explanation for this high adaptiveness other than some kind of passaging in a human body (Zhan et al., 2020). Not even passaging in human cells could have achieved such an outcome.

Two examples illustrate this point. In a follow up to Shang and Ye et al., (2020), a similar group of Minnesota researchers identified a distinct strategy by which the spike (S) protein (which contains the receptor bind domain; RBD) of SARS-CoV-2 evades the human immune system (Shang and Wan et al., 2020). This strategy involves more effective hiding of its RBD, but it implies again that the spike and the RBD evolved in tandem and in the presence of the human immune system (i.e. in a human body and not in tissue culture).

The Andersen authors, in their critique of a possible engineered origin for SARS-CoV-2, also stress the need for passaging in whole humans:

“Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred during cell-culture passage, as such features suggest the involvement of an immune system” (Andersen et al., 2020).

The final point that we would like to make is that the principal zoonotic origin thesis is the one proposed by Andersen et al. Apart from being poorly supported this thesis is very complex. It requires two species jumps, at least two recombination events between quite distantly related coronaviruses and the physical transfer of a pangolin (having a coronavirus infection) from outside China (Andersen et al., 2020). Even then it provides no logical explanation of the adaptedness of SARS-CoV-2 across its whole genome or why the virus emerged in Wuhan.

By contrast, our MMP proposal requires only the one species jump, which is documented in the Master’s thesis. Although we do not rule out a possible role for mixed infections in the lungs of the miners, nor the possibility of recombination between closely related variants in those lungs, nor the potential acquisition of the furin site from a host mRNA, only mutation was needed to derive SARS-CoV-2 from RaTG13. Hence our attention earlier to the figure from P. Zhou et al., 2020showing that RaTG13 is the most closely related virus to SARS-CoV-2 over its entire length. This extended similarity is perfectly consistent with a mutational origin of SARS-CoV-2 from RaTG13.

In short, the MMP theory is a plausible and parsimonious explanation of all the key features of the COVID-19 pandemic and its origin. It accounts for the propensity of SARS-CoV-2 infections to target the lungs; the apparent preadapted nature of the virus; and its transmission from bats in Yunnan to humans in Wuhan.

Wednesday, April 29, 2020

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.

Saturday, April 04, 2020

Shi Zhengli's Student Huang Yan Ling Mysteriously Disappeared


WaPo | The story of how the novel coronavirus emerged in Wuhan, China, has produced a nasty propaganda battle between the United States and China. The two sides have traded some of the sharpest charges made between two nations since the Soviet Union in 1985 falsely accused the CIA of manufacturing AIDS.

U.S. intelligence officials don’t think the pandemic was caused by deliberate wrongdoing. The outbreak that has now swept the world instead began with a simpler story, albeit one with tragic consequences: The prime suspect is “natural” transmission from bats to humans, perhaps through unsanitary markets. But scientists don’t rule out that an accident at a research laboratory in Wuhan might have spread a deadly bat virus that had been collected for scientific study.

“Good science, bad safety” is how Sen. Tom Cotton (R-Ark.) put this theory in a Feb. 16 tweet. He ranked such a breach (or natural transmission) as more likely than two extreme possibilities: an accidental leak of an “engineered bioweapon” or a “deliberate release.” Cotton’s earlier loose talk about bioweapons set off a furor, back when he first raised it in late January and called the outbreak “worse than Chernobyl.”

President Trump and Secretary of State Mike Pompeo added to the bile last month by describing the coronavirus as the “Chinese virus” and the “Wuhan virus,” respectively.

China dished wild, irresponsible allegations of its own. On March 12, Chinese foreign ministry spokesman Lijian Zhao charged in a tweet: “It might be [the] US army who brought the epidemic to Wuhan.” He retweeted an article that claimed, without evidence, that U.S. troops might have spread the virus when they attended the World Military Games in Wuhan in October 2019.

China retreated on March 22, when Ambassador to the United States Cui Tiankai told “Axios on HBO” that such rumors were “crazy” on both sides. A State Department spokesman said Cui’s comment was “welcome,” and Trump and Chinese President Xi Jinping pledged in a March 27 phone call to “focus on cooperative behavior,” a senior administration official told me.