Showing posts with label propaganda. Show all posts
Showing posts with label propaganda. Show all posts

Monday, March 23, 2020

"The problem of SARS-CoV-2 is probably overestimated“ - The conclusion of a new French study in the Journal of Antimicrobial Agents, titled "SARS-CoV-2: fear versus data"

from reddit:

There is an excellent piece of on-going research into the SARS-CoV-2 pandemic being done by a Swiss Doctor over on SwissPropagandaResearch. They are making new updates everyday, and have been doing for over a week.
Here are the updates for today, 23rd March 2020:
  • A new French study in the Journal of Antimicrobial Agents, titled SARS-CoV-2: fear versus data, concludes that „the problem of SARS-CoV-2 is probably overestimated“, since „the mortality rate for SARS-CoV-2 is not significantly different from that for common coronaviruses identified at the study hospital in France“.
  • An Italian study of August 2019 (https://www.ijidonline.com/article/S1201-9712(19)30328-5/fulltext) found that flu deaths in Italy were between 7,000 and 25,000 in recent years. This value is higher than in most other European countries due to the large elderly population in Italy, and much higher than anything attributed to Covid-19 so far.
  • In a new fact sheet, the World Health Organization WHO reports that Covid-19 is in fact spreading slower, not faster, than influenza by a factor of about 50%. Moreover, pre-symptomatic transmission appears to be much lower with Covid-19 than with influenza.
  • A leading Italian doctor reports that „strange cases of pneumonia“ were seen in the Lombardy region already in November 2019, raising again the question if they were caused by the new virus (which officially only appeared in Italy in February 2020), or by other factors, such as the dangerously high smog levels in Northern Italy.
  • Danish researcher Peter Gøtzsche, founder of the renowned Cochrane Medical Collaboration, writes that Corona is „an epidemic of mass panic“ and „logic was one of the first victims.“
  • Former Israeli Health Minister, Professor Yoram Lass, says that the new coronavirus is „less dangerous than the flu“ and lockdown measures „will kill more people than the virus“. He adds that „the numbers do not match the panic“ and „psychology is prevailing over science“. He also notes that „Italy is known for its enormous morbidity in respiratory problems, more than three times any other European country.“
  • Pietro Vernazza, a Swiss infectious disease specialist, argues that many of the imposed measures are not based on science and should be reversed. According to Vernazza, mass testing makes no sense because 90% of the population will see no symptoms, and lockdowns and closing schools are even „counterproductive“. He recommends protecting only risk groups while keeping the economy and society at large undisturbed.
  • The President of the World Doctors Federation, Frank Ulrich Montgomery, argues that lockdown measures as in Italy are „unreasonable“ and „counterproductive“ and should be reversed.
  • Switzerland: Despite media panic, excess mortality still at or near zero: the latest testpositive „victims“ were a 96yo in palliative care and a 97yo with pre-existing conditions.
  • The latest statistical report of the Italian National Health Institute is now available in English.


Saturday, March 21, 2020

Logistical and Technical Exploration into the Origins of the Wuhan Strain of Coronavirus (COVID-19)

 Posted on January 31, 2020 by harvard2thebighouse   

This report is the product of a collaboration between a retired professional scientist with dozens of peer-reviewed publications and 30 years of experience in genomic sequencing and analysis, who worked at the Theoretical Biology Division of the Los Alamos National Laboratory and later helped design several ubiquitous bioinformatic software tools, as well as a former NSA counterterrorism analyst. It considers whether the Wuhan Strain of coronavirus (COVID-19) is the result of naturally emergent mutations against the possibility that it may be a bio-engineered strain – directly altered by genetic manipulation, subject to artificially-guided evolutionary selection, or both – most likely released into the public by accident since China’s rate of occupational accidents is about ten-times higher than America’s, and some twenty-times more than Europe’s, the only other regions with high-level virology labs.

Raising the odds of an accidental release, researchers from China’s only BSL-4 lab in Wuhan were reported to have particularly sloppy field research methods, being both bled and peed on by local bats that host coronaviruses remarkably similar to the Wuhan Strain COVID-19. And they’ve also been reported to smuggle used research animals out of their labs, selling them for cash on the street. Perhaps unsurprisingly, in mid February the Chinese Ministry of Science sent out a directive to all its labs emphasizing the important of carefully handling bio-infectious agents and alluding to slack oversight and past lapses, even mentioning coronaviruses specifically.

Mistakes may have been precipitated by the need to quickly finish research that was being rushed for John Hopkins’ Event 201 which was held this past October and meant to gameplan the containment of a global pandemic. Research may also have been hurried due to deadlines before the impending Chinese New Year – the timing of these events point to increased human error, not a globalist conspiracy. Beijing has had four known accidental leaks of the SARS virus in recent years, so there is absolutely no reason to assume that this strain of coronavirus from Wuhan didn’t accidentally leak out as well. This is unlikely to be a plot twist in one of the novels Tom Clancy wrote after he started mailing it in.

Simply and horribly, this is likely to become another Chernobyl or Fukushima – a catastrophic illustration of mankind’s hubris and intransigence clashing with Nature, as fate again reaps a once unimaginably tragic toll.

Given that this outbreak was said to begin in late December when most bat species in the region are hibernating and the Chinese horseshoe bat’s habitat covers an enormous swath of the region containing scores of cities and hundreds of millions people, the fact that this Wuhan Strain of coronavirus, denoted as COVID-19, emerged in close proximity to the only BSL-4 virology lab in China, which in turn was staffed with at least two Chinese scientists – Zhengli Shi and Xing-Yi Ge – both virologists who had previously worked at an American lab which had already bio-engineered an incredibly virulent strain of bat coronavirus – the accidental release of a bio-engineered virus from Wuhan’s virology lab cannot be automatically discounted, especially when the Wuhan Strain’s unnatural genomic signals are considered.

UPDATE 2/14, 3:02am EST: A probable smoking pre-print has been released, by the National Natural Science Foundation of China:

    “In summary, somebody was entangled with the evolution of 2019-nCoV coronavirus. In addition to origins of natural recombination and intermediate host, the killer coronavirus probably originated from a laboratory in Wuhan.”

In a predictable turn, that article has been removed and both researchers have since deleted their profiles off of the ResearchGate site completely. Furthering the appearance of a cover-up, back on January 2nd, the Wuhan Institute of Virology’s director sent out a memo forbidding discussion of an “unknown pneumonia in Wuhan” after ordering the destruction of all related lab materials a day earlier, making it abundantly clear that the Chinese government knew about this outbreak long before they took any steps to contain it, or made any public announcement.

These propaganda efforts have been bolstered by possible collusion from American scientists, some of which is detailed below – but also most notably by one Peter Daszak, who had been publishing papers on coronaviruses alongside the primary Chinese person-of-interest, Zhengli Shi, for years. Perhaps most notably, Daszak is listed as a co-author in the paper first documenting the isolation of a coronavirus from a bat that targets the ACE2 receptor – just like COVID-19 – research done in Wuhan’s virology lab and supervised by Zhengli Shi, and led by a second suspect Chinese researcher who you’ll meet below. At best, Daszak is perhaps acting as an unwitting agent of the Chinese government, but regardless holds an enormous conflict-of-interest. And if nothing else, it is wildly irresponsible to speak-out against the possibility that the virus got out of a lab when a natural origin has not been conclusively demonstrated. Daszak’s statement in The Lancet is either incompetence, or is meant to be a smokescreen for the wanton hubris and greed that have fueled the gain-of-function research detailed below: As one possible related project which may have overlapped with this one, coronaviruses have been seen as a viable vector for an HIV vaccine for years – a project with hundreds of millions of dollars dangling over it.

And unfortunately Daszak is far from alone, there are countless “journalists” mindlessly regurgitating statements from the Chinese government and the WHO with no effort to fact-check whatsoever, as well as “scientists” whose real job is running PR for pharmaceutical and research companies who have spent weeks serving China by making extraordinarily misleading and overconfident statements to the public about the origins and capabilities of this virus. And it should be noted that in 2018, the esteemed scientific journal Nature – which has published numerous articles speciously claiming this virus is definitely natural – was revealed to have buckled to censorship demands from the Chinese government, killing over 1,000 articles to placate their Chinese partners.

Many involved in this dissimulation are effectively acting as agents of a foreign government, and they have left most Americans entirely unprepared for the tragedy that’s beginning to occur in our nursing homes and hospitals. If the idea that just maybe this thing came from a lab had been part of the national dialogue from the start – wouldn’t everyone have been much more cautious and open to social distancing and other limitations once the need arose?

And so being an offshoot of this sort of vaccine program, possibly as a Red Team designed to build defenses and therapeutics against, is just one possible gain-of-function pursuit that would fit some of the unusual genomic and logistical picture below. Whether or not it was the exact target of the Wuhan lab’s genomic tinkering – the reality is millions of dollars of funding from multiple world governments have poured into this research, funding that’s dangled over these scientists as they’ve chased it like Icarus, this time not just risking their own lives – but hundreds of millions of others as well.

Subsequently, we are calling for an immediate end to dual-use gain-of-function research.

– In 2002, Stony Brook first assembled a DNA virus from scratch, building a polio-virus, and providing proof-of-concept for the creation, alteration, and manipulation of DNA-virus genomes. Two years prior, a separate team had already built an simpler RNA-virus from scratch – choosing to engineer a coronavirus from the ground up, and even swapping out its vital spike-protein genes to make it more infectious. And a generation earlier, artificially enhancing selection by intentionally infecting countless series of lab animals with different viruses is understood to have created the H1N1 Swine Flu. Its Franken-genome has a mysterious untraceable genetic parentage and a “clear unnatural origin,” and H1N1 became the poster-child for a moratorium against gain-of-function research – experimentation that seeks to increase a pathogen’s virulence, creating a more effective double-edged sword to counter and learn from. A ban that was in place for years, but was recently lifted by the American government. In the case of H1N1, it wasn’t a question of if it’d escaped from a research laboratory, only whether it’d been designed as part of a weapons system, or been part of a vaccine trial.

– When a virus manages to infect a new species of host it’s known as a zoonotic jump, a process that generally takes months or even years to complete. The first stage is when a virus infects one individual in a new host species, which is typically a dead-end the first time it happens since there’s no way for the virus to be adapted to a different species’ biology. The second stage of a zoonotic jump is when the virus manages to move from the first new host into more hosts of the new species, which results in some temporary transmission in a localized area – these are known as endemics and generally fizzle out the first few times they happen as the virus adapts to its new host species, and mutations win or lose the survival battle. The final stage, the only time a zoonotic jump is considered complete, is when there’s sustained host-to-host transmission in the new species. These zoonotic jumps have some predictable characteristics, the primary one is that adapting to a new host inevitably requires mutations that weren’t optimal in the old host. And so the virus gets weakened as its initially attempting to jump into a new host species, which is why the above sequence of steps – one new host, a few new hosts that pass it among themselves temporarily, and then finally sustained transmission – takes at least several months if not years to play out, since a good bit of time is required for all three steps to occur. Viral trial-and-error is required for the virus to find the right mutations that will allow it to prosper in a new host species, it’s never been known to just happen magically all at once.

– And so assuming that COVID-19 emerged naturally in a matter of weeks in the middle of a massive urban metropolis the size of New York City, when the host population of bats was hibernating anyways, requires completely ignoring everything we know about how viruses transfer between species. Not only was Wuhan’s population not interacting with bats since they hardly interact with humans in urban situations to begin with, but any possible host bats were sleeping in their caves anyways. And not only would the circumstances of this transfer require rewriting the textbooks on zoonotic jumps if it occurred it all, but beyond that: supposedly not only did a zoonotic jump happen instantly without the necessary steps, but when it hit humans it was extraordinarily virulent from the start, something that’s supposed to take an extensive amount of time to ever happen as mutations go through selective trial-and-error. This trial-and-error takes time and is why viruses have never made a zoonotic jump and been instantly virulent in a new host species like COVID-19 has been in humans. Nothing we know about how viruses naturally make zoonotic jumps point to that happening here.

– Tinkering with viral genomes is not anything new, but is not something that has ever been fully embraced by the scientific community at large. About a decade ago, two separate research teams successful tweaked the genome of the H5N1 Bird Flu in just two spots and then passed it through ferrets until it became both airborne and pathogenic to mammals, creating a virus that “could make the deadly 1918 pandemic look like a pesky cold.” This involved selecting for a mutation that allowed the virus to access a receptor that’s found in ferret lungs, and was alarming enough that the research was urged to be published without revealing the specific methods involved and data collected – however it appears that only the most technical details were left out, and most of the research is freely available.

– By 2015, conducting research that was met with an enormous amount of concern, scientists at UNC had successfully created a “chimeric, SARS-like virus” by altering the viral genome of a Chinese bat coronavirus’s spike-protein genes – sequences that code for the spikes that poke out from surface of viruses and allow them to unlock entry into hosts, in this case making the bio-engineered coronavirus incredibly contagious. This research raised eyebrows since it was clearly gain-of-function research, a practice banned in America from 2014 until December 2017 when NIH lifted the ban, specifically to allow research on this sort of virus. Looking at UNC’s gain-of-function research on coronavirus spike-proteins, which received its funding just before the ban was implemented and was only allowed to go forward following a special review, a virologist with the Louis Pasteur Institute of Paris warned: “If the [new] virus escaped, nobody could predict the trajectory.”

– But then oddly, in late January right as the pandemic was blooming, Dr. Ralph Baric claimed in an interview that people should be more concerned with the seasonal flu – despite having personally overseen the controversial engineering of a hyper-virulent strain of batty coronavirus just a few years back. Immediately discounting the burgeoning outbreak of an unknown coronavirus as a non-event seems particularly troubling for someone who’d trained two Chinese scientists on how to make hyper-virulent coronaviruses, especially when it’s hard to imagine that Dr. Baric was unaware his past colleagues were now working at the Wuhan Virology Lab, the epicenter of the outbreak. Highlighting the dissembling absurdity of this statement, based on reporting from Who: the Wuhan Strain COVID-19 appears to be thirty-four times more lethal than the seasonal flu.

– Scientists have expressed concern about China’s ability to safely monitor this BSL-4 lab in Wuhan since it opened in 2017: “an open culture is important to keeping BSL-4 labs safe, and he questions how easy this will be in China, where society emphasizes hierarchy. ‘Diversity of viewpoint, flat structures where everyone feels free to speak up and openness of information are important.'” This lab is at most 20 miles from the wet market where the virus had been assumed to have jumped from animal to human. However the idea that a Chinese lab could have a viral sample escape is well-documented – as mentioned, one lab in Beijing has had four separate incidents of the SARS virus leaking out accidentally.

– Notably, the first three known cases from early December had no contact with that market, and roughly one-third of the initial exposed cohort had no direct ties to Wusan’s wild meat wet-market, the original presumptive source of the virus. And in mid February, reporting indicated that COVID-19’s patient zero in fact had no connection at all with the wet-market. This is reinforced by the fact Chinese research has also concluded that COVID-19 “may have begun human-to-human transmission in late November from a place other than the Huanan seafood market in Wuhan.”

– Since its discovery, scientists have been unable to fully determine the zoological origins of COVID-19, it was initially thought to have passed through snakes, but now all that’s agreed upon is that it’s mostly bat in origin. This inability to derive an exact zoological source is exactly what would be expected if the virus had been artificially engineered to target humans as UNC already has, this doesn’t prove an artificial nature – but it is consistent with one. Although there has been speculation that pangolins may have been the missing vector, the only data about the pangolin virome wasn’t entered into NCBI’s system until late January, and couldn’t possibly have been collected any earlier than late September 2019, and doesn’t fully answer the vector question anyways. And further research indicated it was “very unlikely” that similarities between their spike-protein genomes of COVID-19 and pangolins, where they share the most similarities, was due to the virus passing through pangolins at all.

– As explained in Nature, COVID-19’s Franken-genome combines a cornucopia of distinct genetic markers from each of the three other distinct branches of the coronavirus family tree, but is distinct enough from all of them that it in fact forms its own clade. Along those same lines, a full-genome evolutionary analysis of COVID-19 published in The Lancet concluded, “recombination is probably not the reason for emergence of this virus” since it seems that the Wuhan Strain isn’t a mosaic of previously known coronaviruses, but instead draws from distant, discrete parts of the coronavirus family tree – not how these viruses naturally evolve. Because even mixing and matching coronavirus genomes from every known zoological virus, scientists couldn’t find any possible combination that would explain those regions of the Wuhan Strain’s genome. The Lancet muses that a mysterious animal host could still be out there, however since they’ve already searched through every known possibility and been unable to find a match, another obvious explanation is that bio-engineering accounts for the inexplicable nucleotide signature of the Wuhan Strain’s genome

– Early research found that COVID-19 targets the ACE2 receptor, which seems to be distributed in roughly equal proportions across global populations, indicating that the Wuhan Strain was likely developed as part of a defensive gain-of-function project possibly linked to immunotherapy or vaccinations – never meant to leave the lab, but meant to serve as a Red Team to fight back against, not as an offensive weapon targeting one specific global population. But counter-intuitively, researchers have pointed out that the most critical sections of the COVID-19’s protein-spike genome don’t match the previously reported pattern that would be expected for optimal binding to the specific ACE2 receptors found only in humans and ferrets, which indicates that these particular segments wouldn’t have been directly genetically engineered to increase virulence.

– And yet this is exactly what researchers looking for a “safe” vaccine candidate would engineer, and doesn’t rule out a scenario where the virus was passed through a series of ferrets. The research team in fact notes that its spike “appears to be the result of selection on human or human-like ACE2 permitting another optimal binding solution to arise,” failing to directly mention that the only other human-like receptors are found in ferrets – which have frequently been used for years in vaccine trials for viruses with this sort of protein-spike, and is exactly how the H5N1 Bird Flu virus was altered to make it airborne. And so the Wuhan Strain’s unique affinity for the human ACE2 receptor, which a pre-print reports to be 10 to 20 times greater than SARS, may be the exact type of vaccine-related accident that led to the moratorium on gain-of-function research in the first place and caused scientists to unsuccessfully call for the research around H5N1 to be partially sealed-off.

– The Wuhan Strain of coronavirus, COVID-19, appears to be transmissible even before its host shows any symptoms at all, making temperature-scanning at airports ineffective since hosts appear to be contagious for about a week before any symptoms emerge. This is in stark contrast with SARS, whose hosts weren’t contagious until they were symptomatic, allowing for its relatively quick containment. This chart is not from a peer-reviewed source but was claims to capture the comparative rates of infections between recent outbreaks. A recent pre-print now gives COVID-19 a rating of R4, meaning each host passes the virus on to four new victims, a rate significantly higher than any past global viral outbreak.

– The successful end results of the aforementioned  bat coronavirus bio-engineering research at UNC that was critiqued for being too risky in 2015, was published the following year and described the successful bio-engineering of a highly-virulent coronavirus derived from bats which was achieved by tinkering with its spike-protein genes. In this paper, researcher #8 is listed as one “Zheng-li Shi” who’s listed as being attached to the “Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.”

– Zhengli Shi seems to have returned to Wuhan at some point since 2016, specifically to the Wuhan Institute of Virology’s Disease Engineering Technical Research Center,  since she then appears in this September 2019 paper on the human behaviors most likely to lead to bat-borne coronavirus exposure in southern China, and also in the paper claiming that this coronavirus was bat in origin, which was peculiarly submitted in coordination with the announcement of the outbreak. Very, very peculiarly. She also appears in this pending preprint on the current outbreak of COVID-19, just a small sample of the dozens of coronavirus-related papers she’s published over a three decade career.

– Not only does Zhengli Shi provide a direct chain of expertise tying the already successful bio-engineering of a virulent bat-based coronavirus at UNC directly to the BSL-4 virology lab in Wuhan, but back in January 2014 she’d received a $665,000 grant from NIH for a study titled The Ecology of Bat Coronaviruses and the Risk of Future Coronavirus Emergence (NIAID R01 AI1 10964) as well as $559,500 more from USAID for a study titled Emerging Pandemic Threats PREDICT_2China (Project No. AID-OAA-A-14-00102). Beyond this American funding specifically into viral diseases zoonotically transferring from animals to humans which would slipped in just before the ban, over the years she’s also received around $3 million in grants to study these zoonotic viruses from China and other countries, and has served on the editorial board of several virological research magazines. More of her research into the intersection of coronaviruses like the Wuhan Strain and their epidemic potential was funded by the U.S. Department of Defense, the U.S. Threat Reduction Agency, and U.S. Biological Defense Research Directorate of the Naval Medical Research Center.

– And so a scientist who’s been prolifically involved with studying the molecular interaction of coronaviruses and humanity, spending decades and millions of dollars, and having even helped build a hyper-virulent coronavirus from scratch at UNC – just so happens to be working at the only BSL-4 virology lab in China that also just so happens to be at the epicenter of an outbreak involved a coronavirus that’s escaping zoological classification, and has other unnatural characteristics that will be discussed below.

– Another Chinese virologist, Xing-Yi Ge, appears as an author on the 2016 UNC paper and is also attached to the lab in Wuhan. Previously in 2013, he’d successfully isolated a SARS-like coronavirus from bats which targets the ACE2 receptor, just like our present virus, the Wuhan Coronavirus COVID-19 uses. And it turns out that sections of the Wuhan Strain’s ACE2 receptor’s genes are unique: they’re almost identical to SARS’s spike-protein genes – despite the fact that almost none of the two coronavirus’s genomes are similar anywhere else at all. Beyond that, although the Wuhan Strain’s spike-protein genome differs from SARS in four out of the five most important genomic spots that determine binding to the ACE2 receptor, they surprisingly don’t effect the protein-spike’s shape. And in an even bigger coincidence, these four spots also code for the outside region of the spike that allows entry into cells, and do not effect it either – allowing the Wuhan Strain to still use the ACE2 receptor to unlock cells while possibly gaining additional capabilities. The odds that this concordance was bio-engineered into the virus are several orders of magnitude more likely than for this to randomly have evolved in nature, and is exactly the sort of process used to make the H5N1 Bird Flu airborne and highly pathogenic.

– Numerous videos purportedly from inside hospitals in Wuhan depict a crisis that is far greater than the numbers released by China to date. There is widespread but unverified online reporting that Wuhan crematoriums have been running 24/7, which is consistent with a recent peer-reviewed study that claims that as of January 25, Wuhan had over 75,000 infections – when the official number was just 761. Chinese language social media also reflects a sense of panic and desperation that is highly discordant with the numbers being released by the Chinese government. Who, notably, are refusing any direct assistance from the American CDC. (Evidence that China is vastly downplaying this pandemic’s severity: Example 1. Example 2. Example 3. Example 4. Example 5. Example 6.)

– Some of the dystopian carnage creeping across China may be due to the fact that much of China’s population may have already been exposed to coronavirus infection via SARS or other less notorious strains, which would allow the Wuhan Stain COVID-19 to use antibody-dependent enhancement (ADE) to much more efficiently enter into cells, and then become much more virulent since this enhancement hijacks the body’s preexisting immune response to coronavirus infections and allows easier entry. However whether or not people have been exposed to a coronavirus infection before, once it’s been circulating in a population for long enough the Wuhan Strain may be able to reinfect its own past hosts and use this molecular hijacking on antibodies left from its own previous infection to become far more virulent, regardless of whether or not someone has been exposed to other coronaviruses before COVID-19. And early reporting from Chinese doctors indicates that re-infections of the Wuhan Strain are far more lethal than the first. More evidence that ADE is occurring is its much higher affinity for the ACE2 receptor and far higher viral loads compared to SARS – both of these may be due at least in part to ADE allowing COVID-19 to much more efficiently bind to and enter cells. And another hint that the Wuhan Strain may be using ADE to more effectively attack its host is the fact that it seems to be targeting its host’s neurological systems, which is explored in depth below. A final clue is the fact that children seem to be far less effected by the Wuhan Strain COVID-19, a phenomenon that’s found in Dengue Fever, which is one of the classic examples for ADE.

– Another peculiar characteristic is COVID-19’s similarities to HIV. And so although another since-retracted pre-print noted several very short genomic sequences in COVID-19’s spike-protein gene that look far more similar to sequences found in HIV than to other coronaviruses – critics quickly pointed out that the shared homology didn’t reach statistical significance. However a closer look at the data reveals that there were a few small shared genomic segments that, despite being physically separated from each other along each strand of DNA, all worked together to code for the Wuhan Strain’s protein-spike’s crucial receptor binding site. Something that is highly unlikely to have happened by chance. And despite most of its protein-spike being shared with SARS, these substituted segments weren’t shared at all – nor were they found in any other coronavirus. One possible but likely reason for these HIV-like segments is that they were meant to be epitopes, or molecular flags meant to mark intruders for a vaccine to target – meaning the Wuhan Strain was built as a monster for a specific vaccine to hunt. It is mathematically possible for this to happen in nature – but only in a ten-thousand bats chained to ten-thousand Petri dishes and given until infinity sense. Alternatively, this pattern could also be produced by infecting a room full of ferrets with a bespoke coronavirus and sifting through the wreckage for your genomic needle.

– Critics have brushed off the Wuhan Strain’s shared homology with HIV as statistically insignificant, however clinical reporting indicates that the Wuhan Strain may be using this shared HIV homology to attack CD4 immune cells just like HIV does, as an unusually high percentage of patients are showing low white blood cell counts, especially the sickest ones. This pathogenicity may well be due to the unique HIV-live genomics of the Wuhan Strain, as one white-paper by LSU’s professor emeritus of Microbiology, Immunology, and Parasitology who’s also a Harvard-educated virologist with a PhD in Microbiology and Molecular Genetics notes: “This is the first description of a possible immunosuppressive domain in coronaviruses… The three key [mutations] common to the known immunosuppressive domains are also in common with the sequence from [the spike-protein]. While coronaviruses are not known for general immunosuppression of the style shown by HIV-1, this does not rule out immunosuppression at the site of active infection in the lung, which would prolong and potentially worsen infection at that site.” And early research has indicated that this unique region may make COVID-19 up to 1,000 times more likely to bind to human cells than SARS, which could be due to either this homology or to ADE, or some combination of these or other factors.

– Even more troubling, a peer-reviewed study noted that one particular part of the Wuhan Strain’s spike-protein genome also wasn’t found in any of its relatives, “and may provide a gain-of-function to [COVID-19] for efficient spreading in the human population.”  And according to that paper, this particular type of furin cleavage site makes similar viruses both more pathogenic and more neurotoxic. Additionally, this particular type of cleavage site is a hallmark of being passed through a series of animal hosts in a lab. Evidence for the Wuhan Strain’s neurotoxicity arrived in late February, in a published paper which notes that “the most characteristic symptom of COVID‐19 patients is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously.” Combined with the observation that “some COVID‐19 patients also showed neurologic signs such as headache, nausea and vomiting,” this paper asserts that since SARS was found heavily concentrated in the brainstems of its autopsied victims, COVID-19 is also probably crossing the blood-brain barrier and killing its victims not just via pneumonia, but also by causing neurological respiratory failure. Indicating that ADE may be occurring, but at a much faster rate than nature allows since reinfections of Dengue Fever that use ADE typically have years pass between them.

– And it should be noted that SARS – much ballyhooed as a close relative to the Wuhan Strain – didn’t notable effect white blood cell counts.  Additionally, clinical treatment guides published online in late January by established Chinese medical sources note the progressive reduction of white blood cells, as well as the importance of monitoring this decline. And reporting from Thailand indicates that adding a cocktail of two different anti-HIV drugs to the typical flu treatment regime seemed to effectively knock back the Wuhan Strain. Additionally, one of the only autopsies performed outside of China to date found that the deceased had a severely depleted white blood cell count. These lowered counts may come from this shared similarity with HIV, or it could also be the result of ADE as well, since this phenomenon primarily targets white blood cells for its hijackings and may help explain why consecutive infections are so lethal.

– In a highly concerning turn, scientists have noted that the Wuhan Strain can have a “striking” short term rate of mutation which doesn’t indicate an artificial origin but captures the unique threat posed by this coronavirus regardless of its providence, since a faster mutation rates makes it more likely this virus can dodge testing and neutralize vaccines. Something there is already early evidence for. Further concerning are reports out of China that even patients who appear cured still harbor COVID-19 in their system, and although the full implications of this are not yet known – none of them are good.

– One of the worst possible scenarios for COVID-19’s mutation rate would be if it falls into the Goldilocks range that would allow it to form mutant viral swarms: too many mutations will cause a virus to eventually implode, not enough allows host immune systems to catch-up, but if things are just right mutant swarms can form and spread across host populations, burrowing into host nervous systems and causing permanent neurological damage. Mutant swarms form when a virus produces mutationally-damaged copies of itself inside a host, some of which aren’t infectious but find their way into the nervous system where they burrow in causing damage, and others that combine with complimentary broken copies inside host cells to produce working infectious copies of the virus. So a host can not only become crippled with neurological issues, but also still be producing infectious copies of the virus. And it seems as if COVID-19 has many characteristics that indicate the potential to form mutant swarms: the “striking” mutation rate mentioned above and the fact a second widespread mutated strain seems to have already emerged in Washington State with many other isolated strains reported elsewhere, crossing between species is another factor and a dog in Hong Kong appears to have tested positive, the fact that the Wuhan Strain can infect not only the respiratory tract but feces as well – multi-organ involvement is an important contributor to viral swarms, and finally the markedly viral load rate of COVID-19 compared to SARS – SARS produced a viral load several times lower which decreased over time, while COVID-19 produces a “very high” viral load that appears to increase over time and can peak several orders of magnitude higher than SARS was measured to reach. And alarming evidence that this phenomenon is occurring emerged from a Chinese pre-print which noted that over one-third of the roughly 200 patients studied has some neurological symptoms, with nearly half of the most severe patients exhibiting neurological issues. And further evidence for the possibility of both mutant swarms and ADE is witnessed by a study published in Lancet, which notes that the case fatality rate in Wuhan could actually be as high as 20% – the outbreak’s epicenter would be expected to have the highest rates of both phenomena as different variants of the Wuhan Strain infected and reinfected overlapping hosts.

– Another exceptional and atypical trait of the Wuhan Strain COVID-19 is that not only does it form its own clade, it’s calculated to have diverged from SARS and its other sister coronaviruses some 260 years ago. And yet in all that time, while it every other branch of the coronavirus tree was busy branching-off into countless variants, if it emerged naturally, COVID-19 somehow spent a quarter of a millennium as the lone known example of its clade, somehow not mutating into related lineages in all that time. Another simpler explanation is that this apparent hereditary distance and genetic uniqueness is the just the result of being altered in a lab. And although two distinct strains of COVID-19 have been identified, there’s no reason to believe this mutational differentiation happened before contact with humans in the winter of 2019. Additionally, when neutral sites, the specific points in the genome which most reliably show evolutionary change, were examined: COVID-19 looks even more evolutionarily distant from any of its possible relatives, which would make sense if all that evolutionary distance was gained by artificially accelerated generational turn-over in a lab.

– Also giving credence to the idea that the Wuhan Strain was bio-engineered is the existence of a patent application registered to a scientist from Wuhan that looks to modulate a coronavirus’ spike-protein genes – the precise region altered by Zhengli Shi at UNC to make a hyper-virulent strain of coronavirus, and whose alteration and adaptation would explain the Wuhan Strain’s unusual behavior as discussed above.

– And curiously, the head of Harvard’s Chemistry Department, Dr. Charles Lieber, was arrested in the midst of this outbreak on charges that he’d been accepting millions of dollars in bribes from the Chinese government. According to his charging documents, Dr. Lieber first went to the Wuhan University of Technology (WUT), in November 2011 to participate in a nanotechnology forum, which was when he was recruited into a bribery scheme that would net him several million dollars to “establish a research lab and conduct research at WUT,” which became known as ” Joint Nano Key Laboratory,” as well as mentor and advocate for graduate students. By 2015, Dr. Lieber appeared to be fairly intimately involved with what seemed to begin as simply a nanotechnology lab, but now had shifted to involve biology as well, since he described visiting the lab multiple times per year “as we try to build up the nano-bio part of the lab.” Whether or not this nano-bio part of the Nano Key Laboratory is related to Wuhan’s BSL-4 virology lab isn’t clear, however if the Wuhan Strain was bio-engineered, technology classified as “nano-bio” would’ve almost certainly played a role.

Given the above facts, either:

– A coronavirus spontaneously mutated and jumped to humans at a wet market or deep in some random bat cave which just so happened to be 20 miles from China’s only BSL-4 virology lab, a virus with an unusually slippery never-before-seen genome that’s evading zoological classification, that may be as much as twenty-times more contagious than SARS and whose spike-protein region which allows it to enter host cells holds an unique HIV-like signature with the concomitant clinical response, that somehow managed to infect its patient zero who had no connection to this market, and then be so fined-tuned to humans that it’s gone on to create the single greatest public health crisis in Chinese history with approaching 100 million citizens locked-down or quarantined – also causing Mongolia to close its border with its largest trading partner for the first time in modern history and Russia to ban Chinese citizens from entry into their country.

– Or, Chinese scientists failed to follow correct sanitation protocols possibly while in a rush leading up to an international virological conference and during their boisterous holiday season, something that had been anticipated since the opening of the BSL-4 lab and has happened at least four times previously, and accidentally released this bio-engineered Wuhan Strain – likely created by scientists researching immunotherapy regimes against bat coronaviruses, who’ve already demonstrated the ability to perform every step necessary to bio-engineer the Wuhan Strain COVID-19 – into their population, and now the world. As would be expected, this virus appears to have been bio-engineered at the spike-protein genes which was already done at UNC to make an extraordinarily virulent coronavirus. Chinese efforts to prevent the full story about what’s going on from getting out are because they want the scales to be even since they’re now facing a severe pandemic and depopulation event. No facts point against this conclusion.

An immediate international moratorium on all dual-use gain-of-function research must be instated and all existing experimentation must be autoclaved, only greed and hubris have ever been served by attempting this type of genetic manipulation. Humanity does not need a vaccine against HIV derived from a coronavirus, nor do we need to be tinkering with genetic material that holds the potential to wipe a significant percentage of us off the face of the Earth.

Failure to embrace such a ban may effectively become a death sentence for our species, assuming we aren’t already on our last mile.

Debunking Nature Magazine's "COVID-19 Definitely Didn't Come From A Lab" China Propaganda

Maybe you shouldn’t blindly believe everything you read? Even if the source has a pretty solid reputation?

Nature magazine has censored over 1,000 articles at the request of the Chinese government over the past several years. And it seems pretty clear that their recent article, “The proximal origin of SARS-CoV-2” is just one more example of their influence.

China bought off the head of Harvard’s chemistry department, you don’t think they could buy off run-of-the-mill research scientists scrambling for tenure and funding and publication? It’s absolutely horrific that so many scientists and researchers are taking part in what’s really clearly a disinformation campaign orchestrated by the Chinese Communist Party, and willfully spreading a smokescreen about something that’s already killed thousands and is projected to kill millions more across the planet.

And while the mainstream corporate media mindlessly regurgitates claims from the Chinese government that are falsifiable with the simplest of google searches, allowing the public to be lulled into a false sense of security and complacency, and Reddit rapidly censors and moderates anything that might indicate that this virus leaked from a Chinese lab and so the Chinese government is to blame for this pandemic  – sites like ZeroHedge, that have been at the forefront of keeping the lines of investigation open, have been banished from Twitter and marginalized.

Below is a takedown of that article, and the good news is a much more nuanced and honest look at the origins of COVID-19, the Wuhan Strain of coronavirus is just a click away.

    Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

    As our report mentions right at the start, scientists passed the H5N1 Bird Flu through a series of ferret hosts until it gained ACE2 affinity and then became incredibly virulent, which is what’s seen with COVID-19 since its affinity to ACE2 is orders of magnitude higher than SARS. That process would leave a genome that appears “natural” and not purposeful as well since it wouldn’t leave a genomic smoking gun and would simply appear to be the result of “natural” selection. However the addition of artificial generations produced by this process of passing through ferrets in the lab would create a lot of genetic distance from any possible relatives – precisely what is seen in COVID-19: it forms its own clade and appears very distant from all other bat coronaviruses. So this is lazy research, they’re either unaware of the Bird Flu study or are willfully ignoring it.

    Given the level of genetic variation in the spike, it is likely that SARS-CoV-2-like viruses with partial or full polybasic cleavage sites will be discovered in other species.

    This seems like pretty intentional dissimulation. It’s “likely” that other viruses with this cleavage site will be found? What? How likely? 1 in 10? 1 in 10 million? Is it likely that if my aunt grew balls she’d become my uncle? Is it “likely” that a natural intermediate animal vector will be found? Well… likely or not, until it happens it seems incredibly disingenuous to state that “likely” means a damn thing here.

    The functional consequence of the polybasic cleavage site in SARS-CoV-2 is unknown, and it will be important to determine its impact on transmissibility and pathogenesis in animal models. Experiments with SARS-CoV have shown that insertion of a furin cleavage site at the S1–S2 junction enhances cell–cell fusion without affecting viral entry14.
    This doesn’t seem to address the virus’s provenance at all, but just as an aside it seems like a lot of the viruses with furin cleavage sites engage in ADE, which COVID-19 appears to be doing from a clinical perspective: neurological damage, the second infection is worse, and areas like Wuhan with extended infections have much higher CFRs as infections overlap.

    The acquisition of polybasic cleavage sites by HA has also been observed after repeated passage in cell culture or through animals17.
    Exactly. Passage through a series of ferret hosts in a lab would have given COVID-19 this distinct cleavage site.

    It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus. As noted above, the RBD of SARS-CoV-2 is optimized for binding to human ACE2 with an efficient solution different from those previously predicted7,11.

    Yes, again we aren’t arguing that this thing was built nucleotide-by-nucleotide as the perfect bespoke bio-weapon. This efficient solution is exactly the kind of thing that would be selected for after passage through ferrets in lab, which was already done to the Bird Flu that created a horrifically virulent strain. Isn’t it funny that no one’s mentioning that experiment? Or Baric’s work at UNC? How come every single public-facing virologist seems to be leaving these studies out? Are they really unaware of them? That seems exceedingly hard to believe when I was able to find them on the front page of a single google search. Seems a lot more likely everyone’s just covering each other’s asses since they realize the magnitude of what’s happening and how deep into the cover-up they already are.

    Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used19
    This is an utterly vacuous statement. Probably doesn’t mean a damn thing in science. “Okay folks, we probably won’t get an earthquake anytime soon, so no reason to prepare for one or try and detect one coming!” Seriously?

    Instead, we propose two scenarios that can plausibly explain the origin of SARS-CoV-2: (i) natural selection in an animal host before zoonotic transfer; and (ii) natural selection in humans following zoonotic transfer.

    As we’ve explained before, there was no trace of this virus before November 2019, and full zoonotic jumps don’t just magically happen, especially not of a virus that’s so incredibly adapted to humans and able to infect us undetected and spread undetected, and then kill us after more than enough time has passed to find multiple new hosts. It’s funny so many virologists are throwing out the book of how zoonotic jumps happen… all that money in gain-of-function research must be quite blinding. Kind of amazing they don’t matter how many thousands of people are dying. As far as the intermediate animal host goes: It might as well be a unicorn at this point. Until someone finds it, it’s just conjecture.

    Malayan pangolins (Manis javanica) illegally imported into Guangdong province contain coronaviruses similar to SARS-CoV-221. Although the RaTG13 bat virus remains the closest to SARS-CoV-2 across the genome1, some pangolin coronaviruses exhibit strong similarity to SARS-CoV-2 in the RBD, including all six key RBD residues21 (Fig. 1). This clearly shows that the SARS-CoV-2 spike protein optimized for binding to human-like ACE2 is the result of natural selection.
    The most recent study, covered in our article, that examines the neutral sites that are assumed to best show heritage found that pangolins are “very unlikely” to have served as a host at all. Their assertion that natural natural selection is clearly shown is raw steamy bullshit. Serial passage through ferrets fits the overall big picture far better than this pangolin crap.

    For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog.
    WAIT WAIT WAIT!! You mean exactly like a bunch of ferrets, which have the same ACE2 receptor as humans, all jammed into a bunch of cages together and then infected over and over again in a lab?! That’s crazy talk!! Other than the fact it was exactly the process used to make the Bird Flu into something that “could make the 1918 pandemic look like a pesky cold.”

    It is possible that a progenitor of SARS-CoV-2 jumped into humans, acquiring the genomic features described above through adaptation during undetected human-to-human transmission. Once acquired, these adaptations would enable the pandemic to take off and produce a sufficiently large cluster of cases to trigger the surveillance system that detected it.

    Hence, this scenario presumes a period of unrecognized transmission in humans between the initial zoonotic event and the acquisition of the polybasic cleavage site. Sufficient opportunity could have arisen if there had been many prior zoonotic events that produced short chains of human-to-human transmission over an extended period.

    Sure this would be plausible… other than the fact that, as we cover in our report, that statistical analysis shows that this thing didn’t hit humans until November of 2019, which this article agrees with. But zoonotic jumps only occur after a genomic trial-and-error process where the virus jumps to one host, spreads to a few new hosts, and then fizzles out. There is absolutely no evidence anywhere of this occurring. Every single data points to this thing hitting humans in November and being immediately adapted and dangerous. There is no trace whatsoever of it creating small clusters of infections and dying out – stating there could have been doesn’t mean it’s been seen. It hasn’t. And as our report covers, this would require sustained interaction with the intermediate host – how does that happen in the middle of a massive modern urban metropolis the size of NYC? And where is this intermediate host anyways? If an intermediate host isn’t needed, is it some magical sleep-flying bat that decided not to hibernate and fight crime in Wuhan when it’s buddies were all hibernating, creating the sustained interactions with humans as it fought for Justice? Because that’s about as plausible as what’s being proposed here.

The presence in pangolins of an RBD very similar to that of SARS-CoV-2 means that we can infer this was also probably in the virus that jumped to humans.

    Again, analysis of the neutral sites shows that pangolins were almost certainly not in play.

    Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described

    This means nothing. There is no open-source shared database of viruses. No one has any idea what viruses are in China’s BSL-4 lab, where they’ve been collecting these viruses for years. As mentioned, one of our persons-of-interest was the very first person to isolate a coronavirus from a bat that uses the ACE2 receptor. He also worked at UNC in Baric’s lab making the hyper-virulent bat coronavirus in 2015.

    Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described.
    The fuck it hasn’t.

    Retrospective serological studies could also be informative, and a few such studies have been conducted showing low-level exposures to SARS-CoV-like coronaviruses in certain areas of China26. Further serological studies should be conducted to determine the extent of prior human exposure to SARS-CoV-2.
    Beyond the statistical analysis that indicates it only hit humans in November in 2019, is the fact that the version of COVID-19 found in the first few dozen hosts was exactly the same – there aren’t any variants whatsoever, just one version. This is not what would be found with the genomic trial-and-error of a full zoonotic jump, which requires sustained human-to-human transmission as different variants of the virus try and fail to adapt to human biology. Here, only one variant was found in all the initial infected humans, instead of the multiple variants that would be expected. But does fit what would happen if a virus that already had high affinity to the ACE2 receptor, which is the same in human and ferrets, leaked out of a lab. But addressing this point in particular, oh weird, the study they cite from March of 2018 was done mostly on people who live in villages barely a kilometer away from bat caves. A far cry from a massive urban city bout the size of NYC. Oh, and how many of these villagers, who live about a kilometer or less from bat caves, had antibodies indicating exposure to bat coronaviruses? Two-point-seven percent. (There is hand-waving about how long antibodies persist in humans, but I’m pretty sure it’s more than long enough.) That study actually sampled people living in Wuhan too and found… no evidence whatsoever of exposure to “SARS-CoV-like coronaviruses.”  So are these peer-reviewers just straight chugging lead paint, or are they on the take too?

    The finding of SARS-CoV-like coronaviruses from pangolins with nearly identical RBDs, however, provides a much stronger and more parsimonious explanation of how SARS-CoV-2 acquired these via recombination or mutation1
    Again, just demonstrably false.

Get the real story here.

Tuesday, December 15, 2015

Naomi Wolf on Fake News



Former Clinton/Gore political consultant Naomi Wolf explains why we should be skeptical of overly theatrical news stories. Propaganda is legal! This took place at the 2014 Free State Project's Liberty Forum.