This article takes a scientific look at Covid-19 (the disease) and SARS-COV-2 (the virus itself). I need to do this because some of the official information about the virus, and its origin, is plain wrong. It’s hard to work out why the official media message is wrong but I’m guessing that a lot of people don’t want the public to be aware of what went on in virology labs around the world for the last ten years. This article begins by focussing on why the virus is so good at infecting people. It then studies what that evidence, and the latest scientific papers, tell us about its origins.
Covid-19 is a coronavirus, as most people know. In other words, it’s a lot like the common cold, which is actually a group of similar viruses. These mainly consist of rhinoviruses but also some coronaviruses. Cold viruses affect mammals and do make us ill, but they are usually mild in their effects. This is a good strategy, as any established virus survives longer if it only produces mild symptoms. If, instead, a virus makes its host drop dead, then everyone else will run away from that person, thus preventing the virus from spreading. Because of this, nearly all natural viruses are mild but successful in their host species.
Dangerous viruses are usually lethal because they’ve jumped from their host species, where they weren’t lethal, to a species that can’t handle them at all. The downside of this move, for the virus, is that it isn’t tuned to the new species. It is therefore very bad at spreading through the new species. This usually means that a lethal virus spreads slowly, giving people a chance to stamp it out. This is where Sars-Cov-2, the Covid-19 virus, begins to look very weird. It spreads extremely well in people and yet it also kills them. How on Earth did it achieve both these abilities at the same time?
Covid-19 is closely related to a coronavirus that circulates in bats, another SARS coronavirus. These SARS viruses circulate in bats without killing the bats, like any naturally-established virus. According to the official explanation, Covid-19 somehow jumped from the bats to humans. This is not an easy thing to do. It is very difficult for a virus that works well in one mammal to successfully infect and survive in another mammal. This is because mammalian immune systems are very sophisticated systems. The virus has to find a way to get into the target mammal, then avoid the mammal’s immune-systems defences, then get into the mammal’s cells, where it makes the cell reproduce it. It must then make the mammal expel copies of it from their body so that the virus infects more members of that species. This is a tall order, especially as the virus can only naturally gain its new abilities through random mutation. Coronaviruses do mutate easily, due to their structure but this mutability comes at a cost; coronaviruses are fragile structures and can fall apart relatively easily, because of sunlight, humidity or something as simple as soap. This is good news for the natural world, as it prevents the process of a virus, that’s infecting one species, to jump to others.
Once we know all this, it becomes clear how incredibly unlikely it was that a virus that survived in bats could somehow jump across to humans and immediately become extremely good at infecting people. Somehow, Covid-19 immediately was very good at it. It can infect someone, reproduce inside them and then spread from them to others for a week or more without that person showing obvious symptoms. It then can cause havoc in their bodies and, in many cases, kill them. This is an astonishing and incredibly unlikely set of skills to suddenly pick up.
As soon as it was clear that Sars-Cov-2 was a major threat to people, virologists did their utmost to discover the genetic code of the virus and study how it worked. Understandably, they wanted to find out how it was so good at infecting people. In the course of their work, they discovered that the virus possessed a very unusual and special ability. Bat coronaviruses get into host cells by manipulating a certain molecular key on the outside of the cells, known as the ACE-2 receptor, as explained in this Nature article. The above diagram shows how the virus uses the key to sneak into the cell. This is why the virus has a corona of spike proteins, hence its name. These spike proteins are the ‘lock-pickers’. Like any burglar, the setup of these lock-pickers will make a huge difference to how well the burglar breaks in and does his nefarious work.
One crucially important part of this spike protein ‘lock-picking’ is how the virus comes apart in order to infect the cell. Bat coronaviruses aren’t naturally setup to break into human cells and break apart, releasing their viral code, in just the right way. Virologists were intrigued as to why Covid-19, supposedly fresh from bats, was able to behave in just the right way to maximise its infection of humans. They studied the genetic code and spotted something very strange. In the science paper entitled A Unique Protease Cleavage Site Predicted in the Spike Protein of the Novel Pneumonia Coronavirus (2019-nCoV) Potentially Related to Viral Transmissibility, published on the NCBI site, the paper’s authors explain that Covid-19 possesses a special extra property that hugely helps its ability to infect humans. The weird thing was, this extra ability seemed to have come from nowhere. Here is their diagram, showing the genetic code that enabled the virus to have its special extra ability:
For readers who aren’t used to reading genetic code information, the top grey-blue bar shows the position of the site-of-interest on the viruses entire genome, i.e. its entire genetic code. This ball of RNA is stored inside the virus-ball in a coiled-up lump. The list of B-SARS, running down the table, are all the bat viruses that are closely related to Covid-19, which is called SARS-CoV-2 on the list. As we can see from the table, SARS-CoV-2 or Covid-19 has an extra four letters in its genetic sequence; PRRA; this is a set of amino acids, or genetic building blocks. None of the other viruses have this extra code. Somehow, this PRRA code suddenly appeared in the SARS-CoV-2 virus. This was an extremely useful bit of luck because that particular piece of code enabled the SARS-CoV-2 virus to suddenly becomes much, much better at infecting people.
The probability of this new genetic code appearing in SARS-CoV-2 by natural mutation is unbelievably low. Some readers might wonder if the PRRA code appeared later on, because of the virus’s spread, but it’s clear the virus was extremely virulent from the very beginning, as the residents of Wuhan found out. We are left with only one reasonable conclusion, that the PRRA code was artificially inserted. This was the conclusion made by the experienced and respected Norwegian virologist Birger Sørensen. In a peer-reviewed paper published together with Professor Angus Dalgleish of St George’s Hospital at the University of London, Sorensen claimed the novel coronavirus SARS-CoV-2 is not natural in origin. In an interview with NRK in Norway, as reported on this website article, Sørensen points to the PRRA sequence, and other suspicious novel genetic sequences in SARS-CoV-2. He makes it clear that they must have been artificially added. To quote from the article:
“The inserted sequences should never have been published. Had it been today, it would never have happened. It was a big mistake the Chinese made. The inserted sequences have a functionality that we describe. We explain why they are essential. But the Chinese pointed to them first.”
Sørensen goes on to say:
“When we technically describe the virus, we see that it has not come about in a natural development. It’s done by Americans and Chinese, as part of what’s called “gain of function” studies. It is done all over the world. You say you don’t, but it happens all the time in advanced labs.”
Sørensen’s candidness has opened up a can of worms, albeit one that had been sitting in plain sight, in virology circles for a long time, the dangers of gain-of-function research.
Gain of Function
The phrase ‘Gain of Function’ sounds innocuous or dull but it isn’t. Gain of function, in virology, is the strategy of making a Frankenstein virus, from naturally occurring viruses, and adding specific genetic code so that this new virus has a maximum ability to infect and kill a specific host, particularly humans. The logic of this strategy is that if virologists make such a monstrous virus, then they can make a vaccine or pharmaceutical medicine to stop it. By doing that, if the virus did appear and start infecting people, the virologists would already have a cure prepared. Not surprisingly, many people have pointed out a significant issues with this strategy; if the monstrous virus escapes accidentally before a vaccine is made, then the virologists haven’t just made a terrible disease that never existed, they’ve let it loose on the world.
This issue was explored in an article on TheScientist website entitled, Lab-Made Coronavirus Triggers Debate. The first paragraph of this article states:
￼”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 relevant scientific paper, with Ralph Baric as the primary author, is entitled A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence. Here is a quote from its introduction:
“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.”
In other words, Baric and his team made a chimeric virus, a mutant version of the bat SARS coronavirus with parts added to make the virus work in a mouse. Mice are often used as a test case before testing on humans because mice have similar metabolisms to humans. The scientists made this chimeric virus to see what it would do to human airway cells. This is classic ‘gain-of-function’ research. Not surprisingly, as TheScientist article states, there’s been a lot of argument, within science, as to whether this is a good idea. The heated issue is described in this NCBI paper entitled Ban on gain-of-function studies ends. To quote from the article:
The situation has its roots in 2011, when the NSABB suppressed two studies involving H5N1 viruses that had been modified to allow airborne transmission from ferret to ferret. They worried that malign actors could replicate the work to deliberately cause an outbreak in human beings. After much debate, the studies were published in full in 2012. HHS subsequently issued guidelines for funding decisions on experiments likely to result in highly pathogenic H5N1 viruses transmissible from mammal to mammal via respiratory droplets. The guidelines were later expanded to include H7N9 viruses.
In 2014, several breaches of protocol at US government laboratories brought matters to a head. The news that dozens of workers at the Centers for Disease Control and Prevention (CDC) might have been exposed to anthrax, that vials of smallpox virus had been left lying around in an NIH storeroom, and that the CDC had unwittingly sent out samples of ordinary influenza virus contaminated with H5N1, shook faith in the country’s biosafety procedures. Over 200 scientists signed the Cambridge Working Group declaration arguing for a cessation of experiments creating potential pandemic pathogens “until there has been a quantitative, objective and credible assessment of the risks, potential benefits, and opportunities for risk mitigation, as well as comparison against safer experimental approaches”.
The debate is focused on a subset of gain-of-function studies that manipulate deadly viruses to increase their transmissibility or virulence. “This is what happens to viruses in the wild”, explains Carrie Wolinetz, head of the NIH Office of Science Policy. “Gain-of-function experiments allow us to understand how pandemic viruses evolve, so that we can make predictions, develop countermeasures, and do disease surveillance”. Although none of the widely publicised mishaps of 2014 involved such work, the NIH decided to suspend funding for gain-of-function studies involving influenza, MERS-CoV, and SARS-CoV.
Unfortunately, this ban didn’t last very long. To quote from the paper:
On Dec 19, 2017, the US National Institutes of Health (NIH) announced that they would resume funding gain-of-function experiments involving influenza, Middle East respiratory syndrome coronavirus, and severe acute respiratory syndrome coronavirus.
Here’s the statement from the NIH. The question becomes; was SARS-CoV-2 created as part of gain of function research and then accidentally released? Any attempts to answer that question inevitably lead to the Wuhan Institute of Virology.
Virologists at the Wuhan Institute of Virology have been studying SARS-like bat viruses for years in their level 4 biohazard lab. Here is one example paper. In many ways, they are the world’s leader in studying bat coronaviruses. It was therefore a strange coincidence that their research facility was only twenty miles from the supposed epicentre of the Covid-19 epidemic, the Huanan Seafood Market, as shown in the following map:
Officially, the virus kicked off in December, 2019, but this may be untrue. A French citizen, Amirouche Hammar, in France, contracted the disease and died very early on in the epidemic, in December 2019, without ever having travelled to China. Investigators discovered that he’d had contact with relatives who’d returned from the World Military games in China, which took place in Wuhan in late October 2019. This story was covered in several papers, including the Daily Mail. This intriguing evidence connects with another mysterious event that occurred in Wuhan in October 2019. This NBC news article reports the following:
A report — obtained by the London-based NBC News Verification Unit — says there was no cellphone activity in a high-security portion of the Wuhan Institute of Virology from Oct. 7 through Oct. 24, 2019, and that there may have been a “hazardous event” sometime between Oct. 6 and Oct. 11.
Cellphone meta-data, in other words data about cellphone messages, is relatively easy to gather, at least in terms of activity and location, but it can be very useful. The World War 2 Bletchley Park codebreaker Gordon Welchman pioneered the used of meta-data. He used the location and security level of German encoded messages to work out what the Nazis were planning, without even needing to decode their Enigma encrypted messages. Since then, it has become a major field of data analysis and intelligence work. The NBC News Verification Unit report includes a telling picture:
The official line from the Chinese, that the virus epidemic began in the Huanan Seafood Market in early December, seems increasingly like a red herring (forgive the pun). Instead, something serious may have happened at the Wuhan Institute of Virology months before.
I think this is enough information to make it clear that the official line on the virus – that it was a natural mutation from bats, possibly through a pangolin – is highly unlikely because the virus has properties that are almost impossible to have been picked up naturally. By comparison, there is a lot of evidence indicating that Covid-19 was artificially created and then accidentally released. We’ll probably never find out exactly what happened but hopefully, this evidence shows that those 200 scientists, who petitioned for gain of function research to stop, did the right thing.
Update – 13th December 2020
I originally wrote this article on the 19th August, 2020. Since that time, there has been a prolonged and concerted effort by China, and those who wish to hide all the ‘gain of function’ work, to convince everyone that the virus came from nature. For example, just this week, the Guardian newspaper published an article, entitled Origin story: what do we know now about where coronavirus came from?. This article does its best to convince everyone that the virus came from nature. It is interesting to see how the authors of the article described dissenting voices. To quote:
Despite the strong genomic trail, excitable China-blaming theories took off on rightwing news websites and social media in April, alleging the virus had been made in the Wuhan Institute of Virology lab.
We can see several straightforward propaganda elements in this single sentence. Dissenting voices are not being rational, science-based, impartial or supporting their view with evidence from scientific papers. Instead, they are, ‘rightwing, excitable and China-blaming theorists.’ I can imagine that a right-wing newspaper, in the same vein, would describe dissenters as ‘socialists’. Sadly for this article, it backs up its criticism of dissenters with a very weak argument. The article goes on to say:
They were dismissed in the Nature paper, whose first author was Kristian Andersen from the Scripps Research Institute in California. “Our analyses clearly show that Sars-CoV-2 is not a laboratory construct or a purposefully manipulated virus,” it said. That was important to say, said Josie Golding, Wellcome’s epidemics lead: “It was a bunch of prominent researchers coming together to say this is why we don’t think it’s made in a lab: because you would never make a virus like this and there are too many links to other viruses that have been found in the wild.” Nor is it likely to have escaped accidentally from the Wuhan lab, said Golding, who used to work in a high containment facility in Pirbright, Surrey. The idea that one person got infected in the lab and spread it to the entire world is the stuff of movies, she said. “Show me the evidence … It just doesn’t seem very realistic.” It is far more likely that animals were infected and people picked up the virus from them.
The argument that the virus can’t have come from a lab, ‘because you would never make a virus like this and there are too many links to other viruses that have been found in the wild,’ is blatantly false. Virologists have spent the last ten years performing gain-of-function work, creating viruses that have been modified to be maximally infectious. They have published many papers, describing their progress. There is also bioweapons research, which goes on all the time, all round the globe. Sars-Cov-2 is understandably linked to wild viruses because it is an artificially modified version of them.
The idea of that an accidental release of a virus ‘doesn’t seem very realistic’ is also refuted by the earlier quotes in this article. The massive increase in biohazard labs around the world, in the last two decades, combined with the increasing sophistication of the gain-of-function work, made the likelihood of a virus slipping out more and more likely. That is why 200 scientists petitioned for gain-of-function work to end. They did force a moratorium but tragically for the world, the moratorium on that work was ended by the NIH in 2017.
I think we are now in a seriously worrying situation, with regard to our mainstream media. The coronavirus has shown that we can’t trust them to give us accurate information, even supposedly objective and rigorous publications like the Guardian newspaper. The blatant lies that we suffered earlier in the year when we were told by many media outlets, that masks were a bad idea, even though that was scientifically ridiculous, only reinforces this conclusion. Because of this, I will continue to write articles on this website that are based on solid science, and are balanced and objective. If you spot any errors in them, feel free to add a comment. In that way, at least one corner of the internet can be a place of free-speech and intelligent, honest views.
Update – 31st December 2020
We’re nearly out of 2020 and the world of virology is still at war over Sars-Cov-2. Fortunately, some virologists are stating openly that Sars-Cov-2 looks very fishy. Dr Alina Chan, from the Broad Institute in the US, says as much in today’s Times Newspaper article, Hunt for Patient Zero has become caught in a clash of Great Powers. The article reports that other virologists, particularly Dr Balloux and Dr Daszak, still insist there’s no evidence of artificial tinkering with Sars-Cov-2. They state that only ‘the seedier elements of the internet’ are making claims that Sars-Cov-2 was artificially modified. I guess that includes me. (I guess I should include some porn on this website, just to fit the profile!) Amidst this mud-slinging, there was no mention of gain-of-function research at all in the article, which is a telling omission. I’ve sent a letter to the Times, explaining my findings on gain-of-function work and the comments of key virologists. If all goes well, they’ll take note and print it.
Update – 9th February 2021
At the beginning of this month, the World Health Organisation headed off to Wuhan, China to study the origins of the virus. To be honest, I wasn’t hoping for much, since the WHO didn’t exactly cover themselves in glory at the beginning of the pandemic. They didn’t recommend the stopping of air travel to and from China during the pandemic’s early stages and they only declared Sars-Cov-2 a pandemic after it was blindingly obvious it had become one. I was also unhappy about this WHO visit to Wuhan because the team included Peter Daszak, who has significant connections with the Wuhan Institute of Virology. Daszak has been ridiculing the lab-leak theory in the press since the start of the pandemic. He is also, by interesting coincidence, President of the EcoHealth Alliance, which is partnered with the Wuhan Institute of Virology. As this nature article, entitled ‘Heinous!’: Coronavirus researcher shut down for Wuhan-lab link slams new funding restrictions, states:
To carry out its research, EcoHealth Alliance partners with the Wuhan Institute of Virology (WIV) in China, which has been at the centre of unfounded rumours that the COVID-19 pandemic was caused by a coronavirus released from its laboratory. The NIH cancelled EcoHealth Alliance’s grant in April, days after US President Donald Trump told a reporter that the United States would stop funding work at the WIV.
EcoHealth Alliance and Daszak have been working with Shi Zhengli, a virologist at the WIV, for more than 15 years. Since 2014, an NIH grant has funded EcoHealth’s research in China, which involves collecting faeces and other samples from bats, and blood samples from people at risk of infection from bat-origin viruses. Scientific studies suggest that the SARS-CoV-2 coronavirus most likely originated in bats, and research on the topic could be crucial to identifying other viruses that might cause future pandemics. The WIV is a subrecipient on the grant.
It’s therefore reasonable to assume that Daszak would be reluctant to pin any blame on the Wuhan Institute of Virology and Shi Zhengli, who is known as the ‘bat lady’ in virology circles. It’s therefore not surprising to see in today’s Guardian report on the WHO press conference that Peter Ben Embarek, the WHO’s food safety and animal disease specialist and chairman of the investigation team, stated:
“The lab leak hypothesis is an extremely unlikely pathway for Covid-19 and will not require further study as part of their work in studying the origins of the virus.”
I can’t find any sign of why they think it’s ‘extremely unlikely’ even though, scientifically, it’s highly likely. I guess we’re supposed to take their word for it.