For Angela Rasmussen, the problems with Elaine Dewar’s book, On the Origin of the Deadliest Pandemic in 100 Years, begin with the title.
“While SARS-coronavirus-2 has been absolutely terrible and has upended all of our lives, it actually isn’t the most deadly pandemic in the last 100 years,” the University of Saskatchewan virologist points out. “That would be HIV, at least for now.”
When Rasmussen, who works at the university’s Vaccine and Infectious Disease Organization, heard CANADALAND’s recent episode spotlighting Dewar’s theories, she found it “somewhat jarring.” Because while it may be superficially possible to draw connections suggesting that SARS-CoV-2 had its genesis in a mine in Yunnan via a lab in Wuhan, that doesn’t necessarily mean such a conclusion is plausible or scientifically sound.
Hi @JesseBrown @CANADALAND. I’m a virologist in Canada who authored a peer-reviewed paper in Cell on the evidence to date on the origin of SARS-CoV-2. Happy to come on your show and discuss what the evidence actually shows and why Ms. Dewar’s speculative claims are unsupported.
— Dr. Angela Rasmussen (@angie_rasmussen) September 28, 2021
On this week’s CANADALAND, Rasmussen joins host Jesse Brown to break down why a zoonotic (natural) origin remains the most likely source for the virus that causes Covid-19 and how journalists can best navigate experts and evidence:
Here’s an edited summary of several of her key points:
On the RaTG13 coronavirus, discovered years earlier in a Yunnan mine, being a possible progenitor of SARS-CoV-2:
“It is correct that RaTG13 is 96% similar to the genome of SARS-CoV-2. However, when we’re talking about viral genomes, a 4% difference is actually huge. There is no way that RaTG13 could have become SARS-CoV-2, because that 4% difference is actually scattered throughout the entire genome of the virus. So in effect, what this would mean is that this virus — in a very short period of time, according to this hypothesis — would have had to acquire over a thousand different mutations scattered throughout the genome randomly, which is just not something that SARS-CoV-2 is capable of. Coronaviruses do have a high mutation rate, as do all RNA viruses, but it’s not that fast.”
On human manipulation potentially accounting for that 4% difference:
“It’s not impossible that somebody could insert over a thousand point mutations into the genome of a progenitor virus — but there’s no reason why anybody would, because that would be incredibly tedious and difficult to do. Also, as a virologist, as somebody who myself has cloned viruses, it’s challenging. It’s not like you can just type in a sequence and print out a virus. It actually is technically very difficult. So there’s no reason why anybody would think to insert all of those different mutations, and that also is not really the point of so-called gain-of-function research.When people are doing this type of research — when they’re inserting different elements into a virus to see if that increases infectivity in human cells or to see if it increases pathogenicity or transmissibility — usually what people are doing is inserting one element.”
On whether the Wuhan Institute of Virology (WIV) could have conceivably done so, anyway:
“The hypothesis that this had its origins in RaTG13 and the Mojiang mine is absolutely, demonstrably untrue. That simply wouldn’t happen, even though they were engaged in some gain-of-function research. I’ve read the papers on coronaviruses that have come out of the Wuhan Institute of Virology very carefully, and they actually were not making chimeric viruses from scratch. They were using known backbones: they were taking viruses that they already had discovered and already had cloned, and they were putting some little pieces into them. Those viruses were isolated by traditional virology means — they were not sequences that they obtained and then cloned and then started screwing around with. And none of those viruses, importantly, none of the backbones they use, none of the modifications they’ve made that they’ve published, are anything like SARS-CoV-2, and they could not have become SARS-CoV-2 with evolution in the human population or in transgenic mice or in anything else — certainly not in cell culture. Could SARS-CoV-2 have resulted from gain-of-function research? Yes, but not if they didn’t have a backbone that is consistent with the SARS-CoV-2 genome. And everything that Shi Zhengli [the virologist who heads up coronavirus research at the WIV] has said over and over again is that they did not have that virus.”
On the notion that the WIV could have been secretly keeping a virus that was closer to SARS-CoV-2:
“I would just say that if they are covering it up, that’s actually a conspiracy. It’s an unproven theory. So in fact, it is a conspiracy theory that we have no basis in evidence for. And I have to say, I don’t personally know Dr. Shi, but I certainly work with people who have worked with her and know her very well. They say that she’s fundamentally an honest person and a good collaborator, and I think without evidence that suggests that she’s in fact lying, I don’t think that we should make the assumption that she is, just because the Chinese government is not transparent.”
On the idea that the virus was suspiciously suited to spreading among humans:
“This virus is not uniquely born ready to infect humans. A lot of viruses can infect humans and many other species. And in fact, SARS-CoV-2 is a very generalist virus: it can infect humans, it can infect raccoon dogs, it can infect cats, it can infect dogs, it can infect palm civets, it can infect badgers and hedgehogs. It can infect a lot of different species besides just bats. That is not unusual in the virus world. SARS-CoV-2 has all the hallmarks of a recently emergent virus in the human population that can infect a number of different species, and that’s really determined by chance encounters. The fact that SARS-CoV-2 can infect all these other species provides a number of different possible routes for how it could have gotten into the human population naturally. We just need to look at the evidence that has unfolded right before our eyes during the course of the pandemic. We’ve seen variants emerge that are either more transmissible or more capable of binding the ACE2 receptor in people; those would be the so-called immune-evasive variants, Beta and Gamma. And then there are the more transmissible variants, Alpha and Delta. Those mutations suggest that this virus was in fact not well-adapted to the human host and these adaptations were only acquired after the virus spread to a great extent throughout the human population.”
On the fact that we still haven’t figured out what animal it might’ve come from:
“I’m so tired of the idea that that we have to find this smoking gun, whatever it is, whether it’s evidence of a lab leak or a zoonotic spillover, because the reality is for a lot of viruses, we’re never gonna find that. During the most recent WHO mission to China, they did test tens of thousands of animals, but that’s really a drop in the bucket when you look at the overall wildlife trade in China. In June, a paper came out that was done by people who are not virologists. They were actually tracking the wildlife trade in China, and they did very comprehensive surveys of the live animals that were available for sale in the markets in Wuhan all the way until November of 2019. And based on that paper, we know that species that are susceptible to SARS-CoV-2 were being sold live in the markets in Wuhan. We also know that these animals actually come from a common supply chain, so they’re farmed in many cases and transported to Wuhan together, usually in pretty crowded, pretty inhumane conditions. And then they’re sold at the various markets. So we know that these viruses are there, we know that they’re circulating in these wildlife farms and in these animals that are being sold in the markets. And it’s circumstantial, but that’s exactly the circumstances under which [the original] SARS coronavirus emerged.”
On determining which scientists have a firmer grasp of a given subject matter than others:
“I think that both scientists and journalists need to be very careful about how journalists are sourcing their stories. I get asked all the time about epidemiology. I’m not an epidemiologist. When that happens, I refer a reporter to somebody who is. I think it’s journalists’ responsibilities, especially science journalists’ responsibilities, to know who they should be talking to, to source the scientists that they’re speaking with correctly, and to be able to distinguish between somebody with a PhD who is an expert in a topic versus somebody who is not.”
Top screencap from Rasmussen’s February 2021 appearance on CNBC’s The News with Shepard Smith
