Why? I think you’ve misunderstood my answer to @Rumraket. Please read it again.
I’ve never said that the chimeric virus was more dangerous relative to the two others. My point was that before performing their experiments, the WIV researchers had no absolute guarantee that the chimeric virus wouldn’t happen to be more dangerous. That’s all!
So what? The fact remains that the authors have constructed genuine infectious chimeric viruses as can be seen in the Mehods section (see below):
Construction of SARS-like chimeric viruses.
Both wild-type and chimeric viruses were derived from either SARS-CoV Urbani or the corresponding mouse-adapted (SARS-CoV MA15) infectious clone (ic) as previously described27. Plasmids containing spike sequences for SHC014 were extracted by restriction digest and ligated into the E and F plasmid of the MA15 infectious clone. The clone was designed and purchased from Bio Basic as six contiguous cDNAs using published sequences flanked by unique class II restriction endonuclease sites (BglI). Thereafter, plasmids containing wild-type, chimeric SARS-CoV and SHC014-CoV genome fragments were amplified, excised, ligated and purified. In vitro transcription reactions were then preformed to synthesize full-length genomic RNA, which was transfected into Vero E6 cells as previously described2. The medium from transfected cells was harvested and served as seed stocks for subsequent experiments. Chimeric and full-length viruses were confirmed by sequence analysis before use in these studies. Synthetic construction of chimeric mutant and full-length SHC014-CoV was approved by the University of North Carolina Institutional Biosafety Committee and the Dual Use Research of Concern committee.
Namedropping Redfield doesn’t change anything. AFAIK, Redfield hasn’t offered anything that makes a lab leak more probable than natural emergence. His stance is one not strongly supported by the entire body of evidence.
Sigh. Rum asked if the “transmission and virulence” of the backbone (mouse-adapted SARS-CoV, MA15) used to hold the bat coronavirus (SCH014-CoV) spike protein in the article cited by Wade was greater in human cells or mice relative to the wild-types, SARS-CoV Urbani (human-adapted strain) or SARS-CoV MA15 (mouse-adapted strain) respectively and he answered with a no. You disagreed with that conclusion, probably thinking Rum was making a comment about such type of research in general, but he was just talking about the findings of the article Wade cited. That’s why your response missed the mark.
You did when you disagreed with Rum and that’s because your response was based on a misunderstanding.
Do you realize you are not making any sense here? Scientific experimentation is conducted to determine causal relationships between two or more variables under controlled conditions, making it a useful tool for hypothesis testing. The researchers, based on computer modelling, predicted the spike protein of SCH014-CoV when inserted into the mouse-adapted SARS-CoV backbone would fail to efficiently bind human ACE2 receptors, hence, show poor replication in human cells. However, after experimental evaluation, it was found that the spike protein of SCH014 promoted efficient entry of chimeric SCH014-MA15 into human cells, leading to robust viral replication, falsifying the hypothesis based on the computer modelling.
In summary, scientists conduct experiments to test hypotheses. You never really know what you get until the experiment is over, whether its in virology, biochemistry, physics, chemistry, geology or any other field of science. If scientists had a guaranteed outcome following some event, that would obviate the need for experimentation. With the experimental findings of the study Wade cited, we now know SCH014-CoV has the potential to cause epidemics in the future, a conclusion we did not know (and didn’t expect) prior to the experiments.
Another response of yours that has gone off the rails. We are talking about pseudoviruses used in virology research, then you show me a study that did not use any pseudoviral system. More so, no one denied the study Wade cited used a chimeric virus to study the spike protein of SCH014-CoV, so its pointless mentioning it.
MA15 used in the study you cited is lethal to mice and is replication-competent, which is not so for pseudoviruses used in virology research, just so you know.
Because it’s certainly going to confuse people, and I’d say it’s also wrong.
What’s he’s saying is that the variants (among which he seems to include the early D614G mutation) aren’t more transmissible; they’re just more fit. Now, ‘more fit’ for this kind of virus means that each infection on average creates more new infections per time period than some other version of the virus. ‘More transmissible’, on the other hand, means that each infection on average creates more new infections per time period than some other version of the virus. In other words, when people are saying that the virus is more transmissible, they mean the same thing as saying it’s more fit. Except that sometimes ‘more transmissible’ is treated as distinct from ‘escapes immunity’; in that case, higher fitness can be broken down into higher transmissibility and immune evasion.
So when he says that there are lots of ways besides higher transmissibility for a virus to be more fit, and that immune escape is only one of them, his statement makes no sense in the context of the actual conversations that are going on about these variants within the field.
Also, it’s very clear in the case of D614G that immune escape had nothing to do with its increased fitness, since the increase can at a time when almost no one was immune to any version of the virus. And there’s good evidence that multiple mutations present in these variants increase infectivity in human cells, produce higher viral loads, probably produce worse disease, and yet have no effect on antibody neutralization. Which is to say, yes, some of the variants, at least, are more transmissible.
(He also makes a passing reference to lineages increasing neutrally, by chance. That’s certainly not the case for some of these variants, so it’s not relevant here.)
I think what he probably means by transmissibility is how likely you are to infect someone per exposure, or something like that. There’s nothing wrong per se with using that terminology, but that’s not what others mean by the term in the conversations I’ve been listening to among epidemiologists and public health people. (And I’ve listened to quite a few.)
Ok, I will. But note that you’re yet again, actively avoiding examining any evidence for yourself, Gil.
So how eminent is Redfield, exactly? Was he the CDC director as a result of his alleged eminence, or for political reasons?
Doesn’t he own responsibility for the pathetic US response to COVID-19, particularly the CDC’s horrible failure in manufacturing a fairly simple RT-PCR test?
That was a nice interview although he said nothing which hasn’t been mentioned here already. However, the interview condenses all the arguments into a concise and easy-to-read format for those seeking science-based information on the origins of SARS-CoV-2.
In addition, for those who want to know how science works, Kristian’s actions early in the pandemic are very informative. Thanks for the share Dan.
A quote from the article that reiterates our exposure of the falsehood that a study cited by Wade, wherein Dr Shi was one of the authors, was proof that gain-of-function experiments were done by Dr Shi. Wade needs to publicly retract that claim in his article because it is serious misinformation, deceptive enough to have led someone like @Giltil astray and smearing Dr Shi’s reputation:
Isn’t that rather like asking the one on trial if they committed the crime. Of course, they have the right to testify to the crime they are being charged with. But one expects the defendant to deny any culpability, even if they are guilty. And that this is coming from China? Do they even acknowledge what they did in Tiananmen square?
It seems similar to asking the Russians if their athletes have been doping with the sanction of the state. Apparently, the Russians deny it. Ok, case closed we believe them.
I can see that most people here think the natural origin of the virus is way more likely than a lab leak. Maybe it is. But Shi Zhengli’s testimony lends not an once of credibility to the case.
And just to be clear this is not an anti-Chinese rant. As I recall NASA tried its best to cover up its culpability in the Challenger disaster. The accused is expected to deny their guilt. In similar fashion the friends and family of the accused can’t sit on the jury.
I’m pretty sure that she did not do anything there. I notice that in your post, you did not acknowledge the many societies committed by Americans throughout history. Why would either be relevant to virology? [asking as a virologist🙂]