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The authors “speculate that the direct ancestor” of the SARS virus may have been a result of recombination — or the natural combining of genetic material — of precursors of these bat coronaviruses. And the authors found that the bat coronaviruses had the potential for direct transmission to humans.
A few of their experiments combined different elements of viruses to better understand what’s required to infect human cells. Specifically, the 2017 research used the backbone of WIV1, a bat SARS-like virus reported in 2013, and swapped in the spike protein of two newly identified bat coronaviruses to see if they, like WIV1, can use the human ACE2 receptor to enter human cells. The researchers found that both chimeric viruses could use ACE2 to infect and replicate in human cells in culture. (The researchers attempted to make six other chimeric viruses, but when put into monkey cells the viral constructs did not replicate.)
Is that gain-of-function? Again, there are different definitions and opinions on that. We reached out to the NIH asking for a more detailed explanation of why the 2017 paper didn’t meet its definition, and we’ll update this story if we get a response.
In the current study, we successfully cultured an additional novel SARSr-CoV Rs4874 from a single fecal sample using an optimized protocol and Vero E6 cells [17]. Its S protein shared 99.9% aa sequence identity with that of previously isolated WIV16 and it was identical to WIV16 in RBD. Using the reverse genetics technique we previously developed for WIV1 [23], we constructed a group of infectious bacterial artificial chromosome (BAC) clones with the backbone of WIV1 and variants of S genes from 8 different bat SARSr-CoVs. Only the infectious clones for Rs4231 and Rs7327 led to cytopathic effects in Vero E6 cells after transfection (S7 Fig). The other six strains with deletions in the RBD region, Rf4075, Rs4081, Rs4085, Rs4235, As6526 and Rp3 (S1 Fig) failed to be rescued, as no cytopathic effects was observed and viral replication cannot be detected by immunofluorescence assay in Vero E6 cells (S7 Fig). In contrast, when Vero E6 cells were respectively infected with the two successfully rescued chimeric SARSr-CoVs, WIV1-Rs4231S and WIV1-Rs7327S, and the newly isolated Rs4874, efficient virus replication was detected in all infections (Fig 7). To assess whether the three novel SARSr-CoVs can use human ACE2 as a cellular entry receptor, we conducted virus infectivity studies using HeLa cells with or without the expression of human ACE2. All viruses replicated efficiently in the human ACE2-expressing cells. The results were further confirmed by quantification of viral RNA using real-time RT-PCR (Fig 8).
originally posted by: Stupidsecrets
He should have got permission to proceed with the funding from a higher source. The line is very blurry. He did not and for that alone he is wrong. It would have never got approved that's why he did it anyway.
originally posted by: 1947boomer
originally posted by: Stupidsecrets
He should have got permission to proceed with the funding from a higher source. The line is very blurry. He did not and for that alone he is wrong. It would have never got approved that's why he did it anyway.
He probably did get approval from a higher source. Fauci's lab is under the National Institutes of Health (NIH). NIH is run by Dr. Francis Collins, and NIH would have to set the policies for approval of funded projects.
originally posted by: BatSars
I posted this in response to your similar comment in another thread:
This SOUNDS troubling, but is actually not gain-of-function. Using bacteria to infect with parts of a naturally-occurring virus to detect virility does not constitute gain-of-function because nothing was gained. They merely sequenced the backbone (much like the vaccine mfg did with the spike protein) and used something to infect certain cells to determine whether it acts upon certain receptors, etc.
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. Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used19.However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone20. 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. We also discuss whether selection during passage could have given rise to SARS-CoV-2.
This is really no different from adenovirus vaccines, or mRNA vaccines. It's similar to using a chemical process to determine whether something will react to it. There was no change or gain of function with any of the viruses.
There is not enough there to say "yes he lied" because it's a debate of semantics (or as you said, splitting hairs) at this point, which is not enough to charge Fauci with perjury.
a reply to: bloodymarvelous
a reply to: bloodymarvelous