Is it time to start a new moratorium on laboratory serial passage & direct genetic manipulation of potentially pathogenic viruses? Yes!! Dr. James Lyons-Weiler makes the case in this stunning 2008

by Paul Alexander

piece on genetic manipulation that involved Ralph Baric and it may go back to even 2005, that they were already engaging in laboratory viral genome manipulation and editing

This is indeed a complex substack yet it raises serious questions as Dr. James Lyons-Weiler poses them. I invite you to read hand to consider his important work.

“Our results therefore support the hypothesis that SARS-CoV-2 could originally result from a recombination of sequences pre-existing in Rhinolophus bats living in the extensive limestone cave systems of South-East Asia and South China41,42. Many species forage in the same cave areas, including R. malayanus and R. pusillus43. In addition, the distribution of R. marshalli, R. malayanus, and R. pusillus overlaps in the Indochinese sub-region (Supp. Figure 5), which means they may share caves as roost sites and foraging habitats44. With the novel viruses here described, understanding the emergence of SARS-CoV-2 does not need to hypothesize recombination or natural selection for increased RBD affinity for hACE2 in an intermediate host like the pangolin before spillover45, nor natural selection in humans following spillover46. However, we found no furin cleavage site in any of these viruses on sequences determined from original fecal swab samples, devoid of any risk of counterselection of the furin site by amplification in Vero cells18.”


‘This passage although only containing the authors’ opinions, is misleading It is incorrect to say that we do not need to invoke natural selection to explain the high affinity of SARS-CoV-2 spike protein for hACE2; their data do not support this. Some affinity binding capacity is not the same as high affinity binding.

The last sentence of the passage is chilling. We already know that the WIV was routinely sampling, growing and characterizing SARS-CoV-2 like sequences. If they were growing them in Vero cells, serial passage without intent could have result in the furin cleavage site. Thus, SARS-CoV-2 laboratory origin now seems all but to have been fated, with our without direct genetic manipulation. This likelihood does not rule out direct manipulation.’

I also include the conclusion and you can study the substack at your leisure. I find the words chosen here are very important and in the white spaces Dr. Lyons-Weiler actually tells us a whole lot:

‘What This All Means

While the SARS-CoV-2 novel S1/S2 cleavage motif (PPAR/S) processed by furin is uniquely associated with greatly enhanced hACE2 receptor binding affinity, the Pathogenicity Motif Pattern I reported in 2020 is associated with hACE2 receptor affinity overall. In fact, the differences between SARS and SARS-CoV-2 like viruses in terms of risk of infectivity in humans resides in this pattern.

The public’s interest in the question of laboratory or natural origin of the SARS-CoV-2 virus is immense, given the massive effect of the SARS-CoV-2 epidemic - and the massive effect of policy responses. Reasonable candidates for a potential “backbone” for SARS-CoV-2 were in fact being studied and manipulated in labs in the US and in China as far back as 2005. That’s profound because the genomes of viral lineages generated in labs are not always reported.

We need to see Dr. Baric’s full laboratory notes and correspondences with scientists in China dating back to at least 2004. We need to see any unpublished sequences over this time period.

And we need to see the same from WIV.

And labs doing research on hACE2 affinity and SARS and SARS-like sequences around the world.

That clearly is not likely to ever happen.

But at least the public now knows the degree to which gene sequence manipulations were possible dating back to 2008 and that serial passage with or without intent can lead to enhanced pathogenicity in humans; they know the was, and is, a group of so-called SARS-like sequences found in the wild indeed have some hACE2 affinity, and and this was known back in 2008; they know that the smoking gun furin cleavage site - and it is a smoking gun for origin of SARS-CoV-2 itself - is only part of the story of hACE2 receptor affinity of SARS-CoV-2 like viruses.

We would be wise to start a new moratorium on laboratory serial passage and direct genetic manipulation of potentially pathogenic viruses.’

Popular Rationalism
SARS-CoV-2-like Spike Protein Sequences with Affinity to hACE2 Were Present in the Public Databases in 2005. Plus, a Hint on SARS-CoV-2 Laboratory Origin
In 2020, I published an analysis of all of the available SARS-CoV-2 and SARS sequences at the time in search of a specific relationship. If any SARS sequences published prior to 2020 were similar to SARS-CoV-2 with respect to functional motifs, then the question of origins of SARS-CoV-2 would have to address how a SARS-CoV-2 like spike protein made its…
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