The Lab Origin of the SARS-CoV-2 Virus

Professor Jeffrey Sachs chaired the Lancet COVID-19 Commission, which was created to help speed up global, equitable, and lasting solutions to the COVID-19 pandemic.

Recently Prof. Sachs said something that created shockwaves.

I’ll add one provocative statement. We could take it up later. It may shock you, it may not. Or you may say I already know that Professor Sachs.

But I chaired the commission for Lancet for the last two years on COVID.

I’m pretty convinced it (the SARS-CoV-2) came out of a US lab, biotechnology. Not out of nature.

Just to mention, after two years of intensive work on this.

So it’s a blunder, in my view, a biotech, not an accident of a natural spillover.

We don’t know for sure. I should be absolutely clear.

But there is enough evidence that it should be looked into and it is not being investigated. Not in the United States. Not anywhere.

And I think for real reasons they don’t want to look under the rug.

I’m not privy to what Prof. Sachs knows.

Still, a paper released two years ago by a group of virologists and vaccinologists expressed concern that the SARS-CoV-2 has the markings of a laboratory origin. That paper was never published in any science journal. You probably know why.

Among all the papers I have read about the lab origins of the SARS-CoV-2, the work of Sørensen, Dalgleish, and Susrud is the most thorough, as it provides a step-by-step account based on several studies on how the SARS-CoV-2 evolved from a bat coronavirus to a highly infectious human pathogen.

At the start of the paper, Sørensen et al. explained that SARS-CoV-2 has several features that make its origin more consistent with purposive manipulation, specifically Gain of Function research

That is a direct contradiction to what Andersen and his group proposed in The Proximal Origins of SARS-CoV-2. [8] 

Bat coronavirus By Naturalis Biodiversity Center, CC0, https://commons.wikimedia.org/w/index.php?curid=44618118

Sørensen and colleagues linked four studies that led to the SARS-CoV-2.

Dr. Zheng Li-Shi, the most experienced virologist and bat specialist at the Wuhan Virology Institute (WVI), is the common thread through all four research projects.

The following are from The Evidence which Suggests that This Is No Naturally Evolved Virus A Reconstructed Historical Aetiology of the SARS-CoV-2 Spike by Sorensen et al.

In 2008, Dr Zheng-Li Si and WIV colleagues successfully demonstrated technical capabilities to interchange Receptor-Binding Domains (RBD) between bat SARS-like and human SARS viruses. [2] The RBD is the part of the spike protein that attaches to the host’s cells.

Building upon this, the 2010 work (Hou et al, 2010) perfected the ability to express (the ACE2 that binds bat SARS-like viruses) receptors on human cells. [3]

On these foundations, the central Gain of Function work that underpins the functionalities of SARS-CoV-2 took place, carrying the WIV spike and plasmid  materials to bond successfully to a UNC Chapel Hill human epithelial cell-line.[4]

This work (Menachery et al.) produced a highly infectious chimeric virus optimised to the human upper respiratory tract.[4]

In convergent support of this hypothesis, both Lu (Lu et al, 2020) and Jia (Jia et al, 2020) have now, in January and April 2020, shown that SARS-CoV-2 has a bat SARS-like backbone but is carrying a Receptor-Binding Domain from a human SARSwith an unusual adaption to humans from the first isolate.

In the 2015 Chapel Hill work it was only ACE2 receptors that were discussed. However, in 2018 Zhou P. et aldemonstrated capabilities to clone other receptors like Amino Peptidase N (APN), and DiPeptidyl Peptidase 4 (DPP4) and to test and compare these against the (intestine) tissue specific Swine Acute Diarrhea Syndrome coronavirus (SADS-CoV) identified.

Then, in the 2019-20 Covid-19 pandemic, profuse symptoms indicating compromise of the bitter/sweet receptors are reported.

Taken all together, this implies that by employing insights gained after 2015, as just deduced, a further optimization of the 2015 chimeric virus for additional binding to receptors/co-receptors such as bitter/sweet specific upper airway epithelia receptors occurred.

That would help to explain the otherwise puzzling high infectivity and pathology associated with SARS-CoV-2 and hence also help to explain the social epidemiology of its spread. 

They conclude,

Henceforth, those who would maintain that the Covid-19 pandemic arose from zoonotic transfer need to explain precisely why this more parsimonious account is wrong before asserting that their evidence is persuasive, most especially when, as we have indicated, we note puzzling errors in their use of evidence.

Slowly, the truth is coming out.

References:

  1. Sørensen, Birger et al. “The Evidence which Suggests that This Is No Naturally Evolved Virus A Reconstructed Historical Aetiology of the SARS-CoV-2 Spike.” (2020).
  2. Wuze Ren, Xiuxia Qu, Wendong Li, Zhenggang Han, Meng Yu, Peng Zhou, Shu-Yi Zhang, Lin-Fa Wang, Hongkui Deng, and Zhengli Shi, 2008, “Difference in Receptor Usage between Severe Acute Respiratory Syndrome (SARS) Coronavirus and
    SARS-Like Coronavirus of Bat Origin”. J Virol. https://doi.org/10.1128/JVI.01085-07
  3. Hou Y, Peng C, Yu M, Li Y, Han Z, Li F, Wang LF, Shi Z., 2010, “Angiotensin-converting enzyme 2 (ACE2) proteins of different bat species confer variable susceptibility to SARS-CoV entry”, Arch Virol, 155:1563–1569, doi: 10.1007/s00705-010-0729-6Hou 2010
  4. Menachery, Zhengli-Li Shi & Ralph S Baric et al., 2015,” A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence,” Nature Medicine, 21(12): 1508–1513. doi:10.1038/nm.3985
  5. Zhou P, Shi ZL, et al. (2018) “Fatal swine acute diarrhea syndrome caused by an HKU2-related coronavirus of bat origin”, Nature 556, 255–258,
    https://doi.org/10.1038/s41586-018-0010-9
  6. Lu et al., “Genomic characterization and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding”. Lancet 2020; 395: 565–74. https://doi.org/10.1016/
    S0140-6736(20)30251-8
  7. Yong Jia, et al. “Analysis of the mutation dynamics of SARS-CoV-2 reveals the spread history and emergence of RBD mutant
    with lower ACE2 binding affinity”. bioRxiv April 11,2020. https://doi.org/10.1101/2020.04.09.034942
  8. Andersen, K. G., Rambaut, A., Lipkin, W.I., Holms, E. C., Garry, R. F., 2020, “The proximal origin of SARS-CoV-2”. Nat Med.