I have previously mentioned that Ron Fouchier described 6 features of SARS-CoV-2 that looked engineered in the memorandum he wrote for Fauci to memorialize the famed Feb 1, 2020 phone call. Possibly there were 2 calls.

In an article I have posted at the end of this piece, Dr. Steven Quay goes further into the weeds on the 3 HIV gp120 peptide sequences that were highly suspected of being engineered by 2 senior Indian scientists on January 31, 2020. Their famous paper was summarily retracted, allegedly by themselves but more likely by Fauci’s boys, in 48 hours. Soon thereafter, Nobel laureate and HIV discoverer Luc Montagnier said on French TV that the GP120 sequences were deliberately inserted into the genome by a highly skilled virologist. Shortly after that, Montagnier died suddenly at age 89.

Steven Quay recently published a preprint on this topic, and while Zenodo says it got published by a journal in December, I am having trouble finding the journal publication in either PubMed or Google Scholar. I made a pdf from the preprint site. The preprint uses the word “providence” twice to mean “provenance.” One paragraph is incomplete.

I am not competent to assess the fine details, but I note that another paper in Trends in Immunology, with the following title and abstract (the rest was behind a paywall) was published in October 2024. Perhaps we are getting closer to understanding the nasty neuropathology of COVID?

You can read Dr. Quay’s paper on the preprint site:

https://zenodo.org/records/14559752

Excerpts below. A pdf of the entire article is below that. It is brief and pithy.

The thrombo-inflammation and neuropathology sequence motifs of the SARS-CoV-2 spike protein appear to have been engineered into the virus

Steven Quay, MD, PhD1

ABSTRACT

A landmark [published in Nature—Nass] paper2 entitled, “Fibrin drives thrombo-inflammation and neuropathology in COVID-19,” was published in August 2024 that concluded the mechanism of the thrombotic and neurological symptoms following a SARS-CoV-2 infection, often called “long COVID,” is attributable to the binding of fibrin to discrete portions of the spike protein, specifically three N-terminal domains. This paper is a high impact publication with >110,000 views, placing it in the 99 th percentile of articles published contemporaneously.

Here I examine the regions of the spike protein that bind to fibrin, fibrinogen, or both. The N-terminus of the spike protein contains the three strongest binding peptides and surprisingly, these regions are also the three insertions in the protein sequence that are unique to SARS-CoV-2 and not found in natural sarbecoviruses….

CONCLUSION

This paper highlights an unusual set of facts:

1. SARS-CoV-2 causes neuro-inflammation and its “long COVID” clinical findings through a mechanism whereby fibrin binds to the SARS-CoV-2 spike protein, forming proinflammatory blood clots.

2. Three of the strongest [fibrin] binding motifs identified by Ryu et. al., are in the N-terminus of the SARS-CoV-2 Spike Protein.

3. These motifs are contiguous to the three inserts identified in January 2020 that are not widely found in related-SARS viruses.

4. These inserts are shown to have primary amino acid sequence homology to portions of the HIV gp120 protein that is responsible for CD4 cell receptor binding. While the sequences are individually small, making their probabilities of being randomly significant unlikely, when they are combined as a continuous 60-amino acid sequence, the homology to HIV is highly significant. The combination is justified because the non-contiguous sequences in HIV are none-the-less brought together to form the CD4 cell receptor binding protein.

5. Antibodies from patients with HIV infections have been found which block the HIV CD4 recognition site and neutralize SARS-CoV-2. This demonstrates the three-dimensional homology of these regions in a functionally significant manner.

6. A hypothesis that both HIV and SARS-CoV-2 can infect CD4 cells via this non-ACE2 interaction is supported by abundant clinical findings.

7. HIV does not share the fibrin binding motifs seen in SARS-CoV-2 and, for the most part, evidence of direct HIV binding to fibrin has not been found.

8. RaTG13 shares 59/60 amino acid homology and, for insert 3, a nucleotide homology of 99.3%. Since there are numerous papers suggesting that RaTG13 has undergone laboratory genetic experiments, one much conclude that there is a likelihood that these unusual properties of SARS-CoV-2 did not arise naturally.

	Quay, Steven Pathogenesis Of Sars Cov 2 … 3.67MB ∙ PDF file
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Note that on January 23, 2020 She Zheng-Li published on RaTG13 and SARS-CoV-2, pointing out that the 3 gp120 sequences were seen in both SARS-CoV-2 and RaTG13. The origin of RaTG13 is uncertain and it certainly could have been manipulated. These sequences have not been seen in any other beta coronaviruses…

However, Jim Haslam points out that yet a third betacoronavirus, found in Laos by the US Navy (NMRC, a small unit that has long been focused on biodefense), also has the three GP120 inserts. The virus is referred to as “Laos Banal-52” on pages 175 and 415 of his book. The provenance of this virus, and identifying which labs had access to it, would be of great interest.

Bottom line:

• IMHO, the GP120 segments were clearly added to a coronavirus spike backbone.
• So were adjacent regions that strongly bind fibrin or related molecules, inducing blood clots and inflammation.
• Ralph Baric’s repeat protestations against these regions being engineered (see Chapter 16 of Haslam’s book), combined with Baric’s reputation as the most accomplished coronavirus engineer, suggest he had something to do with the engineering, or at least knows more than he has said about it.
• It is likely, but uncertain, that the fibrin-binding domains were added to enhance pathogenicity.
• The Navy’s Laos-Banal-52 sample requires further investigation. Was it natural, or might it turn out to be an early iteration of SARS-CoV-2?