Sars-Cov-2 was Lab Made Under Project DEFUSE

Igor Chudov | 23 May 2022

Sars-Cov-2 is a Result of Years of Documented Scientific Work

This long article will explain how Sars-Cov-2, the virus that causes COVID-19, was created as a result of intentional laboratory work. It will also show that the blueprint for Sars-Cov-2 was described in the “Project DEFUSE” proposal by Peter Daszak, which was preceded by years of relevant lab work and virus manipulation.

I intend this to be a comprehensive “popular science” style article, that has references and abundant links but is generally understandable for regular science-minded people, like journalism or computer science majors.

This article does not introduce any new ideas and is instead meant to be a summary of accumulated knowledge about “lab origin”.

I do not set out here to investigate or debunk the coverup efforts to hide the lab origin of Sars-Cov-2. These coverup efforts involve scrubbing data, as well as promoting a so-called “zoonosis theory”, which is pushed by the NIH, EcoHealth Alliance, and its funders and acolytes. I will simply lay out laboratory-designed features of Sars-Cov-2 and will highlight past research where such features were first discussed prior to 2020. This article is non-judgmental and sticks to facts.

My hope is that reading this article will make you want to send it to your smart friend, who will be able to understand it and will become convinced that “lab origin” is not “baseless misinformation”.


  • Prashant’s Jan 2020 article about strange HIV Gp120 and “gag” inserts in Sars-Cov-2 was withdrawn in haste and under pressure during the weekend, which is unusual.
  • HIV-originated Gp120 inserts in Sars-Cov-2, described by Prashant, are meaningful and instrumental to COVID-19’s infecting immune cells, similarly to HIV.
  • Furin Cleavage Site in Sars-Cov-2 does not exist in other betacoronaviruses and is instrumental for pathogenicity.
  • Dr. Fauci is an expert on HIV and Gp120 glycoprotein and is a co-author of many articles and a coinventor of three Gp120 related patents, and no doubt understood what Prashant’s preprint meant, right away. Fauci and his associates, together with the likely creator of Sars-Cov-2 Peter Daszak, set out to cover up the origin of Sars-Cov-2.
  • Peter Daszak’s 2018 “Project DEFUSE” proposal describes exactly what Sars-Cov-2 actually is.
  • Sars-Cov-2 was possibly cultured on a Moderna MSH3 cell line containing a patented Moderna gene sequence CTCCTCGGCGGGCACGTAG.

Hat Tips

While I followed the lab origin theory starting with the Pradhan article, four people were instrumental in expanding my knowledge of the “lab origin” of Covid-19. It is JikkyLeaks (Twitter @JikkyLeaks), Arkmedic (substack), @Daoyu15, and Charles Rixey (Twitter @CharlesRixeysubstack). Many ideas discussed were first brought up by DRASTIC research. They, in addition to the respected scientists I am citing, came up with almost all the ideas.

The only idea that I came up with, around February 2022, is described in the subsection “HIV Inserts Infect Immune Cells”.

“Uncanny Similarity” to HIV Gp120 and gag Protein

In early 2020, as news of a novel virus killing people in Wuhan emerged, the first genomic sequence of the virus was published around January 20. On January 31, a preprint by Prashant Pradhan was published, alleging that Sars-Cov-2 “borrowed” certain genetic sequences from the HIV virus:

Inexplicably, this paper was withdrawn only two days later, on February 2, under murky circumstances. Mind you, Prashant’s article was published on Friday, Jan 31, 2020, and was withdrawn on Sunday, Feb 2, 2020. So urgent and important was the withdrawal, that important editors had to be roused from their weekend activities to withdraw the article.

fact check was promptly posted on Feb 7, 2020, that confidently declared HIV inserts a “baseless conspiracy theory”. Its author, Jessica McDonald, seems to be an intelligent and informed person on a mission to cover things up that her employer wants to cover up. That fact check made a conclusion that was obviously false even in January 2020 but is worth reading if you have time.

What are these inserts? Are they meaningless? Is the story baseless? Who asked to write a fact check calling this story “baseless”?

HIV Gp120 Inserts are Significant and Unusual

To remind my readers, Sars-Cov-2 is an RNA virus, that has a strand of ribonucleic acid (RNA), enclosed within a viral envelope, surrounded by “spikes”. The spikes have unique attachment points (receptor binding domains) that attach to certain receptors on human cells. That attachment allows the virus to open up the cellular membrane, inject its RNA into the cells, and hijack the cell’s ribosomes to make new copies of the Sars-Cov-2 virus, as encoded by its viral RNA. A good basic video of this is here:

What Pradhan found is that the viral RNA contains highly unusual (for betacoronaviruses) sequences that appear to be lifted from the HIV virus and inserted into the Sars-Cov-2 genome.

Fact-checkers stated that these small sequences are meaningless. They are not.

Far from being useless genetic junk, the HIV inserts in Sars-Cov-2 are very important functionally. Despite appearing discontinuously, the proteins that they encode come together in the final coronavirus spikes:

Interestingly, despite the inserts being discontinuous on the primary amino acid sequence, 3D-modelling of the 2019-nCoV suggests that they converge to constitute the receptor binding site. The finding of 4 unique inserts in the 2019-nCoV, all of which have identity /similarity to amino acid residues in key structural proteins of HIV-1 is unlikely to be fortuitous in nature.

Prashant provides a picture, that I further annotated:

These colored proteins that I circled, are on the outside of the spike and are responsible for interaction with human host cells. Prashant explains:

The insert 1 corresponds to the NTD (N-terminal domain) and the inserts 2 and 3 correspond to the CTD (C-terminal domain) of the S1 subunit in the 2019-nCoV spike glycoprotein. The insert 4 is at the junction of the SD1 (sub domain 1) and SD2 (sub domain 2) of the S1 subunit (Ou et al., 2017). We speculate, that these insertions provide additional flexibility to the glycoprotein binding site by forming a hydrophilic loop in the protein structure that may facilitate or enhance virus-host interactions.

A video illustration of HIV Gp120-specific binding sites is seen in this video:

We all have heard that Sars-Cov-2 enters host cells via a so-called “ACE2” receptor, that is abundant in human lungs. This is typical for many coronaviruses, and the original SARS from 2003 also targeted ACE2. This is what makes SARS-Cov-2 airborne.

That is not all it can do, however. SARS-Cov-2 has another card up its sleeve.

Sars-Cov-2’s HIV Inserts Infect Immune Cells, Like HIV Does

SARS-Cov-2 also has a unique secondary mechanism: its HIV inserts also allow SARS-Cov-2 to act just like HIV and infect T cells of the immune system, contributing to post-COVID immune depletion, without using ACE2 receptors at all. I wrote a long substack article about that, but for the sake of completeness let me restate its major points:

  • Nature article, written by, among other people, Shi Zheng-Li (the Chinese Batwoman from Wuhan Institute of Virology), noted that many patients who had severe Sars-Cov-2 had “lymphopenia”, that is, depletion of the all-important immune T-cells
  • The article shows Sars-Cov-2 virus is able to infect T-cells via a unique (to coronaviruses) mechanism that works like HIV, that also infects the same cells, causing AIDS
  • They “show that the infection is spike-ACE2/TMPRSS2-independent”
  • Infection of T-cells occurs via “LFA-1, the protein [that] exclusively expresses in multiple leukocytes”
  • It turns out that HIV’s gp120 protein, parts of which Pradhan found in Sars-Cov-2, is the one that “Activates LFA-1 on CD4 T-Lymphocytes and Increases Cell Susceptibility to LFA-1-Targeting Leukotoxin
  • Just like HIV, Sars-Cov-2 kills T cells: “infection of T cells induced cell death that is likely in mitochondria ROS-HIF-1a-dependent pathways

Igor’s Newsletter

Sars-Cov-2 Kills T-Cells, Just Like HIV

Is Sars-Cov-2 airborne HIV? Two days ago, an interesting article came out: This article was not written by a bunch of random scientists, but instead was written by people from the Wuhan Institute of Virology, including the infamous batwoman Shi Zheng-Li. Just keep this in mind. It was originally submitted in Sep 2021 and revised in January 2022, so it d…Read more4 months ago · 331 likes · 265 comments · Igor Chudov

To summarize this part: HIV inserts in Sars-Cov-2 are translated into instrumental proteins, that form highly important “attachment points” on the spike protein. Those attachment points, or “receptor binding domains”, allow attaching to several varieties of human cells, including ACE2 expressing cells and immune T cells expressing LFA-1. These HIV Gp120 inserts facilitate entry and destruction of T cells, in a manner similar to HIV, using LFA-1.

Furin Cleavage Site

Another, separate feature discussed in Pradhan’s article, is the “Furin Cleavage Site”, or FCS. That site, also located in the spike protein, is a sequence of proteins encoded as “PRRAR”, that cleaves (separates) the spike protein into two parts when it encounters cellular enzyme furin. It facilitates effective infection. FCS is not present in any other sarbecoviruses.

Arkmedic explains:

And just to complete the quad-trick we need the last insert sequence identified in Pradhan’s paper which is QTNS——PRRA. This is a really interesting sequence which we will come to later, because is the furin cleavage site. It’s interesting because beta coronaviruses likes this don’t have a furin cleavage site, this is the only one. Surely this site couldn’t have come from HIV-1? Well, it’s not from the GP120 protein like the other three sequences, it’s completely different and on a different location of the virus which I’ll show you soon but for now let’s run the BLASTp.

This allows for very high infectivity and pathogenicity of Sars-Cov-2:

Unlike regular mutations (changes) usually replacing one nucleotide for another, a complete and functional “insert” is highly unlikely to be acquired by random viral evolution in bats or other animals.

Thus, the PRRAR furin cleavage site insert is a result of human engineering and is key to Sars-Cov-2 pathogenesis.

Arkmedic’s picture provides a highlight of the FCS (colored green on the picture below):

Here’s a video of how Furin Cleavage Site works:

This diagram, made by Antonio Chaves @Antonio41107975, is the clearest explanation on similarities between SARS-CoV-2 and HIV:

Anthony Fauci is an Expert on HIV and Gp120

Around the time Prashant’s article appeared, a lot of secret email activity (h/t @Jikkyleaks) was happening, discussing how to hide the conclusions of Prashant’s article.

To understand this situation, please note that the director of NIAID, Dr. Anthony Fauci, is actually an expert on HIV and Gp120. Fauci is a co-inventor of THREE patents involving HIV’s Gp120:

Dr. Fauci is also a co-author of many articles about HIV’s Gp120 glycoprotein:

Thus, around January 31, 2020, Fauci would have a full and instant understanding of what HIV Gp120 inserts meant for SARS-Cov-2. What did Dr. Fauci do? He convened with his top associates Trevor Bedford and Kristian Andersen, as well as Peter Daszak, and discussed how they can hide these explosive findings.

Who is Peter Daszak and why is Peter talking to Fauci about hiding evidence of Sars-Cov-2 being a lab product?

Well, Peter is the author of the proposal that gave us SARS-Cov-2.

Peter Daszak and the DEFUSE Project

There is a document, called “Project DEFUSE: Defusing the Threat of Bat-borne Coronaviruses”.

This document, oddly enough, described a set of objectives that aligns exactly with what was implemented as Sars-Cov-2 and described above!

I annotated Peter’s 2018 proposal with (numbers) so I can explain how these sentences describe SARS-Cov-2 specifically and make it easy for you to see how they relate to my article.

  1. The search for a furin cleavage site represented Project DEFUSE’s desire to move on from 2003 Sars-1’s less effective trypsin cleavage site to something more infectious, transmissible and pathogenic, which would be a furin cleavage site. This concept was worked on by scientists as early as 2006 when Kathryn Follis et al attempted to replace the SARS-1 trypsin cleavage site with a furin cleavage site. This shows that the DEFUSE Project is based on preexisting laboratory discoveries.
  2. An excellent explanation of interaction of Sars-Cov-2 with DC-SIGN and L-Sign is in a PLOS article “DC/L-SIGN recognition of spike glycoprotein promotes SARS-CoV-2 trans-infection”. Read that link if you have 10 minutes.DC-SIGN is a dendritic cell lectin that binds to HIV’s Gp120 — and Gp120 is what was added to Sars-Cov-2.
  3. Here Project DEFUSE describes testing their new virus on human cells expressing above mentioned DC-SIGN.
  4. Project DEFUSE anticipated problems infecting immune cells (monocytes and macrophages) and thus added specific Gp120 sequences allowing Sars-Cov-2 to infect those specific cells via the above-mentioned LFA-1 mechanism.
  5. Project DEFUSE tested the result in transgenic (humanized) mice, having human ACE2 receptors in their lungs. The mice had to be humanized: as we know, Sars-Cov-2 was able to infect people, but not mice, at the beginning of its history. (Side Note: Later on, another famous virologist, Ralph Baric of UNC, worked on allowing Sars-Cov-2 to infect regular — not transgenic — mice. And guess what, somehow the later variants of Sars-Cov2 (Omicron) do infect mice, a development that may or may not be related to Baric’s research. Baric was also on the email thread with Fauci shown above.).
  6. I believe that “commercial gene blocks” mentioned by Project DEFUSE are HIV’s Gp120 and Gag protein blocks.
  7. Testing on humanized mice was not enough for Project DEFUSE authors, and they finally tested their assembled product on “HAE cells”, which are “human airway epithelial” cells just like the cells you have in your lungs.

The last sentence (7): “test … in Human Airway Epithelial [cells] and in vivo pathogenesis”, semantically, means lab testing in Human Airway Epithelial cells, and then in vivo testing in live HUMANS.

Stop for a second and read that again. What?

I am not sure if the authors really meant that sentence to mean testing Sars-Cov-2 in humans, as English is not my native language. But my understanding is that the plain meaning of the above-quoted sentence is to refer to testing in humans, describing in-vivo testing after in-vitro testing on explicitly human cells.

Whatever “in … HAE cells and in vivo pathogenesis” meant to the author, Sars-Cov-2 has plenty of in vivo pathogenesis in humans, as the families of 6,299,692 dead COVID patients would readily attest to.

Sars-Cov-2 has a Sequence from Moderna Patent 9,587,003 from 2018

Sars-Cov-2 has a nucleotide sequence CTCCTCGGCGGGCACGTAG. Oddly enough, a reverse complement to this sequence exists in a Moderna Patent 9,587,003, that describes certain human cancer cell lines. The probability of that sequence being in Sars-Cov-2 due to random chance is estimated to be around one in 100,000,000,000. The most likely explanation for how that sequence could end up in Sars-Cov-2 is that Sars-Cov-2 was cultured in Moderna-owned MSH3 cell culture at some point.

For people who enjoy trying NIH’s BLAST tool to hunt genes, I wrote an article on how exactly to match the Sars-Cov-2 CTCCTCGGCGGGCACGTAG sequence to the Moderna patent sequence. Try it out and have fun.

Disclaimers and Uncertainties

Let me mention a few things that my article leaves out:

  • I proved (based on the work of others) that Sars-Cov-2 was designed in a lab. I did not identify the lab, or the person who did it (although Sars-Cov-2 originates from the DEFUSE Project). I am very aware that Wuhan is the home of Wuhan Institute of Virology. That said, WIV is not the only possible source of Sars-Cov-2.
  • The DEFUSE Project proposal was rejected by DARPA. However, EcoHealth Alliance was given money by DoD, NIH, and other players such as the Bill and Melinda Gates Foundation. Saying that DEFUSE was never implemented, is incorrect. Project DEFUSE was implemented and the result is Sars-Cov-2, which matches Project DEFUSE. Here, federal money was given via DTRA (Defense Threat Reduction Agency) for the exact purpose stated in Project DEFUSE.
  • The sequence CTCCTCGGCGGGCACGTAG in Sars-Cov-2 does NOT prove or even imply that Moderna was involved in creating Sars-Cov-2. It merely proves lab origin.
  • We do NOT know whether Sars-Cov-2 was released intentionally or accidentally. This article does NOT attempt to identify any specific persons or reasons involved in releasing it.
  • This article does not prove or even imply that Sars-Cov-2 was implemented with the intent, from the beginning, to be released and wreak havoc on humanity. I am leaving this topic out.
  • Whether “Covid Vaccine” was created before Sars-Cov-2 was known officially, is a very important question, that I do not want to discuss in this article, even though I discussed it in the past.

Further Reading

For those curious to learn more, arkmedic provides outstanding details on gp120 inserts, how they look, why they are unusual and lab-made, and their functionality. Please spare a half-hour of your time when you get a moment to read the article below:

Arkmedic’s blog

Absolute proof: The Gp-120 sequences prove beyond all doubt that “COVID-19” was man-made

Following on from December’s article “How to BLAST your way to the truth about the origins of COVID-19” where I explained how the four “inserts” described in Pradhan’s Feb 2020 paper showed definitively that the SARS-CoV-2 genome had to have been man-made, there has been considerable interest and a lot of push-back from those whose reputations are on th…Read more3 months ago · 104 likes · 80 comments · Dr Ah Kahn Syed

Famous economist Jeffrey Sachs wrote an article in PNAS that is pointing out SOME lab-made features of SARS-Cov-2 and is asking for an investigation.

However, unfortunately, Jeffrey Sachs is a brilliant economist and not a virologist. His well-intentioned and extremely well-written article left out HIV-related features, and other facts, that are monumentally important, perhaps due to article size restrictions. Jeffrey’s article is what prompted me to write this post — because I felt that he unintentionally omitted the most crucial details.

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