293 Questions for Ralph Baric
Since Baric won't answer, I will
The Wuhan lab leak sleuths of DRASTIC flagged Ralph Baric as a person of interest before most of us knew his American name. While the public was still wiping down groceries in early 2020, DRASTIC was already examining Baric’s fingerprints on coronavirus engineering.
I didn’t encounter Baric’s name until 2021. A New York Magazine piece, based on DRASTIC’s research, referenced Baric’s work 40 times, twice as often as Shi Zhengli’s. My first thought was: Who is this white guy, and what is he doing in Wuhan?
From 2015 to 2020, the paper trail was blatant: Shi from Wuhan shipped Baric bat samples; Baric from North Carolina shipped her humanized mice. His technology was much more advanced than hers. It looked suspicious, but at the time, there was no document directly tying Baric to the creation of COVID. Baric famously said, “Proximity is a problem” for Shi’s lab.
No one yet understood that engineered genomes can be mailed like any other lab reagent. So the early lab leak narrative assumed Baric must have “taught” Shi how to build something like SARS-CoV-2. After all, neither scientist had publicly proposed inserting a furin cleavage site into a SARS-like backbone.
Baric played the press like a fiddle. He postured as a reasonable voice, leaning toward a natural origin, and gently nudged suspicion toward Shi’s BSL2 lab. Then DRASTIC published the DARPA Defuse bid in September 2021. And Baric didn’t just go quiet—he disappeared for nearly three years.
When Baric finally resurfaced in 2024 testimony, he was asked why he hadn’t disclosed Defuse himself. His answer? He “forgot” and added this remarkable shrug:
After it was released by — I forgot the name of that group, the computer sleuths [DRASTIC] — I saw it on the news. And I was thinking, what’s this? And I read it. Yeah, I wrote the [furin cleavage site] grant.
This is the virological equivalent of finding the Wuhan murder weapon in a North Carolina garage and hearing him say, Oh, that must’ve slipped my mind.
Back in 2021, DRASTIC’s Billy Bostickson published 83 questions for Baric. None were answered. This week, Bostickson added more than 200 new ones, as Baric’s involvement continues to expand the closer one looks.
https://www.researchgate.net/publication/397608384_293_QUESTIONS_FOR_DRRALPH_BARIC_2025
Many fellow lab leakers added to Bostickson’s long list, including myself. Some still defend Baric for various reasons. It’s obvious why they think Baric is innocent if you read through their long list of questions. They still believe Baric “taught” Shi how to create the SARS2 genome. It’s a biosecurity myth that knowledge can be shared since “we can know more than we can tell.” Most lab leak journalists think knowledge crosses borders more easily than genomes.
Lab leakers then focus too much on the genome and not enough on the COVID transmission models. Since Baric refuses to speak to the press, I’ll answer their lab leak questions on his behalf.
This loooong post is inside baseball, so the TLDR on BILLY BOSTICKSON 293 questions:
Do you agree with Dr. Ian Lipkin’s 2021 statement to El País that scientists at the Wuhan Institute of Virology may not have exercised appropriate safety precautions, citing BSL-2 work with bat coronaviruses?
Yes, I recently co-wrote a New York Times (propaganda) piece with Lipkin pointing the finger at Shi’s BSL2, but didn’t disclose my 2018 DARPA Defuse plans to “provide” Shi with SARS2-like genomes.
In your September 2020 Italian interview, you stated that SARS-CoV-2 could be assembled using 3–4 established coronavirus reverse-genetics techniques without leaving detectable signatures. Why did you make this assertion, and what specific techniques were you referring to?
I wasn’t trying to hide the engineering scars for you gullible lab leakers; I was trying to hide them from a bat’s immune system. If my manmade Chinese genome looks like it came from nature, it’s easier to infect Chinese bats. In other words, if my genome leaked from the WIV, it would look like it came from the Wuhan wet market! Or what I previously called the “scapegoat option.”
In the same Italian interview, you stated there is “no proof from genomic data that it wasn’t from a lab” and that definitive answers could only come from inside WIV. Why did you frame the burden of proof this way, and why only to an Italian audience?
I like to brag to hot Italian reporters about my superior biotechnology!
On 22 May 2020, you issued an author correction to your 2015 Nature Medicine paper, adding a new sequence (SHC014-MA15). What prompted this correction five years after publication, and why was the sequence not disclosed earlier?
I never uploaded a novel genome sequence before the pandemic, because I kept my biotechnology “obscure” from the Chinese scientists. So I uploaded the genome post-pandemic to quiet my involvement in the engineering rumors. Shi shared the SHC014 bat sample with me before publication, so I added her name to the 2015 paper. Something similar was planned with RaTG13, and I was going to add her name to an upcoming paper on a bat vaccine, but it leaked from Danielle Anderson’s BSL4 before publication.
The 2018 Scientific Reports paper demonstrated that 2-proline-stabilized SARS-CoV spikes resist conformational collapse after trypsin cleavage at S1/S2, even when furin sites are present. Was this work (a) intended to validate prefusion immunogens for furin-cleavable SARS-like viruses, and (b) directly applicable to SARS-CoV-2 vaccine design?
Yes, since the SARS2 virus is my bat vaccine, I also worked with the Moderna team on the human (mRNA) vaccine. I double-dipped into this cash cow!
Did this research aim to ensure that cleavage didn’t alter conformation or lead to S1 breaking off, so that a 2-proline modified stabilized prefusion protein would be a good vaccine immunogen even if furin cleaved the S1/S2 site, and the S1/S2 cleaved SARS protein still was stable in the desired conformation?
Whatever, but yes. The MERS-MA30 publication further incriminated my proline preference.
If not Baric-led, why was it funded under your NIAID cooperative agreement?
My pre-pandemic research on furin cleavage sites was extensive. If you read the infamous 2017 Moderna mRNA patent and my 2018 DARPA Defuse proposal, you will notice significant overlap (e.g., R667 FCS, live bats, 293-F cells, etc). Now I know why Billy Bostickson wanted to ask me 293 questions!
In 2020, you publicly dismissed pangolins as plausible intermediate hosts for SARS-CoV-2. How do you reconcile this with the near-identical RBD sequences between SARS-CoV-2 and Guangxi/Guangdong pangolin coronaviruses (e.g., GX_P2V)?
After you assholes leaked my DARPA Defuse plans, I finally hopped on board with the pangolin conspiracy, and mixed in some American deer and American mink (ask my buddy Vincent Munster at RML how that happened).
If recombination between a RaTG13-like backbone and a pangolin-CoV RBD occurred, is this event more parsimoniously explained by natural ecology or by serial passage in contaminated cell cultures (e.g., Vero E6 or Calu 3 co-infected with both viruses)?
Prior to 2020, did you know if WIV possessed live isolates or tissue samples of Guangxi/Guangdong pangolin coronaviruses?
Prior to 2020, I didn’t know what a pangolin was.
If so, were any shared with your laboratory?
No, but Shi did share the RaTG13 sample with me.
Did you know that the State Key Laboratory of Pathogens and Biosecurity in Beijing isolated the Pangolin GX_P2 coronavirus series in 2017 and sent samples to BSL2 Labs in China?
No, but before the pandemic, Munster and I planned to send SARS-like sequences to Wuhan for an “experimental inoculation study using Chinese horseshoe bats.”
What is your assessment of the involvement of the Beijing Institute of Microbiology and Epidemiology (State Key Laboratory of Pathogen and Biosecurity, Professors Yang Ruifu, Yigang Tong, Col. Wu-Chang Cao) in sequencing and distributing pangolin-CoV isolates (e.g., GX_P2V series) as early as 2017?
I appreciate Fauci’s former boss, Bob Kadlec, keeping the heat on the Chinese military and off me. He thinks the PLA was doing some SARS2 mind control research or “cognitive dominance through biology.”
Have you ever corresponded or collaborated with Professors Yang Ruifu, Yigang Tong, or Col. Wu-Chang Cao?
I have a hard time with Chinese names, so I’m not sure, but the answer is yes if you suspect them.
If so, on what projects, and what contexts?
As Bob Kadlec claims above, mind control research.
Do you possess, or have you ever had access to, any WIV viral sequence databases taken offline in September 2019, including the 61.5 MB SQL archive or its password-protected sections?
Yes, I was given access to the WIV database after being added to the NIAID R01 grant in 2019. I testified:
My role was to study a couple of the viruses that the Wuhan Institute of Virology found that they were willing to share with me. So I always viewed that as not number one or number two on the list, maybe number five or number six on the list… They did the discovery work and they’re going to choose the priority of what they want to work on first [Shi worked on SARS1-like viruses]. And so I’m not going to get the dregs, that would be an unfair characterization, but I’m not going to get number one. I’m going to get somewhere down the list, which is okay, and I understand that process. Hopefully, it would be something that they felt would be interesting as well. [Baric wanted 25% different SARS2-like viruses like RaTG13].
During the 2014–2017 U.S. GOF moratorium, which specific experiments did you conduct in collaboration with Dr. Zhengli Shi, and under what NIH exemption?
We didn’t collaborate. Shi shared the SHC014 sequence with me because she was unable to isolate the virus. So Shi sent me the plasmid on filter paper, and I did the engineering. I just needed Shi’s bat sequences to engineer a live Chinese virus in my North Carolina lab. My GoF exemption was always a rubber stamp within NIAID.
What exemptions did you request from NIH/NIAID during the moratorium, and what scientific justification was provided?
I got away with a “national security” excuse. I used the same national security language in my 2018 bat vaccine paper, referencing the abandoned Mojiang mineshaft where RaTG13 was collected.
Why were your chimeric coronavirus projects (e.g., SHC014-MA15, WIV1-MA15) not classified as “gain-of-function research of concern” by funding agencies or UNC’s IBC?
It’s the same classification I used in DARPA Defuse: “These use bat-SARS-CoV backbones, not SARS-CoV, and are exempt from dual use and gain of function concerns.” In other words, I’m playing with bat viruses, not human ones, yet!
How did your lab comply with the 2016 NSABB recommendations on GOF oversight while continuing reverse-genetics assembly of novel SARS-like backbones?
It’s called the Baptist and Bootlegger effect of regulation—rules for thee but not for me.
What specific virus was carried by the mice that bit UNC researchers?
I don’t know and I don’t care. But notice my UNC technicians were never “sickened” after a mouse attack. That’s because “adapting coronaviruses to humanized mice makes them less able to infect humans.” I could push the genomic edge of coronavirus research in my safe lab mice. Take up the “edgy” aerosolization research with Munster.
Have you or any member of your laboratory ever been bitten by a humanized (hACE2-transgenic) mouse?
Yes, I have thousands of mice and probably hundreds of bites, but my mice caused zero pandemics.
Since 2018, have you had any communications with EcoHealth Alliance staff members William Karesh, Jonathan Epstein, or Kevin Olival regarding sample transfers or funding?
Had a lot of conversation with my boys at EcoHealth. Billy Karesh and I are buddies. I provided Jon Epstein with the GoF workaround for the DARPA Defuse project. And Kevin Olival helped me recycle DARPA Defuse text under NIAID grants.
How many viable viral isolates has your lab received from EcoHealth Alliance since 2015, and from which countries?
I had access to 700 samples from Wuhan.
Please describe the full scope of your laboratory’s contracts with DTRA and DARPA since 2015, including project titles, funding amounts, and deliverables.
I told DTRA to screw off with only $500,000 grants, and told my wife DARPA was a “persistent bunch.”
With which of the following individuals have you communicated with since 2015, and on what topics?
Fang Li from the University of Minnesota
Fang does biochemistry (RBD) work, and I conduct the dangerous GoF research.
Sina Bavari from Fort Detrick
Sina doesn’t have access to my human airway epithelial cells. Fort Detrick is an Ebola and Anthrax lab. The last time they studied coronaviruses was in 2001, but I’m not a “rogue scientist.”
Jens Kuhn
He is a bioweaponer from Germany and Russia, and he called Kristian Andersen, Eddie Holmes, and Bob Garry the 3 biggest egos, so I like him.
David Franz, who was the ex-commander of Fort Detrick
George Fu Gao of China’s CDC
The only person [from China] that I ever really worked with on a molecular clone was George Gao, and this was prior to the 2020 SARS2 pandemic virus. If you remember, MERS coronavirus transmitted from the Middle East to Korea and infected a lot of Korean citizens. One of those was a Chinese citizen who moved back to China and traveled back to Beijing and infected — that they sequenced the virus from. And they couldn’t culture it. So Gao asked me if I would be willing to help make a molecular clone for that virus. So we designed — we worked with him — actually, we reviewed their design, and so they tried to make a molecular clone. They failed. Ultimately, they never got it to work. They sent the clone to us. This was around 2016. We actually recovered the virus; it’s still sitting in my lab. When I told them we have the virus, he never answered me, and so it’s still sitting in my lab, and I’ve never used it.
How many postdoctoral researchers from mainland China have trained in your lab since 2010?
We never had anyone from Dr. Shi’s lab or any of the Wuhan Institute of Virology come to our lab and train. We never taught them.
Of those, how many subsequently joined BSL-3 or BSL-4 facilities in China (e.g., WIV, Harbin Veterinary Research Institute)?
I only interacted with Dani Anderson both pre- and post-pandemic.
Are you familiar with the DRASTIC research collective (drasticresearch.org) and their published analyses of the missing WIV viral databases and DEFUSE?
Yes, I’m aware of DRASTIC or the “computer sleuths.”
Do you, in principle, support DRASTIC’s call for an independent forensic audit of WIV BSL-2/3/4 facilities and sequence archives?
Hell yes!
After 2018, did WIV request additional hACE2-transgenic BALB/c mice from your breeding colony? If so, how many and on what dates?
I sent them breeder pairs in 2016, and they did their own research. It was part of a Material Transfer Agreement with Wuhan to reproduce UNC research.
Does WIV conduct coronavirus challenge studies in human lung xenograft mice?
If so, under what biosafety level?
The WIV did most work under a BSL2 level, and so did I. My reverse genetic system was so good that I could pre-assemble SARS2 into 6 segments under BSL2 conditions.
Are the unpublished WIV isolates WIV6 and WIV15 members of the SARS-related betacoronavirus clade? Reference: DRASTIC RaTG13/7896 investigation https://www.researchgate.net/publication/350515493_2_INVESTIGATION_OF_R aTG13_AND_THE_7896_CLADE
WIV6 is irrelevant and WIV15 is only 1 of 3 viruses the WIV has isolated. All are closer to SARS1 and SARS2. By the way, I have an unpublished chimera called WIV16.
Why did WIV withhold full-length sequences of the 7896 clade (including RaTG13’s closest relatives)?
Because Shi wanted to publish in Latinne et al in late 2019.
Is it plausible that WIV continued serial passage experiments initiated in Hu et al. (2017) by inserting novel spikes into SARS backbones, using hACE2 mice post-2018?
They developed their own molecular clone, based on WIV1 and closer to SARS1. And into that WIV1 backbone, they shuffled spike genes of other bat coronaviruses. They do not have a SARS2-like molecular clone. That 2017 Wuhan paper also used Vero cells, which delete the furin cleavage site.
Does the Wuhan Institute of Virology possess the technical capability to engineer a betacoronavirus with SARS-CoV-2-like transmissibility from bat precursors?
They use baculoviruses, and their molecular clone is a virus called WIV1, which I don’t think they engineered with class IIS restriction enzymes that don’t leave any sequence. So I think there’s a sequence signature in that virus.
But in general, yes, they had the technology to do it, but they really struggled with trying to develop other molecular clones. They were working on developing the SARS molecular clone from 2016 on, and they failed. It’s not easy technology. So we started three years later and beat them to press, just to show you. And I had no interest in teaching them how to do it faster, either.
How technically challenging is it to derive a human-adapted, highly transmissible coronavirus from a bat progenitor in a BSL-3 laboratory setting?
It’s impossible to create a highly transmissible coronavirus in humanized mice or in vitro research. I made that clear in an NPR interview before the pandemic.
Is it feasible to synthesize SARS-CoV-2 via fragment assembly using a RaTG13/7896-clade backbone and a GX/GD pangolin-CoV RBD, followed by cell-culture selection?
I could do it, and showed something similar in my 2023 Nature publication.
In such a synthetic or passaged construct, how might a furin cleavage site (FCS) be introduced, via directed insertion, serial passage, or recombination, and would it typically be in-frame or out-of-frame?
Notice my conclusion in the 2023 pangolin paper: Although the PgCoV GD strain provides an optimal model to evaluate the impact of a furin cleavage site at the S1/S2 border on replication, pathogenesis and transmission, we urge constraint as such studies should require transparent, independent and rigorous review.
Prior to 2020, did WIV conduct coronavirus challenge studies in non-human primates at BSL-3 or BSL-4?
I don’t know, but I did monkey research (Remdesivir) at RML with Munster.
If so, were you involved in design, analysis, or sample sharing?
Yes, but with Danielle Anderson in the Wuhan BSL4. Not with monkeys but Chinese bats. I had everything in North Carolina, except Chinese bats, which produced fascinating RaTG13 samples.
In your expert opinion, is RaTG13 a naturally sequenced field isolate from an anal swab or bat mating plug, or is there evidence of laboratory reconstruction (e.g., via cDNA fragment assembly)?
Since 2015, I have been searching for a unicorn bat sample like RaTG13. Its spike protein is exactly 25% different from SARS1, which is what I was looking for.
Given documented biosafety lapses at WIV (e.g., BSL-2 bat-CoV work, inadequate PPE during field sampling), do you consider leakage via contaminated cell lines a plausible origin pathway?
Yes, anything that points to Shi’s BSL2 is good news for me.
Why did UNC withhold your email records from 20 March 2019 to 9 January 2020 in response to USRTK FOIA requests?
Because I’m hiding incriminating 2019 emails with Dani Anderson in Wuhan and Vincent Munster in Montana.
Will you voluntarily release these emails or direct UNC to do so for an independent investigation?
Over my dead body.
Pre-2020, did you know that WIV was collaborating with the Wuhan Institute of Biological Products on a pan-betacoronavirus “Disease X” vaccine platform?
No, but the WIBP is near Dani Anderson’s BSL4, so this sounds good!
If so, were you consulted in any way about such a project (Disease X)?
I was busy creating SARS2, not Disease X.
In Ben Hu’s unpublished WIV work, which two novel bat SARS-related CoVs were tested for pathogenicity in hACE2-transgenic mice?
Ask him. Sounds like he was sick, based on a David Asher rumor.
In your 2020 Presa Diretta interview, you noted researchers often insert short “lab tags” into synthetic mutants. Do any such signatures appear in the SARS-CoV-2 genome?
Could the 7-nt deletion (TGGTCGC) at nt 1465–1471, which deletes part of the nsp2 protein in the ORF 1ab of SARS-COV-2, represent a deliberate or residual cloning artifact?
In my 2018 LAV bat vaccine paper, I’m obsessed with this “fascinating” and “unique” sequence motif, found only near the start of Orf1a. It could prevent recombination and make for a perfect bat vaccine.
Are you aware of engineered modifications to SARS-CoV-2’s transcriptional regulatory sequences (TRS) that enhance genomic stability beyond natural betacoronaviruses?
Yes, in 2009, I gave an incriminating presentation on TRS and CRG in Hong Kong:
The claim that SARS-CoV-2’s FCS shares a 19-nt sequence (CTCCTCGGCGGGCACGTAG) with Moderna patent US9587003 (not found in nature) has been widely circulated. Would you agree that this is a misleading claim?
It’s pretty shady because I worked with the Moderna mRNA patent team.
Would you also disagree that it is perfectly placed for a single template switching recombination to paste the CTCCTCGGCGGGCACGTAG into the SARS-CoV-2 genome?
Even the Moderna CEO was perplexed.
SARS-CoV-2’s PRRA FCS exactly mimics the furin-cleavable RRAR motif on human ENaC-α (extracellular domain). Is this mimicry functionally significant?
Yes, but mainly because I had both RaTG13 and Laos BANAL-52 (a unique RSVAS amino acid sequence) by 2018.
Would you agree that the location of this SARS-CoV-2 mimicked peptide in the ENaC-ɑ structure in the extracellular domain suggests that SARS-CoV-2 may have specifically evolved to mimic a human protease substrate?
Humans aren’t the only mammals on the planet. Bat cells also contain furin, and this ENaC research was geared towards rats.
Given co-expression of ACE2 and ENaC-α in the apical membranes of polarized epithelial cells such as primary lung epithelial alveolar type II cells, routinely used in WIV chimera studies, does this convergence support laboratory adaptation?
Yes, I accidentally left a ton of bread crumbs in North Carolina, not Wuhan.
Thus, taking into account the above research, could recombination between FIPV and a bat SARSr-CoV in a feline host explain the SARS-CoV-2’s S1/S2 site?
COVID doesn’t transmit in cats or humanized mice, so no.
Now, moving on to vaccine work, could you briefly describe what makes a live-attenuated vaccine different from an inactivated vaccine?
Live attenuated vaccines are excellent for animals but never approved for human use.
Why was a live-attenuated vaccine necessary for Yellow Fever and what were the difficulties involved in making a vaccine for Yellow Fever?
I only created live-attenuated for Chinese bats, not Yellow Fever for humans. We virologists are just glorified veterinarians, not CIA operatives.
What serial-passage challenges arose, and how do these inform coronavirus vaccine strategies?
In the MERS-MA30, I used 30 serial passages to lock in the Proline found in SARS2.
Describe the 2015 UNC chimeric platform: backbone, spike donor, and intended phenotype.
In 2020, I finally uploaded my 2015 chimera, which resulted in a large 11,000-nucleotide fragment. I testified I would never do this, but here it is:
Functionally, how does your 2015 SARS-like chimera (SHC014 in SARS-MA15) differ from the YF-17D/Japanese encephalitis attenuation chimera?
That’s Japanese technology, not mine, which is based on my Mouse Hepatitis Virus (MHV) model.
If you weren’t making a chimera for vaccine attenuation, what was the goal of your research at UNC in 2015?
To scare NIAID into more risky research by creating risky genomes. The title says it all:
Press reports document multiple UNC select-agent exposures from 2015 to 2018. Were any coronaviruses involved?
I’m sure there were, but my mice are safe and sound science. No pandemic potential created at UNC!
The leaked agents were deemed “non-life-threatening.” Does this align with an attenuated vaccine candidate rather than a wild-type pathogen?
If it leaked from my lab, it was mouse-adapted, not human-adapted. When asked if I was making viruses more dangerous, my dry humor responded, “If you’re a mouse, the answer is probably yes, or at least I was trying to.”
Which SARS-CoV-2 emergence features are incompatible with a vaccine-derived escape (e.g., FCS, RBD optimization)?
I inserted the furin cleavage site to infect bats, and optimized the Receptor Binding Domain (RBD) for Chinese horseshoe bats. Unfortunately, furin and the RBD overlap with humans and bats.
Can you kindly explain why SARS-CoV-2 elicits original antigenic sin of the common-cold coronaviruses (OC43/HKU1), viruses that have nothing to do with bats, when SARS-CoV-2 seems to have derived the majority of its genome from bats?
As I described in my congressional presentation, human coronaviruses originated from bats, rodents, or cattle. The biodefense idea was to vaccinate the bats to prevent another SARS-like emergence. But we accidentally created SARS2. I didn’t bother to mention any of this to Congress, which funded my risky research:
How do you explain this immunodominance shift?
Like everything, I have a paper on that.
Does SARS-CoV-2 exhibit genomic hallmarks of live-attenuation (e.g., codon deoptimization, TRS stabilization) consistent with live attenuated vaccine development?
Yes, but the vaccine hallmarks are immune evasion. My SARS2 genome, without the FCS, acts like a human LAV.
Independent analyses identify BglI-like sites with synonymous mutations at positions 12143–12154 in ORF1a, 17077–17091 in ORF1b (remains of FE-primer), and 22568–22579 (S1, near FCS). These may be “remains” of cloning sites that had been passaged, because these positions are similar to the (original) cloning sites. In addition, we see hotspots of synonymous mutations at/around these sites, which cannot be explained by “natural virus evolution“. These seem to match your “no-see’m” cloning junctions.
You caught me.
Do they represent passaged cloning scars from a backbone + spike-swap assembly?
Maybe.
Would you thus agree that a previously assembled backbone into which just the spike was swapped (possibly just the S1 domain containing RBD and FCS) would agree with these observations?
Possibly.
If you find the above conclusion unacceptable, can you kindly explain: The (synonymous) sequence alterations in the SARS-COV-2 genome at the key positions pos. 12143 – 12154 in ORF1a, pos. 17077 – 17091 in ORF1b and most importantly pos. 22568 – 22579 in spike S1 compared to other SARSr-CoV, since these potential BglI-sites had been used before by “your seamless cloning method” to assemble other SARSr-CoV genomes from contiguous cDNA-fragments or to swap the spike gene.
Dr. Valentin Bruttel figured me out long ago, but thought Shi did it.
From your expertise in seamless assembly, do any SARS-CoV-2 genomic features suggest synthetic fragment ligation?
Yes, I testified that there are 6 fragments in the SARS2 genome, and I always used 6 fragments.
We think our approach is safer because we’ve divided the genome into six pieces, so there’s no way any of those can initiate an infection. And we don’t assemble until we’re in the BSL-3. So it’s fundamentally safer than what was done by others.
Would you agree that WIV Researchers were capable of carrying out these methods (perform trace-free S-gene swaps using your UNC-derived BAC reverse-genetics system) in the years leading up to 2019 in line with published papers and unpublished theses Zeng (2017) and Hu et al. (2017)?
No, I testified they use a different technology that produces 8 or more fragments. I don’t always lie, so here I am in sworn testimony:
If you look at their cloning technology, they use baculoviruses. They may assemble some of the full length molecule using some of the enzymes that we have, but they implant it directly into an insect virus to maintain it as a
baculovirus, which was a technology developed in Europe, not my technology.
Would you agree that the following background summaries are accurate? WIV has
used exactly this technology (described in a recently discovered 2018 doctoral thesis) to “recover“ the Bat CoV named WIV1 (and possibly many more)
No, they use BAC, which is significantly dissimilar from ligating 6 cDNA fragments, then in vitro transcribing and electroporating, like my UNC technology. As I testified:
They use baculoviruses, and their molecular clone is a virus called WIV1, which I don’t think they engineered with class IIS restriction enzymes that don’t leave any sequence. So I think there’s a sequence signature in that virus. I would have to go back and reread the paper.
Would you also agree that the following analysis is accurate? Eight contiguous cDNA fragments of the virus were ligated together using …your UNC based cloning technique?
Unlike the WIV, I use six segments like you found in SARS2, but you keep accusing the WIV, so keep at it.
In WIV1 reconstruction, two synonymous mutations (TGT→TGC, TTT→TTC) created a BglI site in S1 without altering CPFG. Is this standard for your method?
Ask my UNC genomic wizard, Timothy Sheahan.
In all SARS-CoV-2 genomes, we observe that they retain this exact BglI site at nt 22568–22579, absent in SARS-CoV-1. Is its conservation post-passage noteworthy?
Probably.
From a codon-usage and immune-evasion perspective, GGC is suboptimal in human cells compared to GGT, so after passage it results in a codon optimized GGT. Would a natural SARSr-CoV under host pressure retain GGC at a BglI junction unless it conferred a fitness advantage?
I designed the genome for bats, not humans, so we are all lab bats in this pandemic experiment—same answer for the following 5 questions.
Would you agree that in the second of the two mutations, instead of the consensus codon GGA there is either GGC or GGT and that we can observe GGC in only a few virus isolates instead of GGT?
The spike sequence TGC CCT TTT GGC increases CpG content, a known deoptimization signal. Is its presence in SARS-CoV-2 more consistent with synthetic junction preservation than natural selection?
Do you think it makes sense for a virus to acquire additional CpG/GpC unless it leads to a fitness advantage (e.g. increased tropism of the polybasic cleavage site FCS in spike)?
If the CPNG motif (post-BglI mutagenesis) enhances cleavage efficiency, why is it absent in all other known bat SARSr-CoVs?
Are you aware of the full scope, funding, or unpublished data from Zhengli Shi and Ben Hu’s cross-species infection grants (2018–2020)?
Once Shi published RaTG13, she exonerated every Chinese scientist in Wuhan. That’s why I wanted her arrested.
If so, could you kindly provide us with a briefing on them?
I won’t stop you from blaming them for something I did.
After DARPA rejected DEFUSE, were you, or are you now aware that the Chinese Academy of Sciences (CAS) or NNSFC grants funded “DEFUSE equivalent” research, such as immunogen/FCS insertion work at WIV?
I recycled the DARPA Defuse text in 2018-19 into NIAID grants. The Chinese didn’t fund Defuse to protect the American warfighter.
Do you possess any records (emails, call notes, WeChat) of DEFUSE-related research continuing in China post-rejection?
Daszak ratted me out with his sloppy record-keeping.
In DEFUSE, you authored the FCS insertion strategy. Was this informed by a pre-existing SARSr-CoV with a proto-FCS (not RmYN02) in WIV’s collection?
I outlined the rational reason for a furin cleavage site (intracellular protease) in this 2018 bat paper with Munster. I also testified that it was a simple solution to the problem of growing viruses in my lab:
One of the drivers that sort of stopped me thinking about that line of research was we were interested in protease cleavage sites, for example, because it was a second barrier for virus emergence. There were several MERS-related strains and SARS strains that we couldn’t culture. We knew the clone was infectious and the virus could replicate, but it couldn’t spread. So what we realized is that if we add exogenous trypsin, another protease, if you put it in the media, some of those viruses will grow. It’s a simple solution to the problem.
Per DEFUSE notes, which specific chimeric backbones and spike donors were planned for FCS/RBD engineering?
I showed a special interest in HKU3-Smix, which is a precursor to SARS2.
Did you share details of these chimeras or the chimeras themselves with your Chinese colleagues?
I would “provide” this particular HKU3-Smix chimera to Shi and Linfa Wang for testing on Chinese bats.
What does the number “293” denote in DEFUSE? HEK293 cells, Mojiang mine viruses, or another identifier?
DEFUSE specifies “appropriate high-abundant low-risk parental strains.” Beyond WIV16 and SHC014, which others were included?
HKU3-Smix is the main one since its spike is 25% different than SARS1.
Type IIS enzymes (BsmBI, BsaI) allow seamless or scar-leaving assembly. Would retained sites be expected in a modular RBD/FCS screening platform rather than a single construct? (If you want to test several RBDs and FCSs in a virus/several inserts in a plasmid, you would leave them in so that you can easily replace that section)
Most of my UNC publications left the restriction sites in the genome for reproducible reasons.
Do you agree that the restriction sites evident in the SARS-COV-2 genome would have been used in cloning?
Yes, I've always used 5 restriction sites and 6 segments. It’s so incriminating that I tried to cover my tracks by using six sites and creating seven segments.
DEFUSE confirms WIV held BsaI and planned BsmBI procurement. Could this panel generate exactly six SARS-CoV-2 fragments matching observed junction distribution?
Yes, but I priced those in US dollars for my US lab.
Could they, in turn, be easily coupled with read selection in the construction of consensus genomes to generate unique site sets for any panel that yields 6 distinct fragments?
Yes, New England Biolabs is my restriction site vendor, and their founder, Rich Roberts, helped me cover this lab leak mess up.
Would you agree that the putative rWIV1-Spike changer system could only be deployed effectively for spike characterization when prepared in bulk and reused between strains, due to the difficulty in purifying the pre-ligation segments? In 2018 CAS began a “Pathogen Host Adaptation and Immune Intervention” program mirroring DEFUSE’s immunogen goals.
The WIV molecular clone, called WIV1, is closer to SARS1 than SARS2.
When did you become aware of this project, and did it concern you in any way, given your statements regarding “unknown Chinese engineering work?”
I will support your efforts to deflect attention away from my UNC lab.
Do you agree that there was no specification regarding the S2 cleavage site being
specifically “S2’” in the DEFUSE documents? Does this imply both S1/S2 and S2’ sites were targeted?
I specifically referenced R667, which is the S1/S2 border of SARS1.
The DEFUSE document mentions “human-specific cleavage sites”. Would you
consider that the patented ENaC cleavage site would be a good fit for that phrase, especially considering that this is the best matched human protein to the P1’-P4’ sequence, which is equally important to the protease cleavage processes?
Sounds good.
Do you agree that there exists the possibility of a major protease cleavage site mismatch when QTQTNSRSVASQS replaced and completely ablated the primary TMPRSS2 site in SARSr-CoV (the RS(T/V)(G/S)QKS site) and the HTVSLLRSTSQKS cleaved between L and R by Cathepsin L?
In 2018-19, I researched TMPRSS2, cathepsin L, and PRRVR, so I’m caught red-handed.
Would you agree that this putative major protease cleavage site mismatch warranted the insertion of a human-specific cleavage site, such as the human ENaC-Alpha (TMPRSS2 and Furin) cleavage site into the sequence, to restore tropism in the tissue and animal models that are relevant to their study (HAE testing only after the required protease cleavage sites are fixed and can be cleaved)?
Yes, this is a rhetorical question.
One aim of DEFUSE-like projects was to show that few recombination events/mutations enable bat CoVs to cause pandemics, by introducing “human specific” cleavage sites (as such recombination could occur in humans). So, finally, do you agree that the SARS2 FCS is identical to a human lung enzyme FCS?
I agree that humans were collateral damage for my bat vaccine research, since bat cells also contain furin.
DEFUSE states ‘SARSr-CoV S with mismatches in proteolytic cleavage sites can be activated by exogenous trypsin or cathepsin L.’ As FCSs are proteolytic cleavage sites, was it the intention of the authors of DEFUSE to introduce sites into newly discovered proto-FCSs?
As I testified, “The idea of manipulating the protease was clearly mine. No question… we were fundamentally interested in why didn’t sarbecoviruses have a furin cleavage site.”
Do you agree that the resultant infectious clones were to be grown in human/primate cell lines?
I listed human airway epithelial cells in Defuse.
When did you first learn WIV maintained a live Rhinolophus sinicus colony?
In March 2018, during the drafting of DARPA Defuse, I wrote, “I have no bat colony, no way for me to do the experiment, which I definitely think needs to be done, or we have no credibility. My understanding [is] another bat colony exists in China.”
Were you surprised when Peter Daszak publicly denied that WIV had live or dead bats in December 2020, despite being aware that they did since at least 2018, according to FOIA emails from Peng Zhou at WIV?
Yes, but Peng Zhou correctly predicted my bat vaccine “target might be human but not bats.” And four years later, Daszak admitted live bats in Dani Anderson’s BSL4, which threw me under the bus.
Would you agree with Linfa Wang and Christian Dorsten (2020) that due to accelerated viral dynamics in bat cell lines, such rapidly-reproducing viruses would likely generate extreme virulence upon spillover to hosts lacking similar immune capacities to bats (such as humans)?
Yes, Linfa Wang is a better teacher than I am. He explained the bat’s tank-like immune system compared to humans.
Peter Daszak, in his DEFUSE proposal, requested a ~20% spike in RBD divergence from SARS-COV known strains. Was this percentage of divergence identical to SARS-CoV-2’s closest progenitors?
I spoke that line because I patented the SARS2 genome in 2018. The SARS2 spike is 25% different, but the entire genome is 20% different from SARS1 (epidemic strains).
“Bat CoVs have been assembled from viral nucleic acid fragments in the past, where replication capable viruses could not be isolated (e.g. from faeces, BALF, anal swabs etc.)” Are you aware of WIV routinely “recovering” SARS-related viruses apart from the ones that had been published?”
The WIV can only isolate existing viruses like WIV1; it can’t create new viruses like SARS2.
This was usually performed by reverse transcribing viral RNA fragments into cDNA, amplification, and cloning into vectors (concomitant sequencing by Sanger - later NGS). Would a modern virology laboratory such as WIV “recover” usually replication capable viruses by assembly from RNA fragments to test them in cell cultures and on lab animals?
The WIV can’t recreate a full viral genome; it can only shuffle spikes into existing backbones.
Your no-see’m method routinely resurrects “extinct” or unculturable CoVs via 6–8 fragment assembly. Does this risk creating pathogens not currently circulating in nature?
Yes, it’s called SARS2.
Complete viral genomes can be re-assembled using “seamless“ or “no see’m“ cloning technology originally developed by you at UNC, based on taking 6-8 contiguous cDNA strands covering the complete virus genome and ligating them together using adapters at the 5’ and 3’ ends, with restriction enzyme digestion, ligation and transfection into permissive cell lines (such as Vero E6). Does this mean that often (“extinct”) viruses that cannot be isolated from samples and may not even exist in nature anymore risk being brought back to life in a virology lab?
Yes, I proposed to do just that to create SARS2.
Using your method mentioned above, is it often necessary to modify the 5’ and 3’ ends of the amplified fragments in order to generate a suitable restriction site?
You will never know because no one can copy my methods, not even my American colleagues.
Therefore just a few bp (in the cDNA) need to be changed by SDM (site directed mutagenesis) by preserving the amino acid sequence of the ligated virus. This is done by modifying only the wobble bases (introducing synonymous mutations) at the respective cloning sites. The same technology can be used to swap genes, e.g. exchange the spike proteins in a viral backbone. WIV has used this technology (described in a recently discovered 2018 doctoral thesis) to “recover“the bat CoV named WIV1. Are there, from your expert perspective, any signatures in the virus genome of SARS-2 that would hint towards a potential use of such a cloning strategy?
Again, WIV1 molecular clone, which is not SARS2.
Do any SARS-CoV-2 features (synonymous clustering, restriction scars) suggest assembly via your UNC/WIV-shared platform?
We don’t share a reverse genetic platform. I use cDNA; Shi used BAC.
A pristine BglI site at nt 22568 is damaged (C→T) in most SARS-CoV-2 lineages, but retained in early isolates. Does this pattern suggest passaged synthetic junction decay?
You DRASTIC types spend way too much time debating restriction sites and nucleotides. Let me drop a hint:
A potential “smoking gun” would have been an unambiguous BglI site, which is damaged by a C -> T transition, although there are still some isolates with C in pos. 22579. Having looked at thousands of gene sequences, would you agree that this one looks “assembled”?
See above.
The other potential BglI positions in the genome are not that relevant, because they are not required for S swapping.
Good.
You have worked closely with Fang Li in the past, and as you must be aware, Fang Li also worked closely with Lanying Du in recent years, as well as presenting at WIV conferences and collaborating with WIV.
Senator Rand Paul’s office interviewed Lanying Du, and nothing came of it.
Furthermore, in this highly significant late 2009 collaboration (which includes WIV and AMMS) the first authors listed (those doing the bulk of the lab work) are also Fang Li proteges from the State Key Lab of Virology at Wuhan University.
Fang does biochemistry (RBD) work, and I conduct the dangerous GoF research. If Fang Li from Minnesota can’t copy my work, how could the Chinese military?
Have you ever suspected Fang Li or Lanying Du of passing confidential information back to China?
The last time I caught a former UNC postdoc (Menachery) sharing my technology with UTMB Galveston, I wrote the most demaining email in scientific history below:
Immediately after the SARS-CoV-2 genome release (Jan 2020), Fang Li phoned you. No follow-up notes or FOIA record exists. What was discussed: sequence anomalies, FCS, or origins?
Would you agree that this particular insight was the result of prior work (2012) on SARS-1 by Fang Li and his postdocs from the State Key Lab of Virology at Wuhan University, rather than your own work?
I told TWiV in 2015 that I was the one who did this risky research.
Although you have been the leading proponent of the spillover zoonotic coronaviruses via recombinant evolution, since ~1990, do you agree that Lanying Du, Fang Li and his students, as well as other researchers in China, would have had more insight into the structure and mechanisms of coronaviruses than yourself?
D. Janković has my back!
Do you consider it plausible that WIV and AMMS have long exploited your “evolution by recombination” theory as cover for their engineering of synthetic viruses?
As I testified, the Chinese “really struggled with trying to develop other molecular clones. They were working on developing the SARS molecular clone from 2016 on, and they failed. It’s not easy technology. So we started three years later and beat them to press, just to show you. And I had no interest in teaching them how to do it faster, either.”
Do you find it worrying that they provide samples and sequences that purport to support your theory, but only they are permitted to access the caves in which they claim these are found.
My fat ass isn’t crawling around those tiny Chinese caves and sticking Q-tips up a bat’s butt. I’ve never held a bat. As I testified, “I could hold a pangolin and get it close to my face and not freak out. I would have trouble with a bat. I don’t know about the rest of you, but I would have trouble holding a bat close.”
Shi and colleagues crawled on their stomachs through narrow bat caves While it is easy for WIV to send you a sequence or even a synthetic isolate, and for you to verify its viability or its hACE2 affinity, how can you be sure of alleged provenance of the samples as natural?
I resurrected what the bat lady couldn’t isolate: RaTG13. I don’t need her sample, I just need her genome sequence. I’m the only man on the planet who can create something from nothing!
Should Fang Li’s and Lanying Du’s WIV/PLA links be formally investigated?
As long as it takes the heat off me!
Pre-2020, did WIV or Wuhan University use Calu-3 human airway epithelial (HAE) cells for SARSr-CoV propagation?
Yes, but if they used Calu to create SARS2, it wouldn’t favor the ancestral strain (WA1). My former postdoc, Menachery, wrote, “In Calu-3 2b4 cells, the R203M mutant again mimicked the KR mutant.”
If SARS-COV-2 was not completely of zoonotic origin as claimed, and had been passaged in cell lines, in your opinion, which cell lines would most likely have led to the characteristics that SARS-COV-2 has? Please help by ranking these cell lines by likelihood of selecting its phenotype: Huh-7, Vero E6, HCT-8, Calu-3, A549, LLC-MK2, 293T, 293T/hACE2.
Primary human airway epithelial cells
If SARS-COV-2 was not completely of zoonotic origin as claimed, and had been passaged in experimental laboratory animals, in your opinion which experimental animals would most likely have led to the characteristics that SARS-COV-2 has? Please help by ranking these lab animals by order of likelihood: Macaques, Syrian golden hamsters, Ferrets, hACE2 transgenic mice, deer, deer mice, American mink, Chinese tree shrews or any other laboratory animal (please specify).
Munster used Syrian golden hamsters, American deer, American deer mice, American mink, and Egyptian fruit bats. Monkeys, hACE2 mice, ferrets, and any other animals don’t exhibit efficient transmission.
You said: “Based on genomic sequences and contact tracing, estimates place the origin point of SARS-CoV-2 in humans between mid-October and mid-November 2019.” So why do you think there are no recorded cases before December 2019?
I was trying to dissuade people from looking around Wuhan, because I think/hope SARS2 was a natural spillover near the Mojiang mineshaft.
You wrote in one of your early emails that it “looks like we found OUR highly variable virus”. Can you confirm that this term was previously used to describe synthetic viruses assembled with the same type IIs enzyme (BsmBI), which allow for a high degree of variability with regards to replacing viral segments?
Yes, I even used it in DARPA Defuse, but it’s a reference to my 25% difference quote from 2015:
Based on this, would you agree that you immediately recognized the cloning strategy that you developed, and thus Ben Hu and Shi Zheng Li must have known how to adapt his methods to their needs since before 2017?
If you look at their cloning technology, they use baculoviruses. They may assemble some of the full length molecule using some of the enzymes that we have, but they implant it directly into an insect virus to maintain it as a
baculovirus, which was a technology developed in Europe, not my technology.
Regarding the FCS: as suggested in DEFUSE, the one in SARS2 is a “human-specific” sequence. Can you confirm that it is identical to the FCS in ENaC-alpha, which was published by UNC colleagues Kota, Gentzsch, Dang, Boucher & Stutts in 2018?
Yes, Jeffrey Sachs and Neil Harrison caught me.
Can you also confirm that there are also methods to make such viruses without leaving trails (“No See’m”). This was not done with SARS2, as there were too many virus variants, but it could have been content of discussions?
I have a long answer on this, so here it is:
Who was your first contact upon learning of the Wuhan outbreak, and what was said?
I emailed my DARPA Defuse collaborator Daszak, who cc’d our Wuhan collaborators Dani Anderson and Linfa Wang.
Have you ever learned or seen evidence of your Chinese counterparts at WIV or elsewhere, trying to clone/replicate your shared research? For example, doing DEFUSE-like research on their own?
Shi Zhengli had zero input in the drafting of DARPA Defuse.
Prior to the outbreak, have you ever heard of any research based on Mojiang samples?
Yes, I referenced the abandoned Mojiang mineshaft in my 2018 LAV bat paper. I even left the UGGUCGC sequence in the SARS2 genome.
Was BtCoV/4991 (RaTG13) a good candidate for a planned DEFUSE Phase-2 backbone?
Yes, RaTG13 is my unicorn since its spike was 25% different from SARS1.
By end-2020, how many unpublished live SARSr-CoV isolates or synthetic backbones were you aware of (UNC + WIV + EHA)?
“Several CoV infectious cDNA clones are available in UNC lab, including SARS, MERS, CoVs, and bat CoVs with pandemic potential.”
Did you ever discuss with any members of EcoHealth Alliance or the WIV (or of any other research institutions in Wuhan that research SARSr viruses) the possibility and/or implications of adding a furin cleavage site at the S1/S2 boundary of a novel SARSr virus?
“The idea of manipulating the protease was clearly mine. No Question.”
Did you ever discuss details or methods used to construct a reverse genetics system for a novel SARSr virus with members of the same groups?
Yes, if you want to blame them for what I did!
Are you aware of any work being conducted by any members of the same groups between 2018 and 2020, in which the work involved the creation of a reverse genetics system utilizing a previously uncharacterized/unpublished SARSr CoV?
If you believe the WIV inserted the FCS, then published RaTG13, you are a simpleton. It’s biologically impossible to publish something closer.
Are you aware of any work being conducted by any members of the same groups between 2018 and 2020, in which the work involved adding an FCS at S1/S2?
It’s easy to see how obsessed I was with a furin cleavage site at S1/S2 (R667)
Are you aware of any research occurring within the same groups between 2018 and 2020 which relates to the research workflow laid in the DEFUSE proposal & its publicly released drafts, (i.e. RBD/FCS libraries, HAE testing)?
Yes, I did, since I recycled the DARPA Defuse text into the two NIAID grants. Those suckers at EcoHealth and WIV even added me to their ongoing R01 grant.
Were you aware of RaTG13 prior to its February 2020 publication?
I wanted Shi arrested for publishing it, so yes.
If yes, then were any other viruses isolated from the same sera/sample as RaTG13? Who has the sequences?
I don’t know, but I was only interested in RaTG13 because its spike matched my 25% needs:
Were co-isolates from the Mojiang miners’ sera sequenced? Who holds them?
I guess the WIV.
This is a list of tasks within the DEFUSE grant that were leaked to DRASTIC. Are you familiar with the DATA and sequences in this list?
More unpublished data by UNC!
Do you have knowledge of these DATA and sequences? To whom were they made available?
Don’t ask, don’t tell.
Are you or were you ever in custody of these DATA and sequences?
Maybe.
If not then... Who is?
My 2019 records are under lock and key.
If yes then can you provide a complete record of these experiments and sequences?
Over my dead body.
Can you provide the complete details of the workflow that is intended to support the DEFUSE grant?
Something like this?
Where were experiments actually performed?
In Wuhan, because “I have no bat colony, no way for me to do the experiment, which I definitely think needs to be done, or we have no credibility. My understanding [is] another bat colony exists in China.”
Where are the results and sequences that were recorded?
They are called SARS-CoV-2.
What viral sequences that you and your collaborators at WIV-EHA-NUS discovered or created are the most similar to SARS-CoV2?
HKU3-Smix
What experimental collaborations have you had with Zhou Yusen?
The dead guy from Beijing? No. He started working on a SARS2 vaccine months after I did. Moderna contacted me in December 2019.
To your knowledge did he have access to DATA and sequences that were generated by your collaborators UNC-WIV-EHA-NUS?
Yes. Linfa Wang and Dani Anderson even referenced my “consensus” sequence work.
Kindly take time to tell us everything you know about the sequences that were generated for task 4.6 6 (immunogen testing)?
HKU3-Smix = SARS-CoV-2, which I would “provide” to Linfa and Dani
Do you ever, or have you ever since COVID-19 emerged, used Gmail or other communication platforms rather than your work email to communicate with colleagues (US or Chinese) about scientific work funded by NIH?
Yes, my wife and I tried to trick the FBI and USRTK using our Gmail accounts.
What Social networks, Facebook, WeChat, Signal, WhatsApp, Twitter, BlueSky and email platforms do you use to communicate with US Colleagues and Chinese colleagues?
My wife probably has several burner accounts, but I’m too busy in the lab.
Have you ever used or been advised to use a “Burner phone’?
Fauci secretly invited me to the February 1, 2020, teleconference on a burner.
When you first heard of the outbreak in Wuhan, who told you?
ProMED alert on New Year’s Eve.
Can you provide some detail about your discussion concerning the origins of SARS-COV-2 with your colleague Mark Denison, please summarize the discussions?
I don’t kiss and tell.
Can you provide some details about your WeChat communications with Chinese scientists (virologists and molecular biologists)?
Fauci was on WeChat with George Gao, so ask him.
Have you signed the Official Secrets Act (US equivalent, e.g., SF-312)? If so, when?
I, like most high-level academics, have a security clearance.
How many unpublished papers are there currently in preparation or under embargo, that you have collaborated on?
Probably dozens of unpublished UNC papers.
How many unpublished full-length SARSr-CoV viral sequences are there (natural or synthetic), or have there been at your UNC laboratory?
“Several CoV infectious cDNA clones are available in UNC lab, including SARS, MERS, CoVs, and bat CoVs with pandemic potential.”
Did you have access to the WIV viral database before it went offline in September 2019, and did you or any of your colleagues download it?
Apparently, yes. For example, Shi shared SHC014 with me before publication.
What was discussed at the October 2019 meeting of the DEFUSE investigators?
Daszak disclosed that NIAID had funded our Defuse project.
What is the utility of the ‘no-see-em’ methodology, as opposed to leaving restriction sites in after infectious clone assembly?
Future modifications to the prototype.
Did you ever discuss infectious clone construction methods with members of the WIV?
No.
If so, which restriction enzymes were discussed, and was it discussed whether to leave restriction sites in or not after ligation?
The only time I discussed the restriction sites was with my former postdoc, Vineet Menachery, so that we could trick US intel.
Have you ever discussed furin cleavage sites with Dr M. Jackson Stutts of the UNC School of Medicine.
In March 2018, I worked with him.
If so, did you discuss with him the sequence of the FCS of human ENaC?
Maybe.
What protease cleavage sites, other than furin, were you planning to investigate as part of the DEFUSE proposal, (e.g., TMPRSS2, cathepsin, trypsin)?
“So what we realized is that if we add exogenous trypsin, another protease, if you put it in the media, some of those viruses will grow. It’s a simple solution to the problem. So you didn’t exactly have to engineer anything to make it grow. So we published a paper on that, and we used that on a variety of viruses. It’s kind of a simple solution to a more technologically different approach.”
If one wished to introduce a furin cleavage site into the S1/S2 boundary, as described by DEFUSE, what would be the rationale for introducing it as an insertion, rather than mutating existing amino acid residues to create an RXXR motif?
To infect bats!
Did you sign an MTA with Moderna for a CoV vaccine development project in November 2019?
Yes, but my work with Moderna started in 2016.
If so, can you list the reagents, sequences, and vaccine platform (mRNA, spike-stabilized, etc.) that were transferred under the MTA, and any details about the vaccine you were working on?
If you ask nicely!
As you only work with CoV chimeras at BSL3, were you surprised that you needed to inform Peter Daszak of this requirement specifically in the DEFUSE Drafts?
In late 2019, you referenced a 2017 paper by Stanley Perlman, which included “pat7” (a molecular address label), which shows a pattern of 7 amino acids. The first is always proline (P), explaining, for example, the PRRAR furin cleavage site in SARS-COV-2. Is that correct?
That German computational biologist, Andreas Martin Lisewski, caught me!
Yet, you claimed in 2024 that no one would insert a proline as it would have been “a bad engineering decision”: “In the SARS2 sequence, you only need to insert 3 amino acids to make a furin cleavage site. 4 is a nucleotide. 4 amino acids went in asymmetrically. Why would anybody engineer that and do it that way, putting in an extra residue which is a proline, which puts kinks in proteins, it usually screws things up.” Question: Why did you make this strong claim and would you now like to clarify this?
I said that before Andreas cleared peer review, so it was a white lie.
Jeffrey Sachs and Neil Harrison’s 2023 analysis identified a BsaXI restriction site flanking the SARS-CoV-2 furin cleavage site, which, due to the out-of-frame PRRA insertion, necessitates the upstream proline you criticized in 2024. As a pioneer in restriction enzyme-based genetic engineering of coronaviruses, were you aware of this BsaXI signature prior to its publication, and does it alter your view on the FCS as a “bad engineering decision”?
It was genius, if I may say so myself!
Your lab’s 2018-2019 Institutional Biosafety Committee notes document experiments with ENaC-alpha in human airway epithelial cells, incorporating the RRAR/SVAS sequence that matches SARS-CoV-2’s FCS. What specific outcomes from these experiments informed your later dismissal of proline insertions as problematic?
Ironically, I claim to hate prolines!
The Stutts Lab at UNC, which first characterized the ENaC-alpha furin cleavage site (RRAR/SVAS), is located in the same Department of Cell Biology and Physiology as your own lab. Given this proximity, did you or your team consult or collaborate with Dr. Monroe Stutts on ENaC research during 2018-2019, and if so, how did those discussions influence your views on functional furin sites in respiratory proteins?
Now you caught me!
During your review of the January 6-7, 2020, manuscript (later published in Nature as the Zhang et al. paper co-authored by Eddie Holmes), you requested the full SARS-CoV-2 sequence within 12 hours.
Correct.
At that time, did you immediately recognize the PRRA furin cleavage site
January 6, 2020, but never mentioned it in public.
Why was it not flagged in your February 2020 congressional presentation comparing SARS-CoV-2 to SARS-CoV-1?
I lied by omission because this lab leak wasn’t yet a global pandemic.
In the off-the-record discussion with congressional staff about the January 2020 Nature paper, you expressed concerns over confidentiality to avoid identifying the journal. Given that Eddie Holmes was a co-author and later stated he did not suspect engineering at the time, did Holmes share any unpublished WIV sequence data with you prior to the paper’s acceptance, and did it include the FCS?
Good question, someone may have provided me an early copy of RmYN02.
Kristian Andersen’s January 31, 2020, email to Fauci described the SARS-CoV-2 genome as “inconsistent with expectations of evolutionary theory,” specifically citing the apparent PRRA insertion in a 100% conserved 519-amino-acid region flanking the FCS. As a reviewer who saw the sequence by January 7, 2020, why did you not raise similar concerns publicly until May 2022?
It took you, lab leakers, two years to catch up to my cover-up!
On March 4, 2020, you told DHS, DoD, and DTRA representatives that “there is absolutely no evidence this virus is bioengineered.” At that point, had you compared the SARS-CoV-2 FCS to natural betacoronaviruses?
I was blinded by the beauty of my own creation!
If so, why did you omit mention of the proline’s commonality in MERS and other FCS motifs?
To keep you lab leakers off my tail!
Your 2018 presentation slide depicted a chimera of HKU3-S and BtCoV/279-S, resulting in a genome approximately 20% divergent from SARS-CoV-1, closely matching SARS-CoV-2’s profile. This slide also appeared in your 2015 presentation as “HKU3-Smix.” Can you confirm that this chimera formed the basis for the HKU3-Smix construct proposed in the DARPA DEFUSE grant?
I patented SARS-CoV-2 in 2018.
The DARPA DEFUSE proposal outlined testing the HKU3-Smix chimera on humanized mice at UNC and on wild-caught Chinese horseshoe bats at the Wuhan Institute of Virology’s BSL-2 facilities. Which specific WIV laboratory, BSL-2, BSL-3, or BSL-4, was designated for the bat infection studies, and why was BSL-2 deemed sufficient despite the chimeric virus’s potential pandemic properties?
I nominated Dani Anderson, who worked in the Wuhan BSL4.
In a January 10, 2020, email from Vincent Munster linking to the SARS-CoV-2 genome, he wrote, “Perfect! Right between your favorite viruses :-).” Given your prior work on HKU3 (≈30% divergent from SARS-CoV-1) and SHC014 (≈10% divergent), does this suggest Munster viewed SARS-CoV-2 (20% divergent) as a synthetic midpoint of your research strains?
This sounds plausible, but I can’t believe that naive Dutchman sent that email!
In your 2021 email to colleagues, you described Peter Daszak’s assurances about WIV’s BSL-2 containment for coronavirus work as a “load of BS.” What was Daszak’s specific response to this criticism, and were there other instances in 2018-2020 where you documented similar concerns about his representations of WIV biosafety?
Did you know I sent that CYA email from a Gmail account? LOL
As a defendant in the ongoing USRTK lawsuit seeking your 2018-2019 emails, why have you contested the release of communications related to DEFUSE, ENaC experiments, and WIV collaborations? Do these records include discussions of the BsaXI site or proline motifs that contradict your 2024 testimony?
Rules for thee but not for me!
Your wife, Toni Baric, served as UNC’s Grants Specialist and was CC’d on numerous emails involving you, Daszak, and Linfa Wang, including the February 2020 discussion of a natural origins letter. She switched to a personal Gmail account one week after USRTK’s initial FOIA request in early 2020. Was this transition discussed in relation to FOIA obligations, and does her Gmail contain records of DEFUSE-related funding or WIV subcontracts?
We played that poor FBI agent assigned to protect us!
FBI documents indicate that Special Agent [REDACTED] communicated with you not only about threats but also on the substance of the COVID-19 origins debate and UNC’s responses to North Carolina FOIA requests. What specific advice did the agent provide on handling USRTK inquiries into your 2018-2019 emails, and did it influence UNC’s withholding of ENaC or DEFUSE documents?
We played the FBI just like Daszak, forwarding every bit of hate mail and claiming our lives are in danger, while misleading the FBI on our DARPA Defuse bid.
In the February 2020 email chain with Peter Daszak and Linfa Wang, you agreed to distance yourself from the natural origins letter to avoid linking it to “our collaboration,” despite being key DEFUSE co-authors. The same trio (you, Daszak, Wang) appears in both DEFUSE and the 2019 NIAID CREID project. Why did you prioritize perceived independence over transparency about your shared WIV ties in early pandemic messaging?
I blew smoke up the COVID committee’s butt when they asked me about this:
The 2019 NIAID CREID project, awarded $82 million and involving you, Daszak, Wang, and Danielle Anderson, mirrored DEFUSE’s scope for chimeric coronavirus testing in Wuhan. After DARPA rejected DEFUSE for gain-of-function risks, how did CREID modify protocols to address those concerns, and was any HKU3-Smix work transferred from UNC to WIV under this funding?
In an early pandemic email to Daszak, your wife Toni wrote, “we are kindred souls in this mess,” shortly after your CNN appearance promoting “remdesivir. Daszak replied, “welcome to the Resistance,” referencing Trump-era scrutiny. Did these exchanges reflect coordinated efforts to counter lab-leak narratives, and were they part of broader communications with Linfa Wang on the origins letter?
My wife makes me feel good, but sometimes makes me look bad. She likes to watch CNN, so I interviewed from our living room.
Daszak’s emails warned of FOIA risks from Trump administration scrutiny, leading to Gmail use for sensitive discussions. Given that official business on personal accounts is still FOIA-eligible, why did you and Daszak continue using Gmail for WIV-related talks in 2020-2021, and what DEFUSE or CREID details were discussed there?
I essentially lied to Congress and the FBI regarding this Gmail issue. One month after my interview, the committee dug up my Gmail account, and the wife and I will go down as Bonnie and Clyde.
In your January 25, 2020, ODNI BSEG briefing (p. 170), you presented a slide on WIV lab-leak risks due to BSL gaps, yet your February 11, 2020, Congressional Biomedical Research Caucus talk omitted it entirely. What prompted this selective disclosure, and did Dr. Fauci’s February 1, 2020, meeting influence the public omission?
I alluded to a Fauci-led cover-up in my testimony. Fauci will claim he never met me, but if I go, he goes with me!
During the off-record portion of your ODNI briefing discussion (p. 168), you shared excerpts from slides on WIV’s PPE and training deficiencies. Why were these specifics not included in your on-record summary, and what intelligence queries from ODNI directly referenced your 2015–2019 biosafety workshops with Shi Zhengli?
I’m a (BSL2) lab leaker in the sheets, but a zoonati in the streets!
On p. 65, you reiterated your March 4, 2020, DHS/DoD/DTRA statement of “no evidence of bioengineering,” but privately briefed ODNI on lab-leak plausibility weeks earlier. Why the discrepancy, and were any WIV unpublished sequences (e.g., 7896 clade) factored into your intel assessment but withheld from agencies?
I never told ODNI about potential bioengineering. Because that would implicate me. Did you notice that I didn’t mention Shi’s RaTG13 sample? That would incriminate me. But if I report sloppy procedures in Shi’s dirty BSL2 to ODNI, they won’t ask about Dani Anderson’s BSL4.
In the off-record segment on your UNC freezer inventory (p. 135), you listed approximately 15 SARSr-CoV isolates from Shi Zhengli, including 2b clade members. Why classify these as “lab-confidential” rather than public health records, and do they include the “drip-feed” sequences Daszak referenced in 2018 that you prioritized?
There’s a debate about what “DF samples” mean. You think it means drip feed? Someone else claims it’s a USAID project called Deep Forest. I’m not talking, so you will know, but it’s safe to assume every coronavirus ever collected with NIAID and USAID funding is in my UNC freezer.
Your 2015–2019 Galveston meetings with Shi Zhengli (p. 190, off-record) included biosafety training via James LeDuc. What specific gain-of-function risks were discussed privately, and why were they sanitized to “collaborative exchanges” on-record, especially given your ODNI warnings?
Aren’t we a sweet couple?
2018 meeting at UTMB Galveston. Shi is front row left. Baric and LeDuc are 2nd-to-last row in the middle.
On p. 112, you described the SARS-CoV-2 FCS as “easily engineerable” via reverse genetics, contradicting your 2024 proline ridicule (p. 98), yet claimed “no evidence” of manipulation. Reconcile this with your off-record DEFUSE details (p. 79) on proto-FCS candidates from WIV, and why no public call for their release?
I like to have my cake and eat it too.
In response to questions on Fang Li’s January 2020 call (p. 103, off-record start), you vaguely noted “no red flags” but admitted he flagged “sequence anomalies.” What specific anomalies (e.g., RBD, FCS) were discussed privately, and how did they inform your early 2020 “no engineering” stance?
It’s simple, I told Fang Li not to bring attention to my furin cleavage site.
Regarding your evasion of the freezer question (p. 135: “I don’t do bat discovery... look for sequences if interesting”), why not provide an inventory when pressed, especially since p. 201 notes admit receiving “drip-feed” 2b sequences from WIV tailored to your interests?
In your 2006 paper (p. 47), you wrote: “‘No See’m’ sites can be used to insert foreign genes… simultaneously removing all evidence of the restriction sites.” You also testified (p. 112) SARS-CoV-2 FCS is “easily engineerable.” Walk us through how a No See’m BsaXI site could insert PRRA without leaving a trace?
The biological gods tied my hands with that BsaXI site. It forced the out-of-frame insertion and leading proline.
Your 2006 paper (p. 48) stated: “Esp3I sites… systematically removed during assembly… leaving only the desired mutation.” SARS-CoV-2 has BglI-like junctions at 12143, 17077, 22568 (synonymous clusters). Can you now confirm or correct: the claim that these are removed Esp3I scars from your platform?
You lab leakers can’t see my forest through your trees!
Your 2006 paper (p. 51) stated: “Humanize zoonotic viruses by inserting mutations into attachment proteins.” DEFUSE planned “human-specific cleavage sites.” Can you kindly take time to walk us through this, if your 2018 ENaC-α RRAR was the humanization template?
My (bad) idea was to vaccinate against bats against a humanized zoonotic virus.
Your 2006 paper (p. 53) on synthetic genomics, discussed: “Scapegoat option… sequence signature that misdirects origin tracking… build mistrust or precipitate warfare.” SARS-CoV-2’s FCS is unique in sarbecoviruses. Can you confirm that a bioterrorist using your method would choose to frame a natural spillover?
Yes, and it worked! If my artificial genome leaked from the WIV, it would appear to have originated from the Wuhan wet market.
Your 2006 paper (p. 55) discussed “Seamless assembly… coronaviruses mouse hepatitis, TGEV, IBV, SARS-CoV.” You transferred no-see’m to WIV by 2017 (NIC memo). Can you take time to walk us through the first WIV chimera built with your system.
It’s the HKU3 chimera outlined in my Hong Kong presentation.
Your 2006 paper (p. 49) discussed: “Type IIS enzymes… create unique interconnecting junctions… removed from the final product.” SARS-CoV-2 has out-of-frame PRRA forcing a proline. Can you confirm that this could be a No See’m insertion artifact?
BsaXI is a Type IIB restriction site, while BsmBI and BsaI are Type IIS, but I described No See’m in the above presentation. Lab leakers get mad at that Haslam character, but he’s right. I was trying to hide the engineering scars from a bat’s immune system, not you crazy researchers.
Your 2006 paper (p. 57) notes that the “Pathogenicity of chimeric coronaviruses is unknown.” You built SHC014-MA15 (2015) and HKU3-Smix (2018). Can you kindly walk us through the risk assessment you gave ODNI for unknown pathogenicity.
More pathogenic in a mouse. But once I shipped my pathogens to Munster, all bets were off for us humans.
Your 2006 paper (p. 60) stated that: “Knowledgeable experts can reconstruct full-length synthetic genomes for any high-priority pathogen.” You advised CIA/FBI/ODNI (BSEG 2020–2021). Did you brief them that SARS-CoV-2 could be synthetic?
No, I attacked Kristian Andersen before he could notify the CIA or FBI.
Your 2006 paper (p. 62) mentions: “Dual-use… bioterrorists with a scapegoat option.” You called SARS-CoV-2 FCS a “bad engineering decision” (2024). Can you propose why a competent scientist would insert it anyway?
I was trying to infect bats, not humans.
Your 2006 paper (p. 65) mentions: “No regulatory oversight for seamless assembly.” You hold a Top Secret clearance (bioterrorism expert). Did you recommend classified oversight for No See’m tech post-2006?
As I wrote in DARPA Defuse, “These are BSL-3, not select agents or subject to P3CO (they use bat SARS-CoV backbones which are exempt) and are pathogenic to hACE2 transgenic mice.”
During your January 29, 2020, closed-door briefing to the ODNI’s Biological Sciences Experts Group (BSEG), you presented slides warning that WIV’s gain-of-function bat virus experiments may have accidentally released SARS-CoV-2, based on your 2015 collaboration with Shi Zhengli. Why, in your nearly identical February 26, 2020, public briefing to the Congressional Biomedical Research Caucus, did you omit these lab-leak slides entirely, and what specific WIV biosafety gaps (e.g., from your private warnings to Shi) were highlighted in the ODNI version?
CYA baby
The Washington Free Beacon reported on November 4, 2025, that you downplayed the wet market theory in your January 2020 ODNI briefing, noting most early cases had no market exposure. Yet in your February 26 public briefing, you stated, “Bats are used in certain delicacy dishes... so there’s a possibility that bat parts were in the market.” Why did you lend credence to the discredited wet market origin publicly while privately dismissing it to intelligence analysts?
You missed the best part of my congressional presentation. I foreshadowed, “There could be reservoir species in the U.S. that have good matches for ACE2 receptors. So, if the virus comes here, we could have an animal reservoir that the Chinese don’t. And then it hangs around for a long time.” I anticipated that this Old World virus would find a New World home.
Rutgers professor Richard Ebright stated in the November 4, 2025, Free Beacon article that your omission of WIV lab-leak references in the February 26 briefing was “no coincidence” given your “highly unusual one-on-one meeting” with Anthony Fauci on February 11, 2020, as reflected in Fauci’s FOIA-released schedule. What was discussed in that meeting, and did it influence your decision to remove the lab-leak slides from your public presentation?
We discussed the “outbreak and chimera” and arresting Shi for publishing RaTG13, which kickstarted the February 1 teleconference fiasco.
During the February 1, 2020, conference call where Fauci and Francis Collins were warned of WIV’s potential role in the outbreak, you were not directly involved, but Fauci later prompted the “Proximal Origin” paper to disprove lab-leak claims. Given your $132 million in NIAID funding from Fauci (averaging $44 million/year in 2020–2022, covering most U.S. infectious-disease research salaries), why did you not publicly challenge Fauci’s efforts to cast lab-leak discussions as “baseless conspiracy theories”?
I was directly involved. Fauci secretly invited me to that call so I could hear Kristian Andersen’s evidence for lab leak.
Sen. Joni Ernst called on November 4, 2025, for you to testify publicly on why you “pushed the wet market story and stayed silent on the lab leak possibility, even while presenting the opposite in closed-door briefings.” Do you support this call, and if so, what specific evidence from your ODNI slides would you now present to Congress to “unmask” your role in WIV research?
I’ll invoke my 5th Amendment rights, and you will never hear from me ever again.
Fauci’s control of the $6.5 billion NIAID budget gave him “immense influence” over U.S. infectious-disease researchers, including your lab’s $132 million in grants (2020–2022). How did this funding dependency affect your willingness to publicly contradict Fauci’s promotion of the wet market theory after your February 11, 2020, meeting, especially given your private ODNI warnings?
He who pays the piper calls the tune.
In the 2025 Free Beacon article, Ebright highlighted your shift from private lab-leak advocacy to public silence as evidence of Fauci’s coordination to “do great potential harm to science and international harmony” (per Collins’ February 2 email). Walk us through how your post-meeting alignment with the “Proximal Origin” narrative, cited by Fauci in White House briefings, reconciled with your expertise on WIV’s risky experiments.
I was essentially a ghostwriter on the Proximal Origin paper, as it referenced my cover-up papers. In May 2020, I praised Proximal Origin’s “genetic and biological data as strong evidence against deliberate generation, and the arguments are compelling.”
Your January 2020 ODNI briefing warned of WIV’s insufficient biosafety for “virus discovery work,” yet you later testified in 2024 that you had privately warned Shi Zhengli of these gaps. Why did you not include this in your February 26 public briefing, and did Fauci’s February 11 meeting prompt you to withhold it to avoid scrutiny of NIAID-funded gain-of-function research?
Don’t mess with Asian women, or they send you F U emails like this:
The November 4, 2025, article notes that Fauci and Collins, who funded WIV via EcoHealth, ignored lab-leak warnings to promote natural origins. Given your $132 million NIAID grants under Fauci, why did you not advocate for declassification of your ODNI slides earlier, especially as one of the few experts with direct WIV ties?
Because the ODNI slides showed that I was hiding the SARS2 furin cleavage site from US intel.
Sen. Ernst’s November 4, 2025, statement demands “unmasking” your “batty Wuhan research” role. To address this, can you provide us with the full content of the omitted ODNI lab-leak slides, including any references to your 2015 Shi collaboration, and explain why they were excluded from the public record after your Fauci meeting?
My 2015 “collaboration” with Shi was her sending me genomes, and me doing the engineering. Something similar happened with RaTG13.
Your 2015 Nature Medicine paper with Shi Zhengli (first author) created SHC014-MA15 chimera at UNC BSL-3. Shi shipped the SHC014 spike plasmid to UNC. Can you provide us with the shipping manifest and customs declaration for that plasmid, as well as any others received from overseas?
That's a brilliant question, so I’ll give you a non-answer.
In 2016–2019, you and Shi co-chaired UTMB Galveston bat-coronavirus workshops (LeDuc). Can you provide us with the attendee list, agenda, and any minutes where gain-of-function limits were discussed.
David Relman is the only name I remember. And he helped me cover this up. He provided me with an early copy of Dr Quay’s lab leak analysis, so I ambushed Quay during the State Department’s Red Team meeting.
Shi’s 2021 Cell paper acknowledges your lab for “technical assistance” on reverse genetics. Please walk us through the exact protocol you supplied to WIV for WIV1 backbone assembly.
I believe you are talking about my 2020 co-authored Cell paper with Shi. I shared my (safe) humanized mice with her lab. On January 26, 2020, I openly discussed my DARPA/NIAID grant with Daszak and Shi, and my 25% “bookend,” now called SARS2.
Your 2018 EcoHealth progress report (FOIA) lists “Shi Zhengli - UNC exchange” under subcontracts. Please provide the budget line and dates of her 2018 UNC visit.
Where is that? Shi has never visited my UNC facility. But I always had access to her facility. For example, I resurrected the SARS2 isolate from Shi’s lab based on her uploaded genome.
In 2017, you transferred the no-see’m BsmBI system to WIV (NIC memo). Can you provide the training log Shi signed during her UNC bench session?
Where is the evidence for that? Shi used that crappy BAC technology from Spain; I could ligate 6 cDNA fragments, then in vitro transcribe and electroporate. Just like the SARS2 genome, and that’s No See’m technology!
Shi’s lab built 8 SARS-like chimeras in 2017 using pGEM-T Easy (same as your 2006 paper). Can you confirm if you reviewed the constructs before submission?
Your question proves Shi’s technology is about a decade behind my own. My latest and greatest reverse genetic system was also published in 2017. My in vitro ligation-based strategy involves dividing the viral genome into smaller fragments, cloning them into separate plasmids, and then assembling the full-length genome in vitro for transcription and virus rescue. In contrast, Shi’s system utilizes a bacterial artificial chromosome (BAC) vector, where the entire full-length viral cDNA genome is cloned into a single large BAC plasmid. This plasmid is then maintained and manipulated in bacteria before being directly transcribed into mammalian cells for virus rescue.
Your 2015 paper states: “All chimeric work was performed under BSL-3”. Shi’s 2017 paper used BSL-2. Did you send an email to Shi flagging the downgrade?
If you can’t beat them, join them. My 2017 reverse genetic system enables me to perform cell preparation in a BSL1 lab. That’s my kitchen sink!
In January 2020, Shi published RaTG13 (96% SARS-2). Did your freezer log (2024 transcript off-record) list “RaTG13 co-isolate serum”?
I don’t need an isolated RaTG13 virus to work my cDNA magic. I need her sequence, which she partially uploaded in 2018.
Your 2024 testimony (p. 135): “15 unpublished SARSr-CoVs from Shi”. Can you kindly list them with collection dates and the Mojiang mine origin?
You missed the best part of my answer because I self-incriminated:
Regarding Shi’s 2016 grant to you: “UNC will provide reverse genetics training”. Did you provide the training or prepare a syllabus?
You're making up stuff, but I’m training my own UNC staff, not Shi’s!
In your 2018 email, you mentioned the possibility of Wuhan labs working with wildtype SARS-COV, are you aware of any evidence that they did?
No, I made sure Shi worked with safe pseudotypes, and I created the live viruses (chimeras).
In 2019, you and Shi co-authored “Bat SARS-like CoV diversity” (submitted). Can you provide the pre-print and reviewer comments on FCS insertion?
There’s no record of that.
Do you consider it feasible that Shi’s lab used your BsmBI sites in a WIV1-RaTG13 chimera? If so, can you provide the plasmid map you approved?
My plasmid map looks very different from hers (and very close to SARS2)
via Dr. Valentin Bruttel Substack
Shi’s 2013 Mojiang mine samples yielded RaTG13 and 8 other SARSr-CoVs. Did you ever have access to the miner serum metadata (age, symptoms, date of death)?
No, I need sequences, not serum. I did reference the abandoned Mojiang mineshaft in our U01 CREID grant (aka DARPA Defuse TA2)!
Reports from DRASTIC and Independent Science News (2024) indicate your UNC lab holds Mojiang miner-derived isolates beyond RaTG13, potentially a closer relative to SARS-CoV-2. Can you confirm or deny this claim, and provide details on any such samples in your archives?
The committee asked me that question, but I dodged it like a champ!
EcoHealth 2020–2022 subcontract to WIV amounted to $600k/year. Can you divulge UNC’s cut as co-PI?
I’m about 10-20% of EcoHealth’s cut. It’s not about the money from EcoHealth, it’s about access to unpublished Chinese bat samples.
FOIA missed your Gmail. Can you provide us with the login details for your Gmail account that you use to communicate with Shi?
Post-pandemic, we don’t communicate pleasantly:
Moderna mRNA-1273 uses your stabilized spike. Can you provide royalty statements 2020–2025?
FBI agent “John Doe” (real name redacted) logged 37 threats to your family. Please provide the full log and share how you and your family responded to these threats?
They weren’t threats; they were F U emails for blowing up the world.
In the 2015 Beijing Track-II workshop organized by CISAC, you presented alongside Dr. Zhengli Shi and Dr. David Franz on gain-of-function (GoF) risks and synthetic biology. Dr. Franz reportedly criticized the U.S. GoF moratorium as overly regulatory and advocated leaving oversight to lab heads. Did this influence discussions on biosafety standards for WIV’s SARS-like bat coronavirus culturing under BSL-2 conditions, and what was your response to his position during the event?
By 2019, Shi was doing all animal experiments (in vivo) in a BSL-3
Four U.S.-China workshops (2015–2019) via CISAC were held to build “informal” ties amid dual-use concerns, including GoF regulation. As a key participant, what specific risk mitigation proposals did you advance for WIV’s handling of hACE2-using viruses in human cells, and were these documented in follow-up reports shared with BSEG or CIA?
We spent more time in China than Shi did in America. Why? We wanted access to her Chinese bat samples to create Chinese bat vaccines and test them on live bats in Wuhan. Everyone has humanized mice, but only Shi has live Chinese bats. The DRASTIC folks proved this!
That 2015 China meeting with Franz and Baric (shown in red box)
Post-2015 BSEG meeting, the CIA contacted you for a “coronavirus project” just before your Beijing trip. Did this project involve providing intelligence on GoF techniques or viral backbones shared with WIV, and how did it align with the Track-II workshop’s agenda on transparency and regulation?
You saw the 2015 email from the CIA to me. They are clueless on any subject outside of tracking Russian tanks and planes.
On Jan 29, 2020, you briefed BSEG with slides outlining 3 SARS-CoV-2 origins: natural evolution, accidental lab release, and genetic engineering, specifically noting WIV’s role in Slide 22 for a possible accidental scenario. What forensic evidence (e.g., sequence data) supported the lab release hypothesis in your slides, and why was this not publicly disclosed earlier.
Anything that points towards Shi’s BSL2, and away from Dani’s BSL4, is a big win for me.
Your BSEG slides highlighted WIV’s sequencing and culturing of thousands of SARS-like bat coronaviruses under BSL-2, despite hACE2 receptor use and human cell growth, deeming it “inadequate protection.” How did this assessment inform your internal view on the “most likely origins are bats” statement (Feb 27, 2020), and did it factor into any contemporaneous communications with Dr. Shi?
I’ve always said SARS2 came from a bat, because it’s a white lie. Since COVID is the result of a bat vaccine trial gone sideways in Dani’s BSL4, no one is lying, including her!
Your Jan 2020 BSEG briefing has been linked to a potential MI5/Farrar-Fauci call on Feb 1, 2020, regarding lab accident risks. Were you aware of international intelligence sharing on WIV biosafety lapses at that time, and did it influence your Mar 5, 2020, assertion of “absolutely no evidence that this virus is bioengineered”?
As a BSEG member (confirmed in the newly disclosed Sep 2020 full list of 27 experts, including Relman, Inglesby, Brent, and Franz), how did your role intersect with EcoHealth Alliance’s funding of WIV projects? Did BSEG discussions address EcoHealth’s subawards for bat coronavirus work, and were honoraria (e.g., your Jan 2018 payment) reported in BSEG conflict-of-interest disclosures?
Great question, and yes is the answer, I am full of COIs.
CISAC’s “competition” with CRDF and others for budget/influence, using BSEG access (e.g., yours) has been described as an attempt to “hawk US science” in Track-II channels. As both a BSEG and CISAC participant, did this dynamic affect EcoHealth’s role in U.S.-China collaborations, such as DARPA-related dual-use communications you advised on in Mar 2018?
My self-interest is funding my huge UNC lab. If the US biodefense money helps achieve that goal, I will play their silly biogames and make money in the stock market.
The full BSEG membership (Sep 2020: 27 experts) was never previously disclosed, per the thread’s FOIA discovery via the “B Group” alias. As a member, what criteria were used for selection, and why was the list classified despite BSEG’s advisory role on biological threats?
You have seen the BSEG list; it consists of US academics with a security clearance. We are biologists on the US government payroll, via US academic labs funded by government money. David Relman is an excellent example of this. Relman was fully committed to the lab leak theory, delivering hour-long presentations from his Stanford University office. He even discussed the WIV Master Thesis, a short-lived conspiracy since Shi uploaded RaTG13 to NIH databases in 2018. He discussed the missing WIV database, which is now irrelevant since Shi reuploaded RaTG13 on January 24, 2020.
In May 2021, Relman invited me to sign the Science letter calling for a lab leak investigation into Shi’s BSL2. I gladly played Relman and signed it, making lab leakers fall in love with me. Then DARPA Defuse leaked, and both of us went radio silent. Relman claimed Defuse did not “move the needle a lot.” Relman never discussed it or gave an hour-long presentation on my Defuse bid. He’s only continued to implicate Shi’s BSL2.
“They were essentially playing Russian roulette with the virus that the world’s expert [Ralph Baric] had labelled poised for human emergence,” David Relman, a microbiologist at Stanford, said. “It’s the willingness to manipulate them without due concern.”
“It’s not that the scientists would not have wanted to share,” Relman, who has refrained from taking a position on SARS-CoV-2’s origin, said. “It’s that they wouldn’t have been allowed.”
Your late Jan 2020 BSEG briefing on non-natural origins (accidental release or engineering) was uncovered via a likely FOIA redaction error (”BSEC” for BSEG). What other BSEG discussions on WIV lab leaks or GoF risks might remain redacted, and would you advocate for their declassification to align with your Graham & Baric (2020) call for “transparency and open scientific investigation”?
I mentioned this BSEG meeting in testimony, and only this meeting, so there are no others. I would have offered this up as an alibi.
Recent FOIAs show that the CIA, via ODNI (and directly), contacted you post-2015 BSEG for a “coronavirus evolution” project, focusing on “the coronavirus evolution and possible natural human adaptation.” This raises questions on collaboration vs. intelligence oversight. How did this inform your views on balancing U.S.-China virology ties with biosafety monitoring, and why was it not referenced in your Jan 2024 Congressional testimony?
I forgot about it because it’s such a generic request. It sounds like the CIA also contacted clueless Daszak around the same time.
You responded to the CIA officer that you would “be glad to discuss this in more detail” as soon as you returned from a trip to China. Did you discuss the project in more detail, and if so, what exactly was discussed?
I don’t remember, but interestingly, I was in Montana (RML?)
BSEG, established in 2006 under ODNI for classified biological threat advice, included your briefing on WIV’s BSL-2 practices as “inadequate.” What specific recommendations did BSEG make post-Jan 2020 on enhancing WIV oversight, and were these shared with EcoHealth or NIH?
Those 6 segments in SARS2 genome were pre-assembled in my BSL2.
It is claimed that U.S. intel “piggybacked” on Track-II workshops (e.g., 2015 Beijing) for surveillance, with your CIA contact timing. In your experience, how “neutral” were these informal channels, and did they address the “stupid consequences” of competing U.S. entities (CISAC vs. CRDF) in promoting high-risk research?
Sen. Rand Paul’s Oct 30, 2025, document release confirms your BSEG slides on WIV’s potential accidental role. What prompted your inclusion in these classified briefings, and how does it reconcile with your non-response to public leak inquiries in early 2020?
You're missing the bigger picture. I didn’t tell the bozos at BSEG about the pandemic potential of a furin cleavage site. Why? Because I inserted it to help with bat-to-bat transmission.
As the first to highlight your Jan 2020 BSEG briefing (per your Proximal Origin update), the thread credits FOIA “escapes” (e.g., alias errors) for revelations. What steps would you recommend to prevent future redactions from obscuring biosafety intel, especially for WIV-like facilities?
Tell Dani Anderson to be more careful with her BSL4 experiments. She helped me edit that DARPA Defuse document, but left the door wide open when she left town in November 2019.
The UNC meeting minutes on April 1st, 2020, show that Grant ID 74842, to generate a “full length clone of RaTG13, including reporter viruses” was approved. Can you confirm that the PI was you and what results have there been from this experiment, not only regarding host tropism and pathogenesis, but also the viability of generating the clone?
I can generate anything from a sequence.
Why were the results of this experiment not published?
I gladly take taxpayer money for risky research, but don’t publish the results.
On the 17th of March 2020, you wrote a statement for the NIH’s Center for Scientific Review, to the VirB Scientific Review Officer, Neerja Kaushik-Basu, commenting on the RO1 A1110700 proposal “Cell entry, cross-species transmission and pathogenesis of novel coronavirus, SARS2 from Wuhan”, co-directed by you and Dr. Fang Li. Why were so many details of this proposal redacted in the FOIA?
My secrets are greater than China. Did you notice my unpublished chimera in R01AI089728 called WIV16 spike into a SARS1 backbone?
How did this proposed work relate to the other Grant ID 74842, which aimed to generate a “full length clone of RaTG13, including reporter viruses”?
Your money; my results!
Did WIV or other Chinese Laboratories use primary human airway epithelial cells for virus characterization pre-pandemic? If not, what did they use instead?
Did you share your primary human airway epithelial cell expertise with any Chinese scientists at WIV, or in the USA? If so, with who, how and when?
Did you guys ever find a lung transplant department in the WIV?
Did you consider it wise that Dr. Rocke and Dr. Unidad would supervise bat cave transmissible vaccine experiments in China (Yunnan), on behalf of DARPA, for the DEFUSE proposed project, given the underlying goal was to protect the US “warfighter” in future missions?
Do you have $14 million US biodefense bids to justify?
Did you consider possible objections to this research from the Chinese authorities?
Good question, but who cares since we Western virologists call the shots.
Looking back with hindsight, would you agree that there were certain dangers inherent in the DEFUSE research proposed? (see FOIA extract of your draft below):
Technically, my transferable bat technology (top) developed in a humanized mouse model was safe. It was partner Munster who aerosolized agents into a transmissible vaccine (bottom) that was unsafe.
Now, let’s move on to discuss your feelings about SARS-COV-2 related conspiracy theories, for example, that SARS-COV-2 emerged as the result of a live-attenuated vaccine (LAV) experiment: Pre-pandemic, your UNC lab was the only institution worldwide with published live-attenuated SARS-CoV vaccine candidates (WHO Blueprint 2020 list: nsp16 2’-O-MTase mutant and MA-ΔExoN). For the record, can you provide us with the full genomic sequences of both constructs and confirm they remain incapable of sustained human transmission?
By definition, the human oral polio LAV was a perfect model for bat transmission. Does high transmissibility and low virulence sound familiar?
Virologists at RML used CMV (herpesvirus) as a vaccine vector. But others postulated on “well-studied coronaviruses.” From Post #1: “Vaccine transmission is a relatively new concept with few examples, so the possibility of transmission changing in time has scarcely been entertained. The oral polio vaccine (OPV) is perhaps the best documented case of vaccine transmission.”
Independent researchers (Karl & Dan Sirotkin, 2021–2025) have claimed SARS-CoV-2’s phenotype and genomic features resemble a reverting LAV derived from your programme. Every specific marker they cite (CpG suppression, gut tropism, cold-adaptation, ORF10 immunosuppression) has been refuted in peer-reviewed literature. Why do you think this theory continues to circulate despite there being little evidence to support it?
Dan also thinks I taught the Chinese military how to create a human live-attenuated vaccine. I kept my methods from China, and LAV is never approved for humans, but is excellent for animals like bats. Here’s my MERS-MA30 buddy Stanley Perlman:
Your 2015 chimeric viruses (SHC014-MA15) were described in the paper as offering “several different possibilities for attenuation”. Can you kindly confirm that these chimeras were never part of a live-attenuated vaccine development pipeline.
That's a nice question; I forgot I wrote that, but my entire existence was dedicated to the creation of vaccines. Look at this line: “The use of SHC014-MA15 as a live, attenuated vaccine showed potential cross-protection against challenge with SARS-CoV, but the results have important caveats.”
Bull (2015, Virus Evolution) concluded that serial-passage live viral vaccines are inherently prone to reversion and that genetic engineering has so far failed to make them evolution-proof. Please provide us briefly with your current assessment of whether a coronavirus LAV could ever be made reversion-resistant.
Jim Bull and I are buddies from the SARS1 days. He focused on self-spreading vaccines. I concentrated on recombination-resistant, live-attenuated vaccines. You got a hybrid called COVID-19.
Imagine someone did release a reverting SARS LAV in late 2019. What three genomic or phenotypic signatures would you expect to see that are absent in SARS-CoV-2?
Robert Redfield discussed the three phenotypes: aerosolization (oral spread), reinfection (superinfection), and asymptomatic spread (immune evasion). Genomic evidence is in my 2018 HKU3-Smix patented chimera, which “provides a method of producing an immune response to a coronavirus in a subject.” Remember the Laos Banal bat samples? Your human body now has antibodies that protect against those bat samples!
Dr. Baric, for five years, you and your family have lived under death threats, doxxing, and relentless online vilification, much of it amplified by social-media accounts with hundreds of thousands of followers. In your view, did the U.S. government, NIH, UNC, or any federal agency provide you and your colleagues with adequate protection and support during that period, or did you largely have to fend for yourselves?
We had an FBI agent assigned to our protection, then used him to shield us from FOIA laws!
Many journalists and commentators, both mainstream and independent, repeatedly described anyone questioning a natural origin as a “conspiracy theorist,” a label that was then attached to you once the lab-leak hypothesis became more widely discussed. Looking back, do you believe the media’s use of that term was responsible and accurate, or did it contribute to the threats and harassment you received?
I used the conspiracy theorist label first on Kristian Andersen, who threatened to call the FBI and CIA and notify them that my SARS2 genome “looks engineered.” What a prick!
Finally, could you share with us the worst moment you experienced because of this? What did you feel about the role social media, journalists, and public discourse played in bringing that fear to your family, and what, if anything, do you wish had been done differently by institutions or individuals to prevent it?
“Let’s be honest, a fair number that probably wished I hadn’t become a scientist.”
END OF QUESTIONS THANK YOU FOR YOUR COOPERATION, DR. BARIC!
You’re welcome
Ralph Baric and Pfizer funded colleagues were weaponizing Dengue Fever Virus in North Carolina in 2022. They inserted the Furin Cleavage Site that makes Covid19 so Lethal.
https://geoffpain.substack.com/p/directed-evolution-gain-of-function
Great and rapid response to the Baric questions, bravo!
As you know, i have some more answers, extracted by different means ;)