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FTR #1115 This program was recorded in one, 60-minute segment.
Introduction: Against the background of our discussion of the Covid-19 outbreak as what Mr. Emory has termed a “Bio-Psy-Op,” we present archival material about the development of AIDS as a biological warfare agent.
(Programs containing information on AIDS as a BW weapon include: AFA #s 16 and 39, as well as FTR #‘s 16, 19, 63, 317, 324, 557, 597, 606, 642, 644, 682, 820, 912, 1012.)
The program begins with review of an interview with Dr. Wilbert Jordan of Martin Luther King Hospital in Los Angeles (from AFA 16.) Done in December of 1984, it gives perspective on the epidemiological aspects of AIDS–information that undermines the prevailing theories at the time concerning the origins of the disease.
Noting that a disease as lethal as AIDS was at the time (before anti-virals developed to treat HIV infection), Dr. Jordan is dismissive of the notion that such a lethal ailment could have been present in either Zaire or Haiti and then retrospectively traced there after being discovered in the U.S.
The notions of Haiti and/or Zaire being the point of origin of the disease played into the anti-immigrant/xenophobic dynamic that has become prevalent in the era of Donald Trump.
Dr. Jordan concludes by hypothesizing that the disease was created in a laboratory, in all probability in the United States.
Next, the program highlights information from FTR #686, setting forth information about the National Cancer Institute’s Special Viral Cancer Research Project.
After the [official] abandonment by the U.S. of offensive biological warfare research, the Nixon administration declared a “war on cancer” in 1971. As part of the War on Cancer Nixon turned Fort Detrick (the Army’s top BW research center) over to the National Cancer Institute for its Viral Cancer Project. The Viral Cancer Project was inextricably linked with biological warfare research and may well have served as a cover for ongoing BW work. (Listeners interested in this material are encouraged to check out, among other programs, FTR #‘s 606, 682.)
For the purposes of the present discussion, it is worth noting that it was the National Cancer Institute’s VCP that was at the epicenter of AIDS research in the United States.
The VCP/NCI biological warfare connection utilized strong connections to university research facilities. The Naval Biosciences Laboratory (managed by the University of California), as well as Fort Detrick were profoundly involved with the NCI’s VCP. The Cell Culture Laboratory at the Naval Biosciences Facility provided the seed stock for the production of vast quantities of carcinogenic and immunosuppressive viruses that were generated by the National Cancer Institute.
The production of those viruses for the NCI was overseen by Drs. James Duff and Jack Gruber, both longtime veterans of Fort Detrick and its biological warfare research.
The aerial transmission of deadly pathogenic agents was a major focal point of the NCI’s VCP, apparently overlapping BW research projects. Two other key researchers for the NCI, Drs. Alfred Hellman and Mark Chatigny also had biological warfare research backgrounds, including work with aerial transmission of pathogenic agents.
Yet another component of the NCI/VCP/BW connection was the incorporation of pharmaceutical companies in the research programs. The Pfizer company produced viruses for the NCI’s VCP, including the immunosuppressive Mason-Pfizer monkey virus, like HIV, a retrovirus.
Among the most significant and alarming aspects of the NCI’s VCP program is the fact that, when Fort Detrick was converted to the Frederick Cancer Research Center, it was administered by Litton Bionetics, a biotechnology subisidiary of Litton Industries. Litton was a major defense contractor and a frequent vehicle for covert operations.
Prior to assuming stewardship of Fort Detrick for the NCI, Litton Bionetics had employed Dr. Robert Gallo (the “discoverer” of HIV).
Of paramount importance in this investigation is the fact that the NCI’s VCP program involved numerous experiments and operations designed at getting organisms to “jump species.” Prominent researchers familiar with these efforts expressed alarm and the conviction that such work should be outlawed, lest it lead to the creation of new, deadly organisms that would infect humans.
Obviously, this broadcast and the line of inquiry approached in Mr. Emory’s decades-long investigation of AIDS as a man-made disease highlight the possibility/probability/near certainty that HIV is just such an organism.
The program concludes with review of an excerpt from testimony before a House appropriations subcommittee that was drawing up the defense budget for the following year. (The hearings were in 1969.) The testimony discusses the possibility of using genetic engineering to produce a disease that would be “refractory” to the immune system. This is virtually the clinical definition of AIDS. It is worth noting that the project was funded, and just such a disease—AIDS—appeared in just the time frame posited. It is also worth noting that, in the 2002 edition of A Higher Form of Killing, this passage is omitted!!
. . . As long ago as 1962, forty scientists were employed at the U.S. Army biological warfare laboratories on full-time genetics research. ‘Many others,’ it was said, ‘appreciate the implications of genetics for their own work.’ The implications were made more specific that genetic engineering could solve one of the major disadvantages of biological warfare, that it is limited to diseases which occur naturally somewhere in the world. ‘Within the next 5 to 10 years, it would probably be possible to make a new infective micro-organism which could differ in certain important respects from any known disease-causing organisms. Most important of these is that it might be refractory to the immunological and therapeutic processes upon which we depend to maintain our relative freedom from infectious disease.’ [Italics are Mr. Emory’s.] The possibility that such a ‘super germ’ may have been successfully produced in a laboratory somewhere in the world in the years since that assessment was made is one which should not be too readily cast aside. . . .
Program Highlights Include: Litton Bionetics’ work on the Mason-Pfizer monkey virus while under contract to the NCI and when it employed Dr. Robert Gallo; research emphasis on “zoonoses” (diseases that jump from animals to humans) by the joint military/civilian consortium; Gallo’s work with NCI VCP/Ft. Detrick veteran Dr. Jack Gruber in a mass viral inoculation program undertaken by Litton Bionetics; the use of the Mason-Pfizer monkey virus in the Litton Bionetics mass inoculation program.
1. The program begins with review of an interview with Dr. Wilbert Jordan of Martin Luther King Hospital in Los Angeles. Done in December of 1984, it gives perspective on the epidemiological aspects of AIDS–information that undermines the prevailing theories at the time concerning the origins of the disease.
Noting that a disease as lethal as AIDS was at the time (before anti-virals developed to treat HIV infection), Dr. Jordan is dismissive of the notion that such a lethal ailment could have been present in either Zaire or Haiti and then retrospectively traced there after being discovered in the U.S.
The notions of Haiti and/or Zaire being the point of origin of the disease played into the anti-immigrant/xenophobic dynamic that has become prevalent in the era of Donald Trump.
Dr. Jordan concludes by hypothesizing that the disease was created in a laboratory, in all probability in the United States.
2. Next, the program highlights information from FTR #686, setting forth information about the National Cancer Institute’s Special Viral Cancer Research Project.
After the [official] abandonment by the U.S. of offensive biological warfare research, the Nixon administration declared a “war on cancer” in 1971. As part of the War on Cancer Nixon turned Fort Detrick (the Army’s top BW research center) over to the National Cancer Institute for its Viral Cancer Project. The Viral Cancer Project was inextricably linked with biological warfare research and may well have served as a cover for ongoing BW work. (Listeners interested in this material are encouraged to check out, among other programs, FTR #‘s 606, 682.)
For the purposes of the present discussion, it is worth noting that it was the National Cancer Institute’s VCP that was at the epicenter of AIDS research in the United States.
The VCP/NCI biological warfare connection utilized strong connections to university research facilities. The Naval Biosciences Laboratory (managed by the University of California), as well as Fort Detrick were profoundly involved with the NCI’s VCP. The Cell Culture Laboratory at the Naval Biosciences Facility provided the seed stock for the production of vast quantities of carcinogenic and immunosuppressive viruses that were generated by the National Cancer Institute.
The production of those viruses for the NCI was overseen by Drs. James Duff and Jack Gruber, both longtime veterans of Fort Detrick and its biological warfare research.
The aerial transmission of deadly pathogenic agents was a major focal point of the NCI’s VCP, apparently overlapping BW research projects. Two other key researchers for the NCI, Drs. Alfred Hellman and Mark Chatigny also had biological warfare research backgrounds, including work with aerial transmission of pathogenic agents.
Yet another component of the NCI/VCP/BW connection was the incorporation of pharmaceutical companies in the research programs. The Pfizer company produced viruses for the NCI’s VCP, including the immunosuppressive Mason-Pfizer monkey virus, like HIV, a retrovirus.
Among the most significant and alarming aspects of the NCI’s VCP program is the fact that, when Fort Detrick was converted to the Frederick Cancer Research Center, it was administered by Litton Bionetics, a biotechnology subisidiary of Litton Industries. Litton was a major defense contractor and a frequent vehicle for covert operations.
Prior to assuming stewardship of Fort Detrick for the NCI, Litton Bionetics had employed Dr. Robert Gallo (the “discoverer” of HIV).
Of paramount importance in this investigation is the fact that the NCI’s VCP program involved numerous experiments and operations designed at getting organisms to “jump species.” Prominent researchers familiar with these efforts expressed alarm and the conviction that such work should be outlawed, lest it lead to the creation of new, deadly organisms that would infect humans.
Obviously, this broadcast and the line of inquiry approached in Mr. Emory’s decades-long investigation of AIDS as a man-made disease highlight the possibility/probability/near certainty that HIV is just such an organism.
Discussion Highlights Include: Litton Bionetics’ work on the Mason-Pfizer monkey virus while under contract to the NCI and when it employed Dr. Robert Gallo; research emphasis on “zoonoses” (diseases that jump from animals to humans) by the joint military/civilian consortium; Gallo’s work with NCI VCP/Ft. Detrick veteran Dr. Jack Gruber in a mass viral inoculation program undertaken by Litton Bionetics; the use of the Mason-Pfizer monkey virus in the Litton Bionetics mass inoculation program.
3. The program concludes with review of an excerpt from testimony before a House appropriations subcommittee that was drawing up the defense budget for the following year. (The hearings were in 1969.) The testimony discusses the possibility of using genetic engineering to produce a disease that would be “refractory” to the immune system. This is virtually the clinical definition of AIDS. It is worth noting that the project was funded, and just such a disease—AIDS—appeared in just the time frame posited. It is also worth noting that, in the 2002 edition of A Higher Form of Killing, this passage is omitted!!
. . . As long ago as 1962, forty scientists were employed at the U.S. Army biological warfare laboratories on full-time genetics research. ‘Many others,’ it was said, ‘appreciate the implications of genetics for their own work.’ The implications were made more specific that genetic engineering could solve one of the major disadvantages of biological warfare, that it is limited to diseases which occur naturally somewhere in the world. ‘Within the next 5 to 10 years, it would probably be possible to make a new infective micro-organism which could differ in certain important respects from any known disease-causing organisms. Most important of these is that it might be refractory to the immunological and therapeutic processes upon which we depend to maintain our relative freedom from infectious disease.’ [Italics are Mr. Emory’s.] The possibility that such a ‘super germ’ may have been successfully produced in a laboratory somewhere in the world in the years since that assessment was made is one which should not be too readily cast aside. . . .
Uncle Sam and The Swastika
For those Dave Emory listeners who need a visual reference to the CIA’s weaponized immunological genetics research, particularly in the early 1960’s, have fun with the following link:
https://www.cia.gov/readingroom/docs/CIA-RDP80-00247A004200090001‑4.pdf
Has the US found a new home for its various ‘dual use’ biodefense projects? Projects like the EcoHealth Alliance and Metabiota? It sure sounds like it, although we don’t really know yet. What we do know is that there’s a new ‘ARPA’ in town: ARPA‑H. It’s like DARPA for health and medicine. At least that’s the sales pitch. The details have yet to be worked out. But we do know who will be leading it: Dr. Renee Wegrzyn, a biotech executive with extensive government experience. Experience that includes work five years of as a program manager for DARPA, where she oversaw projects using synthetic biology to counter infectious disease and bolster biosecurity. And while it’s certainly possible Wegrzyn’s work had absolutely nothing to do with the kind of ‘gain-of-function’ work that that EcoHealth Alliance was working on in the years leading up to the COVID19 pandemic, there’s also no denying that her resume sounds a lot like the resume of someone who would be very familiar with that kind of work.
So in light of the NIH’s recent decision to rescind the EcoHealth Alliance’s grant over concerns about a lack of oversight with of the Wuhan Institute of Virology, while keeping open the possibility of more grants in the future after these ‘oversight issues’ get worked out, we have to ask: is ARPA‑H the intended new home for for the US’s dual use ‘biodefense’ research? Because if so, it sounds like they chose someone with the appropriate experience to lead it:
“Modeled after the Defense Advanced Research Projects Agency, the new agency is known as the Advanced Research Projects Agency for Health. (In the argot of Washington, where every agency has an acronym, the defense research agency is called DARPA and the health agency is ARPA‑H.)”
A new DARPA. Or rather, the latest ‘ARPA’. And while President Biden was emphasizing its potential role in his ‘cancer moonshot’ initiative, it’s pretty clear that ARPA‑H isn’t limited to cancer. It’s also pretty clear that this new agency is going to be on the hunt for some high profile early ‘wins’ to justify its existence. What isn’t clear is what exactly it’s actually going to be focusing on. Because it sounds like the projects this agency could be involved with are basically anything tangentially related to health and medicine:
So what should we expect from ARPA‑H? At this point the biggest clue is probably the person tapped to lead it: Renee Wegrzyn, biologist with extensive work in both government and the private sector. As the following piece describes, Wegrzyn spent more than five years working as a programme manager at DARPA, where her portfolio included projects that used synthetic biology to counter infectious disease and bolster biosecurity. Now, “synthetic biology to counter infectious disease and bolster biosecurity” could mean a lot of different things. It’s not at all obvious from those scant details that Wegrzyn was in any way involved in the EcoHealth Alliance’s gain-of-function work on coronaviruses in the period leading up to the COVID19 pandemic. But boy does that portfolio sound like someone who would at least be aware of that kind of research and familiar with many of the technologies and risks involved.
So given that we already know that the NIH is cracking down on the EcoHealth Alliance’s work — but doing so in a manner that appears to be designed to end EcoHealth Alliance’s collaboration with labs in China and not end EcoHealth Alliance’s overall work in creating synthetic viruses — we have to ask: is ARPA‑H the intended destination for the next generation of dual use biological warfare ‘biosecurity’ research? It sure seems like an obvious home for that kind of work. And while we don’t have clarity on Wegrzyn’s background, it’s hard to ignore how well “synthetic biology to counter infectious disease and bolster biosecurity” could describe exactly what the EcoHealth Alliance has been doing all along:
“Wegrzyn spent more than five years working as a programme manager at DARPA, where her portfolio included projects that used synthetic biology to counter infectious disease and bolster biosecurity. At the agency, Wegrzyn led its Safe Genes programme, a four-year, $65-million initiative aimed at safeguarding against the potential dangers of the gene-editing technique CRISPR. Doudna says that Wegrzyn was “gifted” at bringing different types of researcher to the table — bioethicists and geneticists alike — to discuss a new and ethically challenging technology.”
You can see why Biden picked her for the role with a background like that. And note that Wegrzyn was working at Booz Allen Hamilton at the time when she was working as a program director for DARPA. She has extensive experience in both the public and private space, in particular in the areas where the private sector is contracting for the government. It’s exactly the kind experience you expect for a pick like this. But, again, it’s also the kind of experience we would expect if the plan was to make ARPA‑H the new home for the US’s dual use biowarfare ‘biosecurity’ research. So when we read that ARPA-H’s foundational details have yet to be established at the same time many basic questions about the agency — like where it will be housed — remained unanswered, it’s a reminder that the ARPA‑H isn’t simply going to be an extension of Joe Biden’s ‘cancer moonshot’. This is the kind of agency that could be leading all sorts of biological research. Especially ‘dual use’ research that would be difficult to get approval for under agencies with more stringent oversight:
And let’s not forget about ambitious initiatives like Metabiota. ARPA‑H is clearly about creating new businesses too, not just research. And we already know Metabiota received funds from both the CIA’s In-Q-Tel and the Pentagons Defense Threat Reduction Agency (DRTA). Are there going to be any Metabiota-related contracts issued by ARPA‑H? It sounds very possible. But also keep in mind that if part of the unwritten intent of this new agency is to house the US’s dual use ‘biodefense’ research, the EcoHealth Alliance and Metabiota are just warmup acts for the bigger and better ‘high-risk-high-reward’ projects to come.
We just got an absolutely fascinating update to the biology of SARS-CoV‑2. Although it’s really an update to the biology of how the human immune system responds to the virus and why it is that some people really are ‘superdodgers’ who don’t even show symptoms no matter how much exposure they have to the virus. New research appears to have elucidated those super-dodging biological mechanisms. And as the following article describes, their finding s once again show how unusual this virus really is. Because it turns out SARS-CoV‑2 is only the third virus ever discovered with a ‘super-dodging’ population. The other two viruses where this remarkable super-dodging ability has been observed is the norovirus and, of course, HIV. And as with HIV, a single mutation appears to be the source of this super-dodging ability.
Now, the ‘superdodging’ isn’t quite the same between HIV and SARS-CoV‑2. As we’ve seen, HIV superdodgers have a mutation in the CCR5 gene that literally blocks the ability of the HIV virus to enter the cell at all. The viruses just stick to the outside of the cells without ever entering. That mutation is found in 5–14% of Europeans but is very rare in African, Native American, or East Asian populations.
In the case of SARS-CoV‑2 superdodgers, the mutation doesn’t block the virus from infecting cells. Instead, it turns out some people have a mutation on the HLA‑B gene, which is deeply associated with your body’s immune response. And if you have this single mutation, your body just happens to create T‑cells pre-programmed to recognized SARS-CoV‑2. Normally, when your body gets exposed to a virus, the product of those T‑cells customized to the invader takes days for your body to produce, giving the virus time to spread before your body can mount an effective enough response to quell the infection. But for these superdodgers, their immune systems are so primed to fight the virus right out of the gate that the infection never gets to the point where symptoms appear. So they aren’t exactly superdodgers but superfighters.
The only require for these ‘lucky’ individuals is that they previously get infected with a different coronavirus. So there’s something about this mutation in the HLA‑B gene that causes these people to elicit a somewhat different T‑cell response to coronaviruses in general, and that difference in T‑cells makes all the difference when it comes to fighting off SARS-CoV‑2. Recall how we’ve already seen indications that common-cold coronavirus exposure is helpful is fighting off the virus and it’s speculated that some of these common-cold coronaviruses started off as COVID19-like killers when they initially jumped to human populations. So it would appear that the benefits of common-cold coronavirus exposure are super-benefits for these superdodgers.
This is also probably a good time recall how the various ‘gain-of-function’ projects involved with EcoHealth Alliance’s coronavirus research involved looking at coronaviruses as a broad group. And then there’s Moderna’s lawsuits over alleged patent infringements of its the broad-spectrum betacoronavirus vaccine, including human clinical trials as far back as 2015. The point being that a lot of generic coronavirus research involving synthetic coronaviruses took place over the past decade. What was learned about the genetics of the human immune response to coronviruses during this period? Was this particular mutation in the HLA‑B gene previously recognized as having an impact on the nature of the T‑cells generated in response to a coronavirus exposure?
There’s another important element of this story with disturbing echos of the highly race-stratified nature of the CCR5 mutation in HIV (where basically the protective mutation is only found in European populations): the mutation that confers SARS-COV‑2 superdodging abilities is found on the HLA‑B gene, in the HLA region of the genome. That HLA region has been subject to the evolutionary pressures of local environmental dangers and as a result is highly varied across human populations. In other words, we should expect potentially very different rates of this protective HLA‑B mutation across ancestral populations, much like what we saw with CCR5 and HIV.
Now, at the end of the following article, we’re going to hear the lead researcher on this study make the observation that “this mutation is quite common. We estimate that maybe 1 in 10 people have it. And in people who are asymptomatic, that rises to 1 in 5.” But it’s important to recognize that their study appears to have been on self-identified White Europeans. So when we hear about this being a relatively common mutation, keep in mind that this is likely a statement specific to European ancestry populations. Whether or not this mutation happens to be just as prevalent across the world is another question. And, again, the mutations found in these HLA region genes are known for being highly stratified based on ancestry. This the part of the genome dedicated to fighting local environmental insults. It’s going to be highly ancestry-specific.
And that’s the big revelation: SARS-CoV‑2, like HIV, is one of only three viruses known to produce superdodgers cause by a single mutation. And the superdodging might be very ethnospecific. More data needs to be gathered to make that determination, but there’s a good chance of that being the case based on the highly race-stratified nature of the HLA region of the genome. What are the odds?:
“Over the course of human history, scientists have identified only two instances of true virus superdodgers. That is, where a specific mutation in their genes makes people completely resistant to a virus. So that it slides off their cells, “like water sliding off a glass window,” as Casanova puts it.”
Only two other viruses have ever been discovered with this remarkable property: a single mutation can turn someone into a ‘super-dodger’. It’s quite an exclusive club for SARS-CoV‑2. Just SARS-CoV‑2, the norovirus, and HIV get to join this club:
But the single-mutation super-dodging observed in SARS-CoV‑2 patients differs significantly from the mechanism through which HIV and and the norovirus super-dodging was operating: instead of a mutation that blocks the ability of the virus to enter the cell, the SARS-CoV‑2 superdodgers had a mutation that caused their bodies to coincidentally make T‑Cells in response to other coronaviruses — like common-cold coronaviruses — that are pre-programmed to recognize and fight off SARS-CoV‑2. The mutation allows these ‘superdodger’ to immediately fight off the virus so effectively they don’t even develop symptoms:
Now here’s where things because eerily similar to the story of the HIV superdodgers: As we’ve seen that CCR5 mutation that creates the HIV super-dodgers is somewhat common in Europeans (5–14%) but very rare in African, Native American, and East Asian populations. It’s the kind of observation that should raise all sort of chilling questions given all the other questions about the origins of HIV and the networks involved in that research. So what do we find with this SARS-CoV‑2 superdodger mutation? Well, the mutation occurs in the HLA region of the genome. This HLA region is, in turn, deeply intertwined with the functioning of the immune system. And when we’re talking about genetics and the immune system, it’s important to realize that the immune system genetics is one of the most ancestry-stratified areas of the human genome. In other words, it varies significantly depending on where your ancestors came from. That’s because the HLA region of the genome is where evolution in response to local environmental dangers happens. So when we’re talking about a single mutation in a single gene in the HLA region that induces this kind of super-dodging capabilities, we’re implicitly talking about a region of the genome where we can expect the prevalence of that mutation to potentially vary significantly depending on your ancestry. Put bluntly, this is a biological recipe for a very race-specific form of super-dodging, much like HIV:
And that brings us to this assertion by the researchers who identified this genetic connection to superdodging that the mutation is “quite common”, with maybe one in 10 having it. There’s an important caveat that should be appended to that claim: when this same search team published their initial findings on the protective properties of the mutation in the HLA‑B gene back in September of 2021, that study was done on a European ancestry cohort. So when we are told that the mutation is ‘quite common’ we should probably be interpreting that statement as ‘quite common in European ancestry populations (white people). For something like HLA‑B, you shouldn’t assume those kinds of rates globally:
And that’s part of what makes this story something to watch: just how globally prevalent are these superdodging genes? Did Europeans once again exclusively get ‘lucky’ in the face of a novel virus, or will we find that this HLA‑B mutation (specifically, HLA‑B*15:01) is also found in other ancestries?
It’s also worth nothing another aspect of this ‘super-dodging’ that differs from the super-dodging observed with HIV: It sounded like the HIV superdodgers probably didn’t spread the virus either. The virus just couldn’t take hold in their bodies at all. But with these SARS-CoV‑2 superdodgers the SARS-CoV‑2 virus is still able to infect their cells and reproduce. The body just does an exceptional job of clearing the infection before symptoms emerge. But don’t forget that COVID19 is most infectious during the asymptomatic early period. So it would be interesting to know if the super-dogers’s immune systems keep the virus at such a low level that they are effectively non-infectious too, or not. Are these superdodgers infectious superdodgers? Or is their super immune response effectively limiting their infectiousness too?
We’ll see. There’s undoubtedly going to be a lot more research in this direction now that these discoveries are being made. Which means a lot more knowledge about how ancestry, novel viruses, and the immune system interact too. For good or ill.