AIDS: Made in America part 2

Robert Huebner
Adenoids to Alzheimer’s

When Robert Huebner was asked in the early 1950’s by the United States Navy to help solve the recurring problem of a chronic but relatively mild form on pneumonia in Naval recruits, he agreed and set to work. Later, he reported his findings in a 1953 article in the Proceedings of the Society of Experimental Biology and Medicine. But, the article didn’t focus upon the pneumonia. It dealt with a secondary phenomenon: the isolation of a disease agent from the adenoids of his naval recruits. The adenoids in the cases of chronic pneumonia presenting in the recruits were undergoing spontaneous degeneration in tissue culture!
This phenomenon of spontaneous degeneration of living tissue was to set the course for the remaining life and research of Robert Huebner, for it was to lead to the isolation and engineering of one of the critical co-factors of AIDS, and, as you shall learn, it also set Huebner on the path to his own death.
Robert J. Huebner can be pointed to as the father of AIDS.
Huebner followed his 1953 article with a series of further research reports spanning the years to 1971 when in the latter year he is credited with a total of 61 citations in Progress Report #8 of the Special Virus Cancer Program, and by 1978 he appears in Progress Report #15 as a member of one of the SVCP Committees. Among his SVCP committee colleagues are three others worthy of note: Dr. Robert Manaker who as we have seen, contributed his initial “M” to the strange antecedent program titled MK-SVLP; also listed is none other than Dr. Robert Gallo who was to later ‘co-discover’ HIV with Luc Montagnier; and, another key figure in the creation of the AIDS co-factors, George Todaro.
Again, murky isn’t it? But let’s try to sort it all out… We will demonstrate how Huebner starts with an atypical pneumonia [which is a characteristic of AIDS] , moves into the degenerating adenoids [which are lymph tissues] and then he becomes an important researcher in a program mysteriously labeled with a code name: MK-SVLP [where the ‘L’ stands for ‘leukemia/ lymphoid ] and in 1965 [ right after L. B .Johnson had won the election in his own right as President of the USA] the ‘MK’ is dropped from the original code name, and SVLP comes from the covert shadows into the relative light of day, as a mainstream US Government research enterprise, Huebner is still right there.
Then, when Nixon declared his war on cancer in 1971, Huebner made a career change. His friend, Robert Gallo, tells it this way:
“When Huebner announced his virogene-oncogene hypothesis, he had already worked for many years and with much success in the Infectious Disease Institute of the National Institutes of Health. His decision to move at this time to the National Cancer Institute, also at NIH, coincided with President Nixon’s declaration of his ‘great war on cancer’ in 1971.”
We shall see why it was that Huebner made this ‘move’ at this time, but first let’s continue with his pneumonia to adenoids research. When we do that you will see how the spontaneously degenerating adenoids was to lead to his work in cancer and finally, how it came together as a co-factor in AIDS.

Take a look at Figure Two. Note the adenoids at the top and back of the nasal cavity. And note in passing that they are just behind the receptor neuron olfactory node which allows certain air-borne molecules breathed into the nose to enter the brain and register as odors. Later we will demonstrate how this fact figured in the death of Dr. Huebner, but first we must continue with the adenoids.
The adenoids are the first line of defence in the immunological processes in the body (and keep in mind Dr. MacArthur’s statement to the Congressmen reported above, that the new lethal biowar agent the Pentagon’s eminent biologists were working on would be”… refractory to the immunological and therapeutic processes upon which we depend to maintain our relative freedom from infectious disease.”
In the immunological processes upon which we depend to maintain our health, the adenoids play a guardian role. They capture samples of the air that is being drawn into the lungs. If that air has some pathogenic agent, the adenoids will not stop it, but will react to it, warning the immune system of the affected individual that something is wrong with the air that he is breathing. The re-action to one of the pathogens to which humans are vulnerable, is ‘spontaneous degeneration’, which was just what Huebner had noted in his study of pleural pneumonia! That’s why Huebner devoted further attention to the degenerating adenoids. He wanted to find out what it was that was causing the pneumonia and the concurrent adenoidal disease.
At first, he could do no better than label the pathogen as a ‘pleural pneumonia-like organism’ or PPLO. He chose this name because the pathogenic agent found in the infected lungs that was causing the chronic pneumonia in the naval recruits was the same pathogenic agent he found in the degenerating adenoids.
It is worth noting in passing that Huebner had adopted a new name for the lung disease that was interfering with the Navy’s training programs. He called the disease “acute respiratory disease” or ARD. This acronym is startlingly close to another ‘acute respiratory’ illness, the severe acute respiratory syndrome or SARS. We’ll see why in our later article on Shyh-Ching Lo and David Ho.
After Huebner et al had published their findings, several other biologists corrected him. It is not, properly speaking, a PPLO that is causing the ARD and the concurrent spontaneous degeneration of the adenoids they told Huebner. The PPLO, they pointed out, is really a microorganism identified in the late 1800’s by two French scientists [at the Pasteur Institute, Nocard and Roux]. The PPLO is actually a ‘mycoplasma’. Note this word carefully. It is the key to AIDS and CFS, and to a number of other neurodegenerative diseases, including the one that was to kill Dr. Huebner. It is also the feature subject of our forthcoming Aug.27-29 CCMRF Conference in Sudbury, Canada.
A Brief Anticipatory Interlude
Although we will be dealing with the mycoplasma in more detail throughout this Special Edition of JODD, at this point we want to draw your attention to something that you need to know as early as it can logically be introduced. This is just such a logical point.
It needs to be noted that the mycoplasma which Huebner stumbled upon in the late 1940’s and early 1950’s became a subject of much covert research. After all, if the Military is looking for a bioweapon what better than one which causes human tissues to spontaneously degenerate. The resultant research, much of which we have now succeeded in tracking down and which we recount in the coming pages, led to the Patenting of a pathogenic mycoplasma by the United States Department of Defence. The nominal ‘inventor’ of this disease-causing mycoplasma was Dr. Shyh-Ching Lo of the American Registry of Pathology and the Patent was granted on September 7, 1993. [See Exhibit Two, p.30].
The critical details that you need to know are on page 22 of that Patent. On that page it is asserted that persons infected with the mycoplasma will be those who have been diagnosed as having either AIDS or CFS or other disease entities such as ‘ respiratory distress syndrome’ (RDS). Compare the latter RDS with Huebner’s ARD or the current SARS. All have to do with some mysterious disease agent that affects the respiratory system… including the one that got Huebner his job with the Navy in the first place.
End of an Interlude
Just what is a mycoplasma?
A mycoplasma is a species of microorganism lacking a cell wall. It is, apparently, a particle of bacterial deoxyribonucleic acid or DNA. Or, as one researcher expresses it:

“The theme underlying the current evolutionary scheme of mycoplasmas is that of degenerative evolution from walled bacteria.”
In other words, we can begin to understand the mycoplasma by starting with a bacterium. The latter is a one-celled animal. It can take in nutrient, generate energy, and re-produce itself. To place it in perspective, we can contrast its one cell being with the average human adult body, which has between 50 and 100 trillion cells.
Although the bacterium has only one cell it has the ability to re-produce itself. When it does so it draws upon nucleic acids of its DNA for the blueprint of its progeny.
Now, if something kills the bacterium, there is apparently a mechanism to preserve some of the bacterial genetic make-up. In some instances particles of the bacterial DNA or RNA are able to save themselves from destruction by manufacturing a protective protein coat. Such particles are what we know of as viruses. Although such particles in their protein coats are unable to reproduce themselves alone, they can invade certain other living cells where they can in some instances, utilize their host cell’s reproductive system to reproduce itself. This is usually done to the detriment of the host cell and the consequences present as disease.
Unlike the virus, the particle of bacterial DNA/ RNA without a cell wall and called the ‘mycoplasma’ can reproduce itself outside of a host cell. However, many species can do great damage to other cells, frequently leading to cell death. Here’s how that works.
Three microbiological researchers [Rottem, Pfendt, and Hayflick] were able to demonstrate in 1971 how the mycoplasmal damage is done. It seems that certain species of mycoplasma, because they are only particles of a complete DNA/RNA have no capacity to manufacture their own growth requirements. To make up for this short-coming, while still possessing the essential urge to live, these species can up-take pre-formed sterols from their host and incorporate these sterols into their own being. Ultimately the loss of such sterols, especially from their membranes, both external and internal, leads to the death of the host, and further damage is then done. The damage that is done is broadly categorized as ‘degenerative’ and there’s where we came in… studying Huebner’s work with the spontaneously degenerating adenoid tissues in Naval recruits.
Here, apparently, is what was happening, and how this led in turn to AIDS.
The Naval recruits, sharing cramped sleeping and living quarters, were exposed to and inhaled air breathed many times over by all of them. In such an environment any pathogenic microorganism was not received and then exchanged for fresh and non-contaminated air, but was constantly being re-introduced into the lungs to challenge the immune defence processes provided by the body. In time those recruits with the least immune defence, would begin to present with the lung infection and in some cases with degenerating adenoids. And it is at the latter point that we began our study of Huebner with his Naval recruits; acute respiratory disease; degenerating adenoids; PPLO and finally the mycoplasma.
[The same principle appears to be at work today in certain work situations and the incidence of disease. For example, the largest employee groups presenting with chronic fatigue syndrome are schoolteachers, hospital workers and airline flight crews. All are exposed in their work to closed space re-circulated air for lengthy periods of time.]
Huebner followed up his initial work with the help of Drs. Manaker, Todaro and Aaronson and as we shall demonstrate in the article below [The Rockefeller Stable of Talent], all figure significantly in the so-called Special Virus Cancer Program. For example, on page 327 of the Progress Report # 8 of the SVCP Todaro is credited with an article titled “Rapid detection mycoplasma-infected cell cultures” , while on page 282 of the same document, Manaker is reported to have experimented with primates by inoculating 33 chimpanzees with the mashed up tissue of diseased human lymph glands. Finally, on page 303 of the document we find that two of these researchers, Todaro and Aaronson, were busy with Huebner himself working with a mouse sarcoma virus. (You will recall that Kaposi’s sarcoma is an important symptom of AIDS).
Summary
In the late 1940’s and early 1950’s Robert Huebner went to work with the U.S. Naval Medical Research Unit No. 4 to study chronic and recurring respiratory diseases. In the process of doing his research, he realized that the organism which gave rise to one such disease also infected the adenoids of the recruits. Further research showed that the microorganism involved in the adenoidal degeneration, which he had first labeled as a pleural pneumonia-like organism, was actually a bacterial DNA/RNA particle called a mycoplasma. Huebner and his Navy employers quickly realized that the mycoplasma had great potential in a field of research that greatly interested them all: biowar weapons development. Other researchers such as Todaro, Aaronson and Hayflick were recruited to covertly pursue the latter prospect. One of the co-factors of AIDS, the mycoplasma, was well on its way to being put to work to reduce the rate of world population growth.