Ending Plague

by Francis W. Ruscetti

  In July 1961, Luc was sent on a three-year scholarship to the laboratory of Kingsley Sanders, near London, where he would continue to investigate the mechanics of replication by viral RNA. After more than two years of hard work, often including weekends, he was the first to discern the shape of replicating viral RNA, a double helix similar to DNA, but much more rigid. This important discovery was published in the journal Nature in August 1963.1 It was an elegant demonstration of Mother Nature’s ability to recycle and improve upon useful designs. Many have theorized that RNA was used to transmit genetic information for the first life on Earth, or by the first molecules with some of the characteristics of life. When DNA made its appearance on the scene, it replaced RNA in all organisms we know, although every organism would retain RNA, in the form of messenger RNA, as the primary way of assembling proteins within the body.

  In effect, RNA would be tasked by the master, DNA, to do a lot of the chores necessary to keep an organism alive and healthy.

  ***

  From London, England, Montagnier moved to the University of Glasgow in Scotland, where the virologist, Michael Stocker, as well as the visiting Renato Dulbecco, were demonstrating how regular cells were turned into cancer cells by exposure to the polyoma virus. Montagnier demonstrated that both DNA and RNA viruses had the potential to create cancer cells, most notably causing changes in the plasma membrane of the cell, as well as the carbohydrate layer surrounding it.

  One of the great mysteries of the time was how RNA viruses, particularly the retroviruses, were changing their genetic information to function in a DNA organism. Howard Temin had suggested some sort of enzyme was allowing for the transformation of RNA into DNA. This was eventually identified in 1970 as reverse transcriptase. Credit for this discovery was shared by Howard Temin, Satoshi Mizutani, and David Baltimore. This discovery led many to believe reverse transcriptase would be a good tool for identifying RNA viruses in leukemia and cancer in humans.

  In the mid-1970s, Montagnier’s research was on finding human retroviruses by the presence of reverse transcriptase when an unexpected discovery made this work much easier. Frank Ruscetti, working with Dennis Morgan in the Gallo lab, had discovered a growth factor for lymphocytes in cell culture, which would eventually be called Interleukin 2 (IL-2). This made Montagnier’s cell cultures more durable, and made detection of retroviruses easier.

  The search for the first disease-causing human retroviruses, HTLV-1 (human T-cell leukemia virus), was won by Frank Ruscetti, working with Bernie Poiesz in the Gallo lab in 1979.

  Only a few short years later, Luc Montagnier and his team changed the history of the world with their discovery of HIV. Montagnier has often acknowledged the importance of Frank’s Interleukin 2 in his isolation of HIV. In collaborating with Paris physicians, Montagnier received a biopsy sample of a swollen cervical lymph node of a young gay man who had recently traveled to the United States. Lymphadenopathy was already known as a precursor of potential serious illness, including cancer. In this case, the lymphadenopathy was a precursor of AIDS.

  As Montagnier recounted for the biographical section of his Nobel Prize speech in 2008:

  The lymph node biopsy arrived on January 3, 1983, a date which I remember well because it was also the first day of the virology course at the Institute Pasteur, which I had to introduce. I could only dissect the small hard piece at the end of the day. I disassociated the lymphocytes with a Dounce glass homogenizer and started their stimulation in culture with a bacterial mitogen, Protein A, known as the activator of B and T lymphocytes, since I did not know which fraction of the lymphocytes could produce the putative virus.

  Three days later, I added the T-cell growth factor I had obtained from a colleague working in the laboratory of Jean Dausset. The T-cells grew well. As previously established, it was decided with my associates, Francoise Barre-Sinoussi and Jean-Claude Cermann, to measure the reverse transcriptase activity in the culture medium every three days. On day 15, Francoise showed me a hint of positivity (incorporation of radioactive thymidine in polymeric DNA), which was confirmed the following week.

  We had evidence of a retrovirus, but this was just the beginning of a series of questions:

  Was it close to HTLV or not?

  Was it a passenger virus or, on the contrary, the real cause of the disease?

  In order to answer these basic questions, we had to characterize the virus biochemically and immunologically, and to do that, we needed to propagate it in sufficient amounts. Fortunately, the virus could be easily propagated on activated T lymphocytes from adult blood donors. No cytopathic effect was observed with this first isolate. But unlike HTLV infected cultures, no transformed immortalized lines could emerge from these cultures, which always died after 3-4 weeks, as do normal lymphocytes.

  By contrast, subsequent isolates I made from cultures of lymphocytes of sick patients with AIDS were cytopathic for T lymphocytes, and we discovered later, could be cultivated in larger amount in tumor cell lines derived from leukemia.

  Shortly after the virus isolation, my co-workers and I were able to show that it was not immunologically related to HTLV, and in electron microscopy, it was very different from HTLV viral particles. In fact, as soon as June 1983, I noticed the quasi-identity of our virus with the published electron microscopy pictures of the Visna virus in sheep, the infectious anemia virus in horses, and the bovine lymphotropic virus: it was a retrolentivirus, a sub-family of viruses causing long-lasting disease in animals without immune-deficiency.

  This indicated clearly that we were dealing with a virus very different from HTLV, and my task was to organize a team of researchers to accumulate evidence that this new virus was indeed the cause of AIDS.2

  The Nobel Prize was a deserved crowning achievement for Luc Montagnier, a scientist who had first isolated and characterized the virus in young men with the disease.

  However, there had been some bumps in the road, and it mostly involved the Americans. Around 1973, Montagnier met Robert Gallo, when they shared a room at a science conference held at an overbooked hotel.3 Montagnier gives an abbreviated account of his dispute with Gallo and its subsequent resolution in his book, Virus, published in the United States in 2000:

  The NIH [National Institutes of Health] had taken out patents for HTLV-3 which were accepted by U.S, authorities, while the patent for LAV [Montagnier’s original name for the virus was Lymphadenopathy Associated Virus], although submitted much earlier (in December 1983), had not been granted. A long legal battle ensued between the American and French teams, not to come to an end until March 1987, when a historic agreement was signed by the directors of the NIH and the Pasteur Institute and ratified by Ronald Reagan and Jacques Chirac. The two patents would become the joint property of the two institutions, which would share the royalties.4

  I have to add that this is probably the first and last time in history that credit for a scientific discovery had to be approved by the leaders of two different countries. But such was the national pride on the line for each country as to who had discovered HIV. In an interview for this book, Montagnier mentioned how our previous book, Plague of Corruption, had given him some further insight into Gallo’s character and professional life, including his vindictiveness toward Frank Ruscetti, who was getting credit for Interleukin 2, as well as the discovery of HTLV-1.

  As Montagnier recalled his own interactions with Gallo:

  In June of 1983, Gallo and I were friends. A heated debate ensued at a Paris restaurant. I told him that the virus I had isolated was close to the lentivirus of animals. Gallo was not convinced. He insisted that my isolated virus must be from the HTLV-1 family. Despite the efforts of our mutual friend, Guy de The, we could not agree.5

  Montagnier is careful not to ascribe any malicious intent to Gallo. However, many other scientists over the years have repeatedly questioned Gallo’s purported usurpation of the discoveries of other researchers as his own.

  One of the most admirable traits of Montagnier is how he r
emains a true scientist, knowing for certain only what the data tells him, and yet remaining free to theorize where the truth might be found. A question we discussed at length in our previous book, Plague of Corruption, is how HIV jumped into humans. The reigning theory is HIV came from chimpanzees, but how did it jump into humans? Montagnier does not share this view, believing HIV has been in humans for a long time, before it was “discovered.” But unlike many supposed scientists, Montagnier does not stop the conversation, even when it veers into dangerous territory. I was endlessly pondering John Coffin’s statement of July 22, 2009, when Frank heard him say, “Do you mean all those sequences we saw in the 1980s were real?”

  Two theories exist, the first being a natural transmission from either humans eating an infected chimpanzee (known in Africa as “bush meat”) or being bitten by one, the so-called “cut hunter” theory. However, we argued the more likely explanation involved the sacrifice of more than five hundred chimpanzees in the late 1950s in the development of an African polio shot given to more than a million residents of the continent. This hypothesis was covered extensively in the voluminous book, The River: A Journey to the Source of HIV and AIDS, by Edward Hooper, and published in 1999. As Montagnier writes in his book on this question:

  The origin of HIV-1 is even more mysterious. One is tempted to look for an animal source, as with HIV-2, some primate infected with the virus but not sick. For a long time this approach produced no results whatsoever: none of the viruses isolated in monkeys tested in Africa were close to HIV-1. The situation changed in the early 1990s, when one virus and then a second were isolated in chimpanzees.6

  It starts to become clear to me why our investigation into the fourth known human Retrovirus family, XMRV, was so threatening to the establishment.

  The question as to the origin of AIDS almost became a crisis with the publication of Hooper’s book, claiming it was released into the human population through the use of chimpanzee tissue in African polio experiments. However, the “bush meat” theory or the “cut hunter” scenario appeared equally plausible. And besides, the scientific establishment wouldn’t be expected to point the finger of blame at themselves. The question and the controversy around the origin of HIV were mostly forgotten.

  With XMRV, a mouse virus which had somehow jumped into human beings, no plausible explanation other than the use of mouse tissue in medical research for vaccines and other products was possible.

  People had not been eating “mice burgers.”

  And unlike the thrilling action adventure scenes of chimpanzee and human conflict depicted by writers like David Quammen in his book The Chimp and the River: How AIDS Emerged from an African Forest, there had been no heroic battle to the death between a jungle hunter and a wild mouse.

  And as far as variants of XMRV, well, the same thing happened in HIV. I will be the first to admit I don’t know the answers. But when the very questions are banished from the public arena, what other conclusion can be drawn than at the very least, some are very terrified to find out the answers? Montagnier detailed the continuing mysteries of HIV:

  Today, nine subtypes of the major group HIV-1 plus the new subgroup HIV-O have been identified, but the list is far from complete. It is therefore possible the virus existed in an endemic state (that is, at a low level) on several continents before developing into an epidemic.

  If we grant that the virus had been present in humans for a long time, in Africa and probably elsewhere, the question then arises as to why the epidemic is so recent. Why, in just a few years, has the same virus gone from being a sporadic infection to an explosive epidemic?7

  Montagnier doesn’t claim to know the answer to the questions he’s posing, any more than I do. And yet, one is warned against venturing into such dangerous waters. With age comes skepticism, and although you might not know the truth, you get a pretty good sense of when people are lying about claims in your area of research. It wasn’t surprising when Montagnier and I came to similar conclusions about the origins of the SARS-CoV2 virus responsible for the COVID-19 crisis. This is from a French newspaper in April 2020:

  Luc Montagnier, who won the Nobel Prize in 2008 for his work on HIV … said, “We have arrived at the conclusion that this virus was created.” He accused “molecular biologists” of having inserted DNA sequences from HIV into a coronavirus, “probably” as part of their work to find a vaccine against AIDS.

  He said it was not clear how the virus had been able to escape the laboratory, and condemned scientists for doing “the work of a sorcerer’s apprentice.”

  Professor Montagnier has said that he is not the first to suggest the connection, and added that “a group of renowned Indian researchers” had also tried to publish a study showing that the new coronavirus includes HIV DNA, but were forced to retract their claims and had been “smothered.”8

  As a molecular biologist, I appreciate that in order to study retroviruses one must be able to grow them. My entire career in the lab has been focused on developing technologies to produce large quantities of retroviruses for study.

  Those technologies are immortalized cell lines.

  I had worked in the 1990s with the Vero monkey kidney cell line, culturing Ebola viruses.

  Viruses don’t “escape” laboratories.

  They are shipped around the world in those cell lines and walk out in the infected lab workers.

  I think one of the signs of a truly great mind is understanding that even though you may have a deep understanding of your own subject matter, one is continually interested in learning new things. Even though Montagnier is known as one of the world’s foremost retroviral hunters, he is unsatisfied with the lingering questions which remain, such as why cells die prior to the infection becoming severe, a condition known as apoptosis. At the end of his biographical section for the Nobel Prize, Montagnier states the challenge in the following way:

  We have spent a lot of time trying to find the origin of this massive apoptosis, without finding a completely satisfactory explanation: the most likely is the intensive oxidative stress existing in patients since the beginning of their infection. This is also a finding of which I am very proud: although oxidative stress has been – and still is – completely overlooked by AIDS researchers, it is likely to aggravate the wrong activation of the immune system at the origin of its decline and also it triggers inflammation through the production of cytokines.

  Of course, the next question arises: what are the factors causing oxidative stress; viral proteins, fragments of viral DNA, co-infection with mycoplasmas? Even after 25 years, we still do not know the complete answer. But the phenomena does exist and needs to be treated, while most AIDS clinicians do not care about it at all! The treatment by combined retroviral therapy has, without doubt, changed the prognosis of this lethal disease, from a death sentence to an almost “normal” life. However, the virus is still there, ready to multiply when the treatment is interrupted, and not all HIV infected patients in the developing world have access to it. And the epidemic still kills 2-3 million people a year. It is thus absolutely necessary to resolve these problems.9

  A scientist stays on a problem until all of the questions are answered. There have been great strides made in HIV/AIDS. It isn’t enough. Just as we have not answered critical questions about chronic fatigue syndrome (ME/CFS), autism, or even cancer.

  We must do more to answer these questions.

  ***

  When one enters a controversy, you discover your true friends and enemies.

  Yes, it was possible to believe in those heady days of 2009 and through much of 2010 that the public health authorities would take the appropriate action on behalf of the chronic fatigue syndrome community which had been neglected for more than two decades.

  The dangerous question I asked was, “If we are growing viruses in animal tissue, how do we know that other viruses in the animal tissue aren’t coming back in the vaccine, or pharmaceutical product, which is being developed?”

  However, wh
ile much of the scientific establishment and the mainstream media joined the witch hunt against me, Luc Montagnier has always been a stalwart champion of my right to ask questions and go wherever the data leads. He was brave enough to endorse our book, Plague of Corruption, and has consistently supported my research.

  Montagnier is careful not to say he always agrees with my conclusions, but that the scientific process must be followed, and all objections discussed in an open manner, without the public shaming of me that has taken place. However, he acknowledges the risks I have pointed out. This is from my coauthor’s interview with Dr. Montagnier:

  Kent: Is it accurate to say you don’t have much of an opinion, either positive or negative, about Judy’s XMRV work?

  Dr. Montagnier: Yes. But I have to say there is no reason to doubt Judy Mikovits. She had problems because she mentioned vaccines. I have my own concerns about vaccines. She was concerned that some viral material may have been contained in vaccines. I have been concerned about bacteria from plants contaminating the vaccines. They have been found in human cells.

  Kent: Do you consider it a theoretical possibility that since we grow human viruses in animal tissues, that when we create a product from this mixing of human and animal tissue, that we may have unsuspected animal viruses coming back from that product?

  Dr. Montagnier: Yes, it is quite possible. We are so paralyzed.

  Kent: Should science be actively investigating whether there are animal viruses coming back in these products which are developed for use by humans?

  Dr. Montagnier: Quite assuredly, yes. Especially if we use live attenuated vaccines, like in the case of MMR (measles-mumps-rubella.) It is quite possible there could be transmission. We could also have contamination by bacteria. We are changing our environment.10