AIDS a document to read absolutely

[Janic]

a particularly important interview on the history of AIDS (part one)
ELENI PAPADOPOULOS-ELEOPULOS
Is HIV the cause of AIDS?
Interview by Christine Johnson


ELENI PAPADOPOULOS-ELEOPULOS
is a biophysicist and leads an HIV / AIDS research group in Perth * (Australia). For more than 10 years, his group has published a number of scientific articles challenging the HIV / AIDS hypothesis. Here she is questioned about this work and especially about the position of her team vis-à-vis AIDS itself.
*Department of Medical Physics, Royal Perth Hospital, Perth, Western Australia.
Voice int +61 9 2243221; Fax int + 61 9 2243511
CHRISTINE JOHNSON:
Member of MENSA and science journalist. Lives in Los Angeles (USA). Scientific Information Coordinator at HEAL / Los Angeles, Scientific Advisor to C0NTINUUM and Co-Editor of Reappraising AIDS. Christine is a consultant for the Mark Griffiths Association. Her extensive documentary experience in the legal and medical field has set her in pursuit of the truth about AIDS. She specializes in making cryptic information from scientific journals accessible to the general public. For the past four years she has been interested in the PERTH group and the articles she wrote to criticize HIV testing have been published around the world.
Christine Johnson: Thanks, Eleni. to accept this interview.
Eleni P.Eleopulos: Please. With pleasure.
CJ: Is HIV the cause of AIDS?
EPE: It's not proven.
CJ: How is that?
EPE: For several reasons, but first of all because there is no proof that HIV exists.
CJ: It's quite a startling statement, and rather hard to believe!
DE: Maybe, but that's the conclusion of my research nonetheless.
CJ: Yet Montagnier and Gallo already isolated HIV in the early 80s.
EPE: No. The articles that these two researchers published at the time in the journal Science do not provide proof that they isolated a virus from an AIDS patient.
CJ: Yet they claim that it is.
EPE: Our interpretation of their data is different.
CJ: Maybe you could explain to us what made you take such a radical stand.
EPE: To begin with, I think that the easiest would be to ask the question: "What is a virus?". The answer is quite simple: A virus is a microscopic particle capable of reproducing itself inside a cell.
CJ: Don't bacteria do the same?
EPE: Yes, but there is a very important difference. Bacteria are not dependent on the cell to reproduce - we say to replicate -. Viruses, for their part, necessarily need the cell. The bacteria, you see, just like the cell, carries its reproductive material within itself. It only borrows its food and energy from the outside. The virus, on the other hand, being nothing more than a bundle of proteins tied around a piece of DNA or RNA, does not include any machinery suitable for ensuring its replication.
CJ: So if you consider that the cell is a factory, the virus is just a matrix in search of a factory.
EPE: The comparison could not be fairer.
CJ: And how does a virus replicate?
EPE: He must first enter the cell. To do this, its protective envelope fuses with the cell membrane and it passes inside. Once there, it takes advantage of the mechanisms of its host to break up and synthesize the spare parts necessary for the constitution of new viruses. Finally, when everything is ready, these new viruses leave the cell.
CJ: How do they get out of it?
EPE: Either by destroying the cell, or in a more orderly manner by budding through the cell membrane, as is the case with retroviruses. The exception is HIV: although a retrovirus, it is said to destroy the cell.
CJ: Exactly, what about this particle called HIV? According to you, it is not a virus?
EPE: To prove that a virus exists, you need to do 3 things:
1) - First, in a cell culture, find a particle that looks like, that's the least of all things, a virus.
2) - then design a process that allows to isolate this particle, to separate it into pieces and to analyze with precision the elements which compose it.
3) - Finally, see if the particle is able to make exact copies of itself. In other words to replicate.
CJ: Can we, looking through a microscope say, "This is a virus"?
EPE: No, we can't. This is the whole problem with viruses. Not all particles that look like them are viruses. They are only so if it is proven that they can actually make copies of themselves. No replication, no virus. Sorry, but that's how it is. And this is a very important point that no one, especially no virologist, can afford to ignore.
CJ: It seems obvious. I don't see how you could get sick from catching a germ that doesn't multiply!
EPE: Absolutely.
CJ: So what is AIDS research wrong with?
EPE: It's less about knowing what she's wrong about than knowing what she failed to look for. For some reason, the good old method of isolating retroviruses developed in animal research has not been followed.
CJ: Before going any further, could you explain to us what retroviruses are?
EPE: Yes, it would be better. As you probably know, HIV is said to be a retrovirus. Retroviruses are incredibly tiny, almost spherical particles that ...
CJ: What size?
EPE: 100 nanometers in diameter.
CJ: That is to say?
EPE: One ten thousandth of a millimeter. On a pinhead, you could have millions.
CJ: How, practically, do you go about seeing something so small?
EPE: You need an electron microscope. It is thanks to him that we know the size and shape of retroviruses, that we know that they are almost round, that they have an envelope covered with protuberances, like buttons and a heart made of RNA and a few protein.
CJ: If it exists, then HIV is an RNA virus?
EPE: That's it. And there is another important point: retroviruses do not directly use their RNA template to multiply. According to retrovirologists, what sets them apart from all other viruses is that they start by copying their RNA into DNA. This DNA then goes into the nucleus of the cell where it merges into the cellular DNA. This piece of integrated DNA is called pro-virus, and it can sit dormant for years until something comes to reactivate it.
CJ: What happens then?
EPE: The proviral DNA is copied back to RNA and it is the latter, not the original RNA, that governs the production of the proteins needed to make new viruses.
CJ: Why are they called retroviruses?
EPE: Because for a long time biologists believed that in living cells the process of protein production made sense, from DNA to RNA. Since retroviruses do the opposite, at least in the first stage, they have been seen to work against the grain, in a retrograde direction.
CJ: Understood.
EPE: Something else. One of the proteins that make up the virus is an enzyme that catalyzes the process of transcription. It was therefore called: reverse transcriptase.
CJ: So what?
EPE: So it is for this set of reasons that we say: retrovirus.
CJ: You mentioned a decades-old viral isolation method. When does this go back?
EPE: You can look at the period from the 40s to the late 70s. You see, retroviruses were among the first viruses to be discovered. Peyton Rous of the Rockefeller Center in New York discovered them in 1911 while experimenting with malignant chicken muscle tumors. But to really see them, it was not until the invention of the electron microscope (EM) and the ultra-fast centrifuge (CUR). It was then that things started to organize.
CJ: What things?
EPE: The method of identification and purification of retro-viral particles
CJ: That is to say the insulation; it's the same thing, isn't it?
EPE: Yes. To purify particles, whatever they are, the researcher must develop a method that allows them to be separated from everything else.
CJ: How did the electron microscope and the high-speed centrifuge make the purification of retroviruses possible?
EPE: The ME allows you to see tiny particles. CUR plays an extremely important role. It should be noted that the retroviral particles have the particularity of floating at a very precise density and this is used to separate them from other culture products. The process is called "Density Gradient Centrifugation".
CJ: It seems very complicated!
EPE: The technique is complicated but the concept is quite simple. You prepare a solution of sucrose - it is ordinary sugar - but you make the solution so that the solution is weak on the surface and more and more dense towards the bottom of the test tube. In the meantime, you have grown cells that you believe contain retroviruses. If there is, they will be dropped into the culture medium. You decant this liquid and very delicately you pour a drop of it into your sucrose test tube, the density of which is variable. Then you centrifuge at very high speed. This creates enormous gravity and the particles at the top of the test tube will be dragged down the solution until they reach a point where their density is the same as that of the sucrose at that point. They are in equilibrium with the environment and all will eventually come to a standstill at their own level. In the jargon of biologists we say that they "bandage" because they are stacked in bands in the test tube. Each band can be selectively extracted and imaged at the ME.
CJ: And do retroviruses band at a particular density?
EPE: Yes, in the sucrose solution they bandage at a characteristic density of 1.16 gm / ml.
CJ: So under the microscope you can see what kind of fish you caught.
EPE: Not only that; it is also the only way to know if you have caught fish or nothing at all.
CJ: That's right ... didn't Montagnier and Gallo do that?
EPE: Your question raises one problem among many. Montagnier and Gallo did use density gradient centrifugation, but for some unknown reason they did not release any photographs of the material harvested at 1.16 gm / ml, ... which they claimed to be - as everyone has claimed to follow them - "pure HIV". This is very intriguing for the good reason that 10 years earlier, in 1973, those who were to become the greatest experts in HIV had discussed at the Institut Pasteur the method of isolating retroviruses. At this meeting it was established that the photograph of the 1.16 density band was absolutely essential.
CJ: But Montagnier and Gallo have yet published photos of viral particles?
EPE: No not. Montagnier and Gallo did publish photos taken at ME of a small number of particles, but they do not provide proof that they are viral. They call them HIV, but not having followed the method adopted in 1973 they do not prove that HIV exists.
CJ: And what is this method?
EPE: All the steps that I have already described to you. This is the only method that is scientific: to cultivate cells, find a particle, isolate it, tear it to pieces, find what it contains and then prove that it is capable of multiplying without varying in nature in a healthy cell medium.
CJ: So, long before we talked about AIDS, we had a method to prove the existence of retroviruses, but neither Montagnier nor Gallo followed it when it came to HIV?
EPE: They used some techniques that the method requires but they skipped steps. In particular that which consists in demonstrating the nature of the particles found in the 1.16 gr / ml band, a band specific for retroviruses.
CJ: What about their photos?
EPE: Until March of this year (1997) nobody ever published the photo of a density gradient. Photos of Montagnier, Gallo and all the others are from unpurified cell cultures. Not the gradient.
CJ: ... And this photo is necessary if we want to prove that we have isolated a virus.
EPE: Absolutely.
CJ: Does tape 1.16 contain anything other than retroviral material?
EPE: Yes precisely. That's why you need a photo. You have to be able to visually see everything there is in this band. Since long before the AIDS era, it was known that retroviral particles are far from the only ones to sneak up to this density gradient. Tiny pieces of cells, structures inside the cell, or just cellular waste can bind to 1.16 gm / ml. If among them there are nucleic acids, they can take the appearance of retroviruses.
CJ: What are nucleic acids?
EPE: This is called DNA and RNA
CJ: Yet we should be able to avoid contamination by cellular debris since retroviruses do not burst the cell when they leave it.
EPE: Actually, yes and no. Back in the days when they were working on animals, retrovirologists never failed to recommend that cultures be handled with extreme care and that cells be nourished with care to prevent them from breaking down. But when it comes to HIV, avoiding infection is not that simple since we are told that it kills cells. No one can therefore claim to recover only virus in the liquid in which the cultures bathe, nor at 1.16 gm / ml. Another source of confusion is that in many experiments with HIV it is the experimenter himself who is deliberately crushing the cells. Knowing all this, it is even more incomprehensible that no researcher produced the photo of a density gradient. It is a crucial step that has been skipped.
CJ: Could it be because electron microscopy is too specialized and too expensive?
EPE: Maybe in the past, but not anymore. ME has been used daily in hospitals for at least 20 years to diagnose all kinds of diseases. In addition, there is no shortage of pictures of HIV cultures at ME. The point is, until '' until this year, for some reason, none had been caught in the density gradient.
CJ: Heard. So let's talk about these famous photos taken this year. What do we see there?
EPE: Two different groups just posted photos of the density gradient. One is Franco-German, the other American, from the National Cancer Institute. The photos of the Franco-Germans are taken in the band 1.16 gm / ml. On the other hand, it is impossible to know in which band the Americans took their photos. So suppose it is also in the correct band. The first thing that can be said is that these pictures reveal a huge percentage of cellular material. The authors describe this material as "non-viral" and call it "pseudo virus" or "micro-vesicles".
CJ: What are micro-vesicles?
EPE: These are encapsulated cell fragments.
CJ: Is there any virus in these photos?
EPE: There are a few particles that the authors say are retroviral. In fact, they say it's HIV. But they do not provide proof.
CJ: Are there a lot of this HIV?
EPE: Very little. The tape should contain billions of them and in an EM photo it should cover the entire field.
CJ: So the material does not contain very few HIV particles in a particularly impure environment?
EPE: That's it.
CJ: What is the explanation of the experts?
EPE: They say the cellular material settles at the same level as HIV.
CJ: But tell me, do these particles that claim to be HIV look like a retrovirus?
EPE: They only have a vague appearance. It is true that they are closer to the retrovirus than the rest of the material but would they be perfectly identical that this would not be enough to say that it is the retrovirus. Even Gallo admits the existence, in the band 1.16 gm / ml, of particles which have the appearances and the biochemical properties of retroviruses but which however are not because they lack the capacity to replicate.
CJ: Okay, but other than that, what makes these particles different from real retroviruses?
EPE: Gallo and others, like Hans Gelderblom who has done most of the studies on HIV photos, admit that retroviruses are nearly spherical in shape, 100 to 120 nanometers in diameter, and covered in vesicles. The so-called HIV particles described by the two groups are not spherical, none are smaller than 120 nm (many are more than double), and neither have vesicles.
CJ: Is size that important? In biology, many things vary in size. Men twice the size of others are nonetheless men.
EPE: What is true for men is not true for retroviruses. In the first place, retroviruses do not need to grow. They are born adults. The comparison must therefore be made between adult men. And do you know a lot of men of 4 meters? The tallest ever recorded was 2m95. But it's not just the size that's in question here.
CJ: And what else?
EPE: Assuming that the two research groups went to take their particles at the density that corresponds to retroviruses, their particles should have the same density, or 1.16 gm / ml. However in the photos, if you measure the so-called HIV and that to make things easier you consider the spherical particles, you see that the Franco-German particles are 1,14 times wider and the American ones 1,96 times wider than d. 'authentic retroviruses If you cubed the diameters to get the volumes, that gives you particles one and a half and seven and a half times larger than retroviruses. The American "HIV" is obese: it is 5 times the Franco-German!
CJ: What should we conclude from this?
EPE: That the Franco-German particles contain one and a half times and the American ones seven and a half times more matter than real retroviruses.
CJ: And why?
EPE: Because density is the mass / volume ratio. For the same density, if the volume increases, the mass must increase by the same value.
CJ: Sure, but where are you going with this?
EPE: To this: Every true retrovirus contains a very specific amount of protein and RNA. No more no less. In this case, we have particles that are made of much more material than genuine retroviruses. This means that if these particles of different sizes are really HIV, then HIV is not a retrovirus. Another explanation is that the photos are not from tape 1.16. If this is the case, all that remains is to change the definition of retroviruses and stop considering that band 1.16 is that of retroviruses. If we come to this, all the previous research falls apart since until now it is in this band that all the researchers have gone to draw their "pure" HIV. As a result, the RNA and proteins of this band could no longer be used for the manufacture of diagnostic tests.
CJ: You mentioned that these particles did not have vesicles. Is it very important?
EPE: All specialists agree that the vesicles that cover HIV are absolutely necessary for it to adhere to the cell. It is the first step in the infection process. No adhesion, no infection. Their protein, GP 120, acts like a grapple. If HIV does not have this mechanism of collision, how does it reproduce?
CJ: You mean he can't hang on to the cell he has to enter to be able to reproduce?
EPE: Exactly. If it does not replicate, HIV cannot be infectious.
CJ: This is indeed a crucial question. What do specialists say?
EPE: They avoid answering. And this vesicle problem is not new. The German team mentioned above first drew attention to this in the late 80s and again in 1992. As soon as an HIV particle leaves the cell, all of its vesicles fall out! This simple fact has multiple implications. Take hemophiliacs for example. 3/4 are seropositive to have supposedly been infected with contaminated Factor VIII. This Factor VIII is the substance they need to clot. It is extracted from plasma, ie blood without cells. If there is HIV in Factor VIII, it has already left the cells and is floating freely in the plasma. However, if the extracellular HIV does not have vesicles, it does not have the means to enter healthy hemophiliac cells to infect them.
CJ: So how do you explain the seropositivity and AIDS of hemophiliacs?
EPE: My colleagues and I have published several articles on this topic. We give several possible explanations. In a special issue of the journal Genetica from 1995 which deals with the HIV / AIDS controversy we even do a detailed analysis of hemophilia.
CJ: I admit that I find it difficult to accept that hemophiliacs were not infected with contaminated clotting factor. And I bet the same is true for affected hemophiliacs.
EPE: Unfortunately, it's the truth. But maybe you'll be persuaded by a quick little explanation. Tell me, if an HIV positive person cuts and bleeds, how long does their blood remain infectious? Outside of his body?
CJ: From what I've read, a few hours at most.
EPE: And why?
CJ: Because HIV dries up and dies. At least that's what the World Center for Infectious Disease Surveillance (CDC) says.
EPE: Indeed. Now let me ask you a question: How is Factor VIII prepared?
CJ: From donated blood.
EPE: Right. Have you ever seen a vial of Factor VIII?
CJ: No.
EPE: Well I will describe it to you: It comes as a dry, flaky yellowish powder and by the time it is used it already has at least 2 months of storage. Do you see the problem?
CJ: I see. If it is desiccated and several months old. The HIV it contains is long dead.
EPE: Obviously. So how does Factor VIII cause HIV infection and AIDS in hemophiliacs?
CJ: I don't know, but I'm starting to understand why you are frowned upon in some circles! We might be better off not getting caught up in a discussion about hemophilia. I have another question. This is about the contents of the 1.16gm / ml band. : How come, in your opinion, most HIV experts mistook it for pure HIV. At least until recently?
EPE: I think it is premature to believe that these photos from March 97 changed anything in general opinion. The 1.16 gm / ml band of the density gradient is still taken for pure HIV.
CJ: Oh well ... And what does your group think of these photos?
EPE: They provide proof that the photographed material is impure, that it does not contain particles of the retroviral type, much less retroviral particles and certainly not a retrovirus as specific as HIV. This confirms our research and the position we took from the start that there is no evidence for the isolation of a retrovirus from patients or those at risk of AIDS.
CJ: OK Let's put those photos aside. What other evidence has been produced that HIV exists?
EPE: They were already pictures of particles, taken at the ME, but coming from cultures. Not the density gradient. What we can say is that these cultures contain a wide variety of particles, some of which may pass for retroviruses. That's all. No additional data has been collected on these particles. No purification, no analysis and no proof of replication. Several researchers specializing in this field, such as Hans Gelderblom and his colleagues at the Koch Institute in Berlin, have found not one type, but an incredible profusion of particles of different types. This raises many questions:
- If one of these particles is really the retrovirus that experts call HIV, then what are all the others?
- Which of these particles is 1.16 mg / ml?
- Assuming that the HIV particle causes AIDS, why wouldn't another, or others, do the same?
- Why shouldn't all particles cause AIDS?
- Or, why wouldn't it be AIDS, or just crops, that produce HIV?
Not to mention the fact that when it comes to the nature of HIV itself, no one agrees. Among the three known subfamilies of retroviruses, HIV has been classified by different groups of researchers in two of them and, what is more, classified under three different species.
CJ: Where are we today?
EPE: We still don't know anything about these particles. None in particular has proven to be a retrovirus. None whose RNA and proteins could be used to test for infection or experiment. And without this precondition, how to understand what is happening, how to know if it is really a virus which causes AIDS?
CJ: Good. Now suppose we have a photo of a density gradient, that it contains nothing but thousands of particles, and that they do have vesicles, the size and shape required to apply as a retrovirus. . What should be the next step?
EPE: The next step is to disaggregate the particles, analyze their RNA and proteins, prove that one of these proteins is an enzyme capable of changing RNA into DNA, and finally prove that particles are exactly identical in shape and form. to the constituents are produced in a culture of virgin cells, from a sample taken in the density gradient. 1.16.
CJ: Was this experiment done?
EPE: No. But no doubt I can explain things to you more clearly by telling you about what was done in 1984 by Gallo.
CJ: 1984? Isn't that going back a bit far?
EJE: No, because that was when the research on HIV isolation was the most valuable. It was then that we built up everything we believe and teach today about HIV.
CJ: Everything, really?
EPE: Absolutely. Down to the smallest detail. Because what is decisive is to have isolated the particle. By the fact of having isolated it, you have proved its existence; everything else follows. For example, with its proteins you test for antibodies, with its RNA you test for infection in children who have not yet made antibodies, you measure the famous "viral load" as we do now, etc. . . But the question is whether the initial experiences were sufficient.
CJ: Sufficient?
EPE: Good enough to claim that a new virus called HIV exists and is the cause of AIDS.
CJ: Good. So tell us about Gallo's experiences. But in fact, why was he interested in AIDS?
EPE: In 1984 Gallo had already spent more than ten years on retroviruses and cancer. He was part of this army of virologists mobilized by President Nixon for his crusade against Cancer. In the mid-70s, Gallo believed he had discovered the first human retrovirus. It was in patients with leukemia. He claimed that his work proved the existence of a retrovirus which he called HL23V. At the time, as he would do later with HIV, Gallo used the reaction of antibodies to detect which proteins belonged to the virus among the proteins present in the culture. Soon after, the same antibodies were found in many people who did not have leukemia. After a few years it was found that these same antibodies appear naturally and are directed against many substances which have nothing to do with retroviruses. It was then realized that the HL23V was a huge blunder. There was no HL23V. Gallo's work became a thorn in the side of science and the HL23V was never discussed again. Despite this, what is interesting for us in this story is that the evidence that Gallo gave for the existence of HL23V is the same that it emerged for HIV. In fact, they were even stronger.
CJ: Stronger? In what sense?
EPE: Well, unlike the case of HIV, Gallo found reverse transcriptase in fresh tissue without having to do any cultures. In addition, he published pictures of the material found at the density gradient 1.16 gm / ml.
CJ: And despite that, it turned out to be a false trail.
EPE: Gallo did not insist on his HL23V. But in 1980, he announced the discovery of another virus, still in relation to leukemia. He named it HTLV-1 and claimed it was the cause of a particularly rare disease, ATL (Adult T4 Leukemia). In fact, there are some very remarkable parallels and paradoxes between this HTLV and HIV.
CJ: What are they?
EPE: These two viruses are believed to infect the same type of cells (T4) and spread in the same way. However, unlike HIV, HTLV-1 remained at the discovery stage. Its incidence is too low and affects only a few people in Africa and southern Japan. Less than 1% of people who test positive for HTLV-1 develop this leukemia, and the latency period can exceed 40 years. So, next to AIDS ... but I'm sad. What I wanted to explain was how Gallo used HTLV-1 to conceive HIV. At the onset of AIDS, patients suffered from cancer, Kaposi's sarcoma, and T4 deficiency, which had only just been learned to count because the appropriate technology was developed at precisely that time.
CJ: So it was assumed that HIV killed T4s.
EPE: Not right away. HIV had not yet entered the scene. It was only assumed that something was killing the T4s. So Gallo thought of the HTLV-1. But that was not easy. First because the leukemia caused by HTLV-1 is a proliferation of T4 and not a deficiency, second because, in southern Japan, despite the high prevalence of anti-HTLV-1 antibodies, there is no had no AIDS. Despite everything, because of the association cancer / T4 dysfunction in many homosexual AIDS patients, Gallo persisted in demonstrating that a virus could explain everything.
CJ: What happened next?
EPE: With his group, he embarked on a whole series of experiments, the results of which were published by the journal Science, in 4 consecutive articles, in the issue of May 84. It was a year after the French published on the same subject, in Science too. Gallo's group had initially grown lymphocytes from AIDS patients, but apparently no culture produced enough reverse transcriptase to convince researchers that they had a retrovirus. Gallo and Mikulas Popovic, a Czech who worked for him at the time, came up with the idea of ​​mixing the fluids from the cultures of 10 AIDS patients and pouring this mixture onto leukemia cells. The cells in question had been taken years earlier from a patient with ATL. The preparation then produced enough reverse transcriptase to convince Gallo and Popovic that they finally had a retrovirus.
CJ: You mean that a retrovirus that did not grow in cultures of individual AIDS patients began to grow when the specimens were mixed and then grown together?
EPE: Yes.
CJ: Isn't that a little weird? If a germ is present in a specimen, it should grow anyway, as long as the cultures are done the same.
EPE: This is what we are entitled to expect.
CJ: And if you mix all the specimens, how will you know which virus was originally in? The virus may have been present in only one patient. Gallo has he never been questioned about it?
EPE: It was. On a TV show in 1993. He said he didn't care whether the virus came from an individual or a pool of patients.
CJ: Didn't you say that the cells used for the culture were from ATL Leukemia?
EPE: Yes.
CJ: So the culture must have contained a lot of T4?
EPE: Indeed.

[Janic]

second part
CJ: How does a virus like HIV grow on T4 cells that it is supposed to kill?
EPE: This is yet another paradox of HIV / AIDS. HIV is believed to kill T4 cells and cause immunosuppression (that's what AIDS stands for). However, the cells that Popovic used, as well as their H9 clone, are immortal and remain so even when they are infected with HIV. In other words, far from dying because of HIV, or rather what we take for HIV, cells allow it to grow indefinitely. This is how it is cultivated to provide the raw material for tests made from its proteins and RNA. Its H9 clone is widely used in research.
CJ: Good. But what did Gallo actually do to prove that he had isolated a new retrovirus from AIDS patients?
EPE: If you read his first article, what he called "isolation" consists of photos of rare particles, in culture and not in the density gradient, plus the discovery of reverse transcriptase, and the fact that some antibodies from hemophiliacs and rabbits reacted with certain proteins in the culture.
CJ: Is that all that was reported in lieu of isolation?
EPE: Yes.
CJ: Is it really insulation?
EPE: No. To isolate means "to separate from everything else". It is not just detecting a few phenomena. The only way to prove the existence of an infectious agent is to isolate it. That is the whole point of this debate.
CJ: Yes but, isolated or not, how do you respond to Gallo when he says that his cultures have grown a retrovirus?
EPE: Allow me to insist: there has never been isolation. Gallo did not isolate a virus. He did not take pictures of the specimen at the density required to have only retroviral particles. He did not take any photographs of the centrifuged material. Just snapshots of cells, a dozen particles scattered around them, but no extraction, no analysis, no proof that these particles can replicate, can produce identical particles. One is entitled to wonder if Gallo had any proof whatsoever. In our opinion, he did not have one. It is essential to remember here that finding particles and reverse transcriptrase does not provide proof that a retrovirus exists.
CJ: Yet you said that retroviruses contain reverse transcriptase.
EPE: They contain it. In fact, reverse transcriptase was discovered in a retrovirus. But beware of the pitfalls! There are two. One is that TI (reverse transcriptase) is not the exclusive domain of retroviruses. The other is in the IT highlighting process. Its demonstration is indirect. We put a little RNA in a culture and we see if the DNA that corresponds to it appears.
CJ: You mean the IT presence is inferred from the culture's ability to do this sleight of hand?
EPE: Yes. It is the reverse transcription process that is demonstrated. Like many enzymes, the test measures what the enzyme is doing, not its presence itself. For TI, the DNA production resulting from the copy of a synthetic RNA probe introduced into the culture is measured. The problem is that IT is not the only one that can do this "sleight of hand" as you say. Ordinary cellular enzymes can do the same. They even do it very well, including on this probe that all researchers introduce into their cultures to prove that there is TI and therefore HIV. The worst part is that when you read the AIDS literature you realize that researchers who claim to have isolated HIV have done nothing but detect IT.
CJ: It's disconcerting!
EPE: And that's not all. According to Harold Vamus, Nobel laureate and director of the National Institute of Health, there is IT in normal cells, just like in bacteria. It is also known that among the chemicals necessary for culture medium, some have the property of causing normal lymphocytes to retrotranscribe. If they are leukemia cells, they do it on their own, without additional chemistry or AIDS cells.
CJ: TI can therefore have multiple origins.
EPE: Yes. And yet another concerning Gallo's experiments. Remember he and Popovic used the H9 cell to demonstrate the existence of their HIV. However, as I pointed out, if you go up the line of H9 you arrive at HUT 78, a cell taken by Gallo from a patient in whom he diagnosed a cancer due to HTLV-1. If this virus exists, it will inevitably end up, with its TI, in the H9 that Gallo used to prove the presence of HIV.
CJ: Certainly it wouldn't occur to anyone to look for a new virus in a cell that already contains it!
EPE: Except that at Gallo it was deliberate: a year earlier he had specified that he was using the H9 line, when he had published the genetic sequence of HTLV-1, in Science.
CJ: So IT cannot be used as proof.
EPE: The IT problem is that of all the evidence, including the photographs exhibited by Gallo. The particles may be viruses just as the TI may come from these retroviruses. But the "it may be" is not proof. You are not building scientific theories from assumed situations.
CJ: Despite everything, Eleni, how can you rule out the particles photographed by Gallo in his cultures. They are so convincing: Even though it deviated from the traditional method of isolation, these particles are a fact and many very serious people see them as a retrovirus.
EPE: I appreciate your insistence, but when it comes to particles you have to take a lot of perspective. Particles that look like retroviruses are almost everywhere. In the 70s it was discovered in leukemia tissue, embryonic tissue, in the majority of the placentas of animals and humans. This is important to note because Gallo's H9 line is a leukemic line and because the Montagnier ME photos are taken in umbilical cord cultures. Let's be careful. See for example the group of retroviruses classified "type C": they are found in mammals, fish, snakes, worms, tapeworms, pheasants, quail, partridge, turkeys, field mice, agouti, insects ... in this group that Gallo and Montagnier have decided to place HIV. Without unanimity because officially HIV borrows many other disguises. See also this study by O'Hara and his Harvard colleagues in 1988. They looked at photos of lymph nodes in people with AIDS and non-AIDS patients with lymphodenopathy. They found "HIV" particles in 90% of patients in BOTH groups. They had to admit that the particles alone did not prove HIV infection.
CJ: Okay, okay. Let us leave this domain of particles. What about those antibodies that react with cells in cultures? It is still a sign of a particular phenomenon. Couldn't that indicate the manifestation of a virus?
EPE: Yes, it could be. But it's always the same thing: we do not prove that proteins are those of a retrovirus, nor that antibodies are the result of a retrovirus, nor that we have isolated a retrovirus on the pretext that we have obtained reactions in a test tube.
CJ: Can you tell us a bit more about that?
EPE: Again, don't let the results of the experiments say more than the scientific method allows. The experiments described by Gallo in his first paper show that in hemophiliacs and in rabbits, antibodies react with H9 cell proteins co-cultivated with AIDS cells.
CJ: It's the data.
EPE: These are the working data. What matters is the interpretation. Gallo decides that the antibodies can give him proof that he has isolated a virus. Why does he choose antibodies? For two reasons. First to remove particles that are not viruses. Gallo knew that there are some which mimic retroviruses, bandage at 1.16 gm / ml, contain TI but do not replicate. Then, because the antibodies, it is in the logic of his hypothesis: the AIDS virus exists, it comes from outside, when it infects a patient it makes him produce antibodies. In one of his publications, Gallo also speaks of the need to have a specific agent such as an antibody or a protein to identify a viral particle.
CJ: So it works both ways: The virus produces antibodies and the antibodies signify the presence of the virus.
EPE: Alas, no. That's the whole problem. Antibodies don't work in reverse. We'll get to that in a minute. Right now the important thing is not to forget the question we are trying to answer. We are trying to find out which proteins are found in retroviruses and which belong to them. For me; there is only one way to find out and it is simple: the proteins of a virus are like our arms, legs, kidneys.
CJ: What does that mean?
EPE: Which means my little bits of anatomy are mine because they are part of Eleni Papadopulos' body. Whether inside or outside. If I have a diseased kidney and the surgeon decides to remove it from me, the first thing he will do before opening my stomach is to make sure that it is me that has been laid on the operating table. It's the same with viruses. Virus proteins are proteins that come from particles identified as viruses. It's that simple. If you want to define the proteins of a retroviral particle, you must first prove that you are dealing with a retroviral particle.
CJ: The antibody is too little specific?
EPE: Of course, but the question is not there. Antibodies have nothing to do here. You prove that proteins come from a virus by first isolating the virus and then dissecting it. You don't prove anything by causing chemical reactions in a soup. Culture is broth. Do antibodies and proteins react? So what? There are a thousand reasons for this.
CJ: Which ones for example?
EPE: Antibodies are multitude. An antibody to one thing can react, and in fact does react, to other things. In immunology these are called cross reactions. It is a natural phenomenon and it creates a lot of problems. An antibody that reacts with proteins in a culture may well have been produced by something that is not even in the culture, that has nothing to do with the culture at all. Broadly speaking, the antibodies are unfaithful. As my colleague Val Turner says, they are "womanizers"! The only way to prove that the reaction you are witnessing is a legitimate mating is to see if it only occurs between the partners you are studying. The reaction must be correlated with the presence of HIV in person. The antibody is specific if it only reacts when HIV is there.
CJ: ... and does not respond when HIV is absent?
EPE: Percentage question. 100% specific means that there is no reaction when HIV is absent. My colleagues and I say that antibodies can no more prove the existence of a virus than you can prove which is the first of the chicken or the egg. This is an essential point in our argument, so I hope that I will manage to make myself understood.
CJ: I'm all ears ....
EPE: Think about what we have done so far: we have a good old method, safe, logical, sensible, to prove the existence of retroviruses. It is based on the very definition of the retrovirus and nothing else = particle with a well-defined size, shape, appearance, constitution, plus the ability to replicate. Suddenly, for some unknown reason, this method is abandoned when it comes to applying it to HIV. Do not ask me why, but it is so! In its place we have a collection of disparate data such as photos outside the density gradient, traces of TI in cultures or the 1.16 band of the gradient ... None of them are proof of the existence of a retrovirus by itself. Gallo himself admits it
CJ: Carry on. I follow you.
EPE: In the process then comes the idea of ​​antibodies. If there is a virus, coming from outside, it must induce antibodies in the people it infects. But we say to ourselves: what if these antibodies were specific? what if they were produced as a reaction to HIV only? what if they only reacted with HIV proteins? OK Suppose this highly unlikely specificity exists and make an even more unlikely assumption.
CJ: Yes, which one?
EPE: That there are only specific antibodies: antibodies to tuberculosis bacillus only react with Koch's bacillus, antibodies to hepatitis B virus only react against HBV etc ... OK We take samples tissue on AIDS patients. We water the culture. Hop! it reacts. So what? What have we proven? People with AIDS are full of germs, we know that. Their microbes, or debris from their microbes, end up in their cells; (that's why the lab technicians who handle these specimens are said to be at risk, isn't it?). On the other hand, we also know that despite their immunosuppression, AIDS patients have myriads of circulating antibodies. Including anti-human T cell antibodies, the very one that serves as a substrate for our culture. You can see: even if each antibody reacts only with its microbe partner, we will see a host of reactions between a bunch of different elements.
CJ: I see where you are going with this: since all you see is the reaction phenomenon, you can't tell who reacts with what.
EPE: Exactly. The antibodies react, it flashes; but who put their finger on the switch? For the sake of argument, we have assumed that each antibody is specific, but in reality, they are cross-reacting. It's even worse.
CJ: It's hard to know where each protein and antibody comes from. It's a strange mess.
EPE: That's exactly it. Moreover, let us not lose sight of the fact that we are seeking to know two things that should not be confused. On the one hand nature, on the other hand the origin of viral proteins. The antibody reaction tells us neither about one nor the other. Why would such a protein come from a particle rather than from the planet Mars? Antibodies are just waffles that carry the imprint of their mold.
CJ: Do we know of any microbes in AIDS patients that could be responsible for the antibody reactions that Gallo had in his cultures?
EPE: Of course. A good example is the hepatitis B virus, HBV. Many people with AIDS, and virtually all hemophiliacs, are carriers. And this HBV doesn't just infect liver cells. It also infects T lymphocytes. Strange as it sounds, it also has reverse transcriptase. And the sick make antibodies to this virus ...
CJ: OK, I see the drift ...
EPE: But there is more to say about Gallo's experiences. First about the serum used. It comes from a patient labeled by the initials "ET" However, ET did not have AIDS. He suffered from a condition called pre-AIDS. It is a disseminated inflammation of the lymph nodes. There are many infectious agents that can be responsible for pre-AIDS, even in the absence of pseudo-HIV. They are found in homosexuals, intravenous drug addicts, hemophiliacs.
CJ: So ET might not have had anti-HIV antibodies and still react.
EPE: Exactly. The other mystery is the rabbits.
CJ: Oh yeah. I was going to ask you the question: what is this rabbit thing?
EPE: Well here it is: Gallo claims he had a rabbit serum containing HIV specific antibodies. Imagine the scene in his laboratory. He's finished growing H9 cells with lymphocytes from AIDS and when it comes to determining which proteins in the culture belong to his hypothetical virus, he digs into a cupboard and, by magic, he pulls one out. vial with the label "HIV Specific Antibodies". How did he get it? This is his first scientific communication on the virus he is trying to isolate, and already he has bottled antibodies?
CJ: How did Gallo's lab get these antibodies?
EPE: They say they made rabbits make these antibodies by repeatedly infecting them with HIV. But it had taken pure HIV for the rabbits to make specific antibodies. They should therefore have isolated the HIV before making the first attempt at isolation. Again, that does not hold water!
CJ: But then, if they didn't inject them with pure HIV, what did they inject them?
EPE: At best what can be seen in the photos of the Franco-Germans and the American National Cancer Institute, as long as they have injected the product of the 1.16 gm / ml band, the one that everyone takes for pure HIV. By injecting their rabbits with this product, even centrifuged, Gallo and Popovic injected them with a multitude of cellular proteins. However, any immunology book will tell you, the protein is the most powerful inducer of antibodies there is, especially when injected directly into the blood. The rabbits therefore produced antibodies against all of these proteins. It is obvious that putting these antibodies back into the soup of antigens that induced them, that provoked reactions. This is exactly what you should expect when you mix antigens and antibodies. But that does not provide proof that these antigens are viruses and even less a single retrovirus.
CJ: OK, I got it. you mean that before you identified the virus. Gallo had no way of knowing which antibodies, in ET or in people with AIDS, would selectively target HIV proteins.
EPE: That's it. He couldn't even know if there were any anti HIV antibodies. Before even starting to talk about antibodies against the proteins of a virus, we must prove that the proteins in question are indeed the constituents of a particle that looks like a virus and which replicates. The only way to do this is to isolate the particle and subject it to the treatment I described above. You need to catch the virus BEFORE you run after its proteins and antibodies.
CJ: But what the hell are those antibodies that everyone calls anti-HIV, in people with AIDS?
EPE: No one has proof that these are anti-HIV antibodies. This is what my colleagues and I have tried to remember for so many years. The only way to know would be to compare them to the isolated virus. This is an experiment known as basic calibration. It consists of taking virus isolation as a benchmark, as a completely independent means of determining whether the antibodies are really and only directed against HIV. Imagine HIV being the arbiter. If antibodies are specific to it, they will be revealed by reacting in its presence only. Nothing is simpler. But there is a catch, however, which you may not realize. What happens if, in addition to specific antibodies, there are also non-specific antibodies?
CJ: I'm afraid the reader is starting to get confused. Could you go into more detail?
EPE: Very good. The problem with using antibodies is that there can be two kinds: Specific ones, produced by HIV alone; they react with HIV and nothing else. Nonspecifics, produced by other agents or stimuli, which react with these agents, of course, which will react with HIV as well. In that case, when you put a drop of serum in a culture or in a test and you have a reaction, how will you know what kind of antibody is causing the reaction? In fact, there are three scenarios: all antibodies are specific, all are non-specific, or they are mixed. All you see is the reaction. Something that changes color. That's all. So how do you decide? It's simple: you are going to test a whole panoply of people: patients who have AIDS, patients who do not have AIDS, the healthy. In the same experiment, at the same time, you take HIV as the arbiter to judge the type of antibody. If antibodies appear when there is no HIV, they are nonspecific.
CJ: And has this antibody spotting experience already been done?
EPE: Well no. It should have been done, of course before we put the test on the market. But how would it have been since HIV has never been isolated? What we commonly see is that people who are officially considered uninfected have antibodies and therefore test "positive". There would therefore be non-specific antibodies to HIV. But that doesn't tell us their number or how to differentiate them. In conclusion, this is to say that HIV infection cannot be diagnosed in anyone by antibody testing. This is to say that the very existence of HIV must also be questioned, and for the same reason that the existence of HL23V has been questioned by Sloan Kettering and the National Cancer Institute.
CJ: So your argument basically boils down to the fact that the antibodies that everyone calls anti-HIV are not against HIV.
EPE: That's exactly it.
CJ: Now what about the proof that HIV is the cause of AIDS? Did Gallo bring it in 1984?
EPE: Actually, in the 1984 Science article, Gallo did not claim that HIV was the direct cause of AIDS. He said HIV was the probable cause of AIDS. But in terms of probability, there was already cause for doubt. Because, assuming that he isolated his virus, Gallo only found it in 36% of the AIDS patients he studied (26 out of 271) while 88% of patients had antibodies. In addition, he used the least specific test there is: the ELISA test. No one can diagnose HIV infection using ELISA alone anymore. If the virus was present in 36% of patients, why did 88% of them have antibodies? That's more patients with antibodies and without viruses than patients with viruses. On the other hand he did not have the slightest proof that HIV killed T4s, nor even that a decrease in T4 was responsible for all these diseases called AIDS.
CJ: In 1984, the proof was very thin.
EPE: There was no proof! Two years later, when Gallo defended himself for using the French virus for his version of HIV, he was much more confident than in his initial communication. He claimed to have provided "clear" proof that HIV was the cause of AIDS. He had not changed his mind in 93. Let me quote you his words during a television program called LA PESTE: "The irrefutable proof which convinced the scientific world that this virus is the cause of AIDS comes from us. what we know today about the virus comes from that lab, thanks in large part to Mika Popovic. As well as the development of a sensitive, operational screening test. I don't believe there is to discuss. I think the story speaks for itself. "
CJ: Does the false reasoning that Gallo used while working on cultures also affect the tests for HIV infection, which they do without cultures?
EPE: Do you mean antibody testing?
CJ: Yeah.
EPE: Of course. It's the same thing. Understand what's going on: To convince themselves that they have proteins in their cultures for a virus they call HIV, researchers use antibodies from their patients' blood. This is the first step. After that, they close their eyes and say, "OK, if these proteins are HIV proteins, then the antibodies are HIV antibodies." They use the same chemical reaction to tell who reacts with what. However, it is out of the question for an antigen / antibody reaction to give you the identity of one of the constituents, even if you know the other from the start. This is exactly why you need "basic calibration" as a referee. What makes the difference between testing and cultivation is the technology. In the test the patient's blood is deposited on proteins extracted from the H9 cell line or the like. When the proteins are contained in a test tube, we are dealing with an ELISA test. When they are arranged along a strip of blotting paper, we speak of WERTERN BLOT. When the proteins react with their blood, the patient is found to be HIV positive. In the Western Blot, the number and type of proteins that must react for the test to be positive varies from country to country. This poses a huge additional problem.
CJ: So the HIV testing process is the same as the one used in 1984 to prove the existence of HIV in cultures.
EPE: Yes, and the same one which served in 83 for the French group. And it is always he who was used by Gallo and his colleagues in the 70s to prove the existence of the late HL23V ... I find it appalling that scientists can take the antigens / antibody reaction for proof of viral isolation. ! What do they expect to see next under the microscope? A particle with its nucleus and its buds?
CJ: So you can say that HIV testing is unnecessary.
EPE: No, they are not unnecessary. There is no doubt that if you belong to a risk group and test positive, that is not a good thing.
CJ: What do you mean?
EPE: Because empirically, we see that these people are more likely to fall ill. They develop illnesses classified under the AIDS category, but the test also predicts increased mortality for diseases that do not fall under the AIDS category. This study was published in the "Lancet". On the other hand, what the tests do not prove is that there is an HIV infection, or even that the presence of HIV predisposes to AIDS. You may not realize it, but the only evidence that HIV causes AIDS is testing. However, since the test itself does not prove HIV infection, it cannot be claimed that HIV causes AIDS.
CJ: What is the significance of a positive test in someone in good health who does not belong to a risk group? Should he be worried?
EPE: We have nothing to answer this question, and I think we will never have any. Groups of healthy people should be followed over several years, the only difference being that one group is made up of seropositive and the other of seronegative. We would see who develops AIDS and who does not. The trouble is that it would be very difficult for people with HIV and their doctors not to believe that sooner or later they are going to get very sick and eventually die of AIDS. This state of mind is likely to completely bias the results of the experiment. And this on both sides.
CJ: What do you mean by: on both sides?
EPE: I mean the patient's health will be affected by knowing they are HIV positive and their doctor will feel obligated to treat them for a virus they don't have.
CJ: The treatment can be dangerous in itself?
EPE: Well AZT, the first antiviral on the market and still very widely used, has amply demonstrated its toxicity. Some of its side effects can even sound like AIDS.
CJ: Suppose anyway that the experiment is done, blind. and that HIV-positive people are found to be more prone to developing AIDS than HIV-negative people. What could we conclude from this?
EPE: The same as for groups at risk. At a stroke of poker, Gallo and his colleagues discovered a test that predicts a tendency to suffer from a number of diseases that have been grouped together under the name of AIDS. It does not prove that the link between all these diseases is a retrovirus. That will never prove that until we prove that HIV exists. To do this, it must first be isolated, then use it to validate the antibodies and confirm that they are directed against it. Even after that, you cannot say that HIV causes AIDS just because it is present in people with AIDS. Association is not causation. You may very well be in a bank during a heist and not be the thief. More information is needed to prove causation. Anyway, currently you can be diagnosed with AIDS without actually being infected with HIV. Refer to the official definition of AIDS given by the CDC.
CJ: It's still crazy!
EPE: Yet that's what it says: the CDC's definition requires that, in certain circumstances, the patient be diagnosed with AIDS even if their antibody tests are negative.
CJ: And what about other tests, RNA, PCR, Viral load, etc ...?
EPE: It's a huge subject. I'll just say two words: All of these tests are based on comparing a piece of RNA or DNA from the patient with a piece of RNA or DNA from the supposed virus called HIV. We come back to the story of rabbit antibodies. You have a second bottle in the cabinet, with the label "HIV RNA" on it. But since the virus has not been isolated, purified, who can prove to you that this piece of RNA comes from a virus? HIV experts themselves say that there are nearly a hundred million different HIV RNAs in every AIDS patient. The least likely source of so many variants is a virus. How can he remain the same actor if he varies so much? How can he continue to build the same proteins, to induce the same antibodies? It is magic!
CJ: Tell me, Eleni, if there is no virus, where do all these things that Montagnier and Gallo have found in their cultures come from? I guess you still think they've found something.
EPE: Of course they found something. They even found a lot of things. Everything we discussed. Your question is a good question. In our opinion, the TI and the particles they found would be produced by the diseased cells they cultured. It is also possible that it was produced by the reagents they added to the cultures. Finally, it should be remembered that the production of particles of the viral type is the result of a pathological process as well as a normal process. This is an established fact. There is absolutely no doubt about it. So what exactly are these particles? Well, some must be nothing more than broken cell debris. Some, because they are more uniform, could be viral or even retroviral. But in the context of HIV, what really matters is that there is at least one that shows that it is retroviral. Aside from that, the possibility that the TI and the proteins in management come from an endogenous retrovirus have yet to be ruled out.
CJ: An endogenous retrovirus? What is that?
EPE: Normal human DNA happens to contain retroviral information. The cell was born with it. They were not introduced following contamination as is the case with non-retroviral infectious agents. Let some phenomenon awaken this information, and DNA begins to make RNA which in turn makes proteins. The whole can very well lead to the assembly of retroviral particles. They are said to be endogenous because they do not come from outside. Something that comes from outside, like HIV, would be called exogenous. Long before the time of AIDS, everyone knew that in animal cells the production of endogenous retroviruses could be spontaneous. Just put a cell in culture. Leave it on the bench for a few days or a few weeks. Suddenly, it begins to produce particles of the retroviral type. They seem to come from nowhere. The process can be accelerated millions of times by inducers of cell activation. As luck would have it, these adjuvants are compulsory if we want to obtain HIV! Interestingly, it was not until 1993 that Gallo, Fauci, and other leading AIDS researchers admitted that human RNA could produce endogenous retroviruses. In fact, almost 1% of our DNA is made up of endogenous retroviral DNA. For the record, this is 3000 times the length that experts attribute to the HIV genome. And what is more, new endogenous retroviral genomes can arise from the recombination of existing retroviral genomes.
CJ: So HIV could be an endogenous retrovirus?
EPE: What goes on in the lab about HIV can be explained by many different explanations. We reviewed them all in a very long article written by Continuum in October 1997.
CJ: Can we tell the difference between an endogenous retrovirus and an exogenous retrovirus?
EPE: No. They have the same morphology and the same biochemical properties.
CJ: If HIV is endogenous, why do people with AIDS produce it and others not?
EPE: Because they are sick. They are actually sick before AIDS appears. The disease subjects their cells to stress, such as that required in cultures to induce the production of retroviruses. Conditions to which the patient is subjected or conditions to which the culture is subjected, who plays the main role? I don't know, but it should have been determined long ago if early researchers included control specimens in their experiments.
CJ: That is to say?
EPE: Suppose you are culturing lymphocytes from an AIDS patient. You have mixed a few H9 cells with all the chemicals needed for the culture to produce HIV. Well. You find something. Is that “something” that makes the difference between your AIDS patient and other people? What if you found the exact same thing in people without AIDS? Therefore, to make sure that what you find - and what you call HIV - is only present in people with AIDS (and therefore must be dealing with AIDS), you need to use controls. These are experiments carried out in parallel with yours, in exactly the same way, with the same products, the same equipment. The only difference is a variable that you are trying to highlight.
CJ: Could you explain a little more detail?
EPE: A control would be a culture of cells taken from an individual suffering from diseases which resemble AIDS but which are not, and who would have the same age, the same sex, living in the same living conditions as the patient as you study. It's even more perfect if he has a T4 deficiency and his cells are oxidized. People with AIDS present these two anomalies, but they are not the only ones to be in this case. Remember to add the same chemicals to each crop. It is known in advance that one of these ingredients causes the appearance of reverse transcriptase in normal lymphocytes. When you have finished your preparation, you will compare your two cultures. You may well see particles, TI, and antibody reaction in your non-AIDS control New Yorker. It would be better, in this case, to be careful before claiming that these manifestations are due to AIDS.
CJ: Hasn't there ever been an experience like this, with controls?
EPE: This is yet another problem in AIDS research. It is bloated, and yet hardly anyone uses controls. When there are, they are rarely valid.
CJ: Aren't we taking AIDS backwards? You suggested it
earlier: HIV would come from the patient or the culture, and not the other way around.
EPE: That's right. Being sick with AIDS could cause these biological abnormalities. Retrovirologists themselves have envisioned that retroviruses may arise as a result of disease and not the other way around. Taking the effect for the cause would not be new in medicine. A Nobel Prize was even awarded under these circumstances.
CJ: Time is running out, and I have a few more questions for you. First of all, for how long have you and your colleagues argued that HIV might not exist?
EPE: Since the very first announcement was made in 1983.
CJ: So that's not a conclusion you recently came to?
EPE: No, not at all.
CJ: Have you tried to get your ideas across to the scientific press?
EPE: Yes, of course. Our first article on AIDS dates back to 1988. In it I hypothesized non-viral AIDS and covered some of what we have been discussing today.
CJ: Who published you?
EPE: The journal "Medical Hypotheses".
CJ: It's not a very well-known newspaper.
EPE: In the opinion press category he is well known. The discussion of HIV isolation was not as candid as it has been here, but at the time it was virtually impossible to question the existence of HIV. You had to be cunning to be able to get printed. Even so, it took several years for the article to come out. I had previously offered it to a well-known newspaper which had refused it. On two occasions even ...
CJ: What was this diary?
EPE: Doesn't matter. Again in 88 Val Turner and I wrote another post in which we frankly tackled all of the issues we have stated today. We were targeting the clinical medicine audience and donated the article to a newspaper read by general practitioners in Australia.
CJ: And it happened?
EPE: No. No chance !
CJ: So it was only the readers of "Medical Hypotheses" who could, 10 years ago, know what you were thinking.
EPE: Yes.
CJ: You mentioned your hypothesis of non-viral AIDS. Can you tell me what it is?
EPE: We were the first, in the scientific world, to put forward the hypothesis that non-infectious factors could explain AIDS in homosexuals and the first to propose a non-infectious theory that applies to all risk groups. . Furthermore, our theory predicts that the factors that lead to AIDS are also responsible for what everyone thinks of a retrovirus.
CJ: What were the reactions?
EPE: There was unfortunately very little reaction. Still, some teams of researchers have confirmed many of our predictions, including that antioxidants may be helpful in treating individuals at risk for AIDS.
CJ: Have you succeeded in shaking the inertia against your ideas?
EPE: We have not had much luck with the scientific press, but a few homosexuals and their organizations have become our best allies. Without them, I think we would have achieved next to nothing.
CJ: If you had to point out just one obstacle to the scientific solution to AIDS, what would it be?
EPE: In our opinion, the biggest and only obstacle to understanding and solving AIDS is HIV.
CJ: Is that why you wrote so much against HIV?
EPE: Exactly. In fact, we have written many more articles than we have published. We only managed to get a dozen of them printed in scientific journals. One of the most important was an article in Bio / Technology, which has since become Nature / Biotechnology. We said openly that there was no isolation of HIV. The article was certainly noticed but, once again, no one reacted.
CJ: So you're still a minority.
EPE: Much worse. We are still the only ones to have ever published in the scientific press a questioning of the existence of HIV; as well as questioning the diagnosis of infection by means of the antibody test.
CJ: Eleni, why, despite everything you've just explained, virtually every scientist and doctor in the world seems to easily cope with evidence that you find so hard to accept?
EPE: The problem is not to accept the obvious. The problem is how the obvious is interpreted. This is how I see it: most scientists and doctors who believe in HIV, and believe that HIV causes AIDS, believe it because they accept the interpretation of a minority of experts. It is totally unrealistic to expect everyone who works on AIDS to analyze the results of Research at the level we have done. As for the experts themselves, I don't know why they interpret the obvious the way they do. I can only speculate. Perhaps this is because of the enormous power of photographs. There are photos showing particles that look like a virus and there is TI in those same cultures. It is possible that mentally we connect particles, TI, proteins and antibodies to make it obvious and believe in the existence of a retrovirus. Particularly in the mind of a virologist. I guess the whole problem is there. Let us not forget that we are all at the mercy of our subjectivity and that each of us sees noon at his door.
CJ: But doesn't that also apply to you when you interpret literature?
EPE: Certainly it is. But do not lose sight of a very important thing which is not subjective.
CJ: What then?
EPE: The definition of a virus and the resulting method to prove its existence. This method was certified by the Institut Pasteur in 1973. No one can deny that it constitutes absolute proof of the existence of a retrovirus. And no one can deny that, according to this method, HIV was never a reality. In other words, although AIDS is considered one of the worst plagues of mankind, no one has found it necessary to use a proven method to establish the existence of the presumed cause of this dreadful disease. Instead, everyone opted for an assortment of non-specific criteria and got it into their heads that by mixing it all up the correct answer, by metamorphosis, would come out.
CJ: Doesn't that have some merit? If all these criteria are clues on the trail of a retrovirus, the more there are, the more likely we are to reach the goal.
EPE: Certainly not. What if the real cause was something unexpected? Or something you don't know? Or even something impossible to imagine? In such a case, the more clues you have going in the direction of what you want it to be or what you smell, the more you will go astray. It is like going into probabilities rather than finding facts. This is what I call being subjective. It is like a doctor who sees an exhausted patient, in shock, with fever, diarrhea, vomiting, and who immediately declares that he has cholera. Of course it could be cholera, but there are dozens of other germs that give the same clinical picture. Why would he eliminate them?
What if your life depended on it?
CJ: I understand you. Now that we know what is in a density gradient, do you think the tide will turn and HIV will be challenged?
EPE: I do expect that this new data will constitute a turning point. Especially if a lot of people read it. It confirms what our group has been saying for a very long time. In their introduction, the authors of the Franco-German paper clearly state that their photos give the lie to the belief that "the density gradient 1.16 gm / ml contains a population of relatively pure viral particles". This is precisely our point: HIV has never been isolated and despite this, for the past 14 years scientists and pharmaceutical companies have used this impure material to obtain the proteins and RNA of pure HIV. Photos have the power to impress, and that is a double-edged sword. Here, it can go in the right direction.
CJ: What do you think will happen now in the area of ​​AIDS research?
EPE: I think it is urgent that we start to apply the traditional method of viral isolation. And that we do it well: from cultures of patients who have AIDS but also with appropriate controls. Like I said, we have to find out once and for all if there is something called HIV. It took 14 years to get barely a handful of electron microscope photos in a density gradient. Even if these photos had revealed nothing other than particles perfectly likely to be retroviruses, we would still have to go through all the other steps that separate us from isolation.
CJ: What are the most important steps?
EPE: All the steps are important. Confirm the presence of particles of the retroviral genus in cultures; purify and analyze these particles; prove that these particles can replicate; and finally, to prove that the antibodies in patients' blood are specific to the proteins of the particles in question.
CJ: What if it isn't?
EPE: If this is not the case, i.e. if these phenomena also exist in the control cultures, or if the particles in band 1.16 have the wrong morphology, are not infectious, or if the antibodies AIDS patients are not specific to these particles, so AIDS patients cannot have been infected with a virus called HIV, and we should not talk about it anymore.
CJ: Which means HIV could end up like the same Gallo's HL23V?
EPE: It's very possible. The proteins of the so-called HL23V were identified in the same way as those of HIV, by reaction to the antibodies. When the antibodies were found to be nonspecific, the HL23V vanished. In the case of HL23V this was relatively easy to come to terms with since the antibodies were produced by so many people who would never have leukemia that there really could not be a relationship. And this has been demonstrated by Sloan Kettering and the National Cancer Institute. In our team, we believe that the scientific world will accept that the same is true when it comes to antibodies to HIV. You know AIDS patients have so many infections that they're stuffed with antibodies. It would be nothing special if some of them react with two or three of the 10 proteins in the HIV test. It does not take more to be HIV positive. In fact, it has become quite obvious that this is already the case for antibodies to two infections that 90% of people with AIDS suffer from. I'm talking about mycobacteria and yeast infections, which are responsible for the two most common opportunistic diseases: their antibodies react with all the proteins in HIV. We have just written an article on this for an English journal Current Medical Research and Opinion. If so, who can now continue to claim that these antibodies provide proof that HIV exists, or that these diseases are caused by HIV?
CJ: Eleni Papadopulos-Eleopulos, thank you very much for your time today
EPE. But it was with pleasure, and it is I who thank you. The Perth Group welcomes any scientific discourse on its research.
Eleni Papadopulos - Tel: (Aus) + 618 9224 3221. Fax: + 618 9224 3511
Direct contact: Perth Group of HIV / AIDS scientists at http://www.virusmyth.com/aids/perthgroup/sousindex.html
email : vturner@cyllene.uwa.edu.au Translation: Philippe Krynen, Association Partage, Tanzania. Scanned by Jean-Reymond Cornu for:
The Mark Griffiths Association, La Métairie Blanche, 11190 La Serpent, France.
Phone: 0033 04 68 31 27 91.
Send 12FF in stamps to receive a copy of this text. Christine Johnson, July 1997
PO Box 2424 Venice, California 90294-2424, USA.
Phone: 001+ (310) 392-2177 Fax: 001+ (310) 273-297
See also Continuum Supplement, Vol 4, N ° 3 Sept / Oct 1996.
THE ISOLATION OF HIV: HAS IT REALLY BEEN ACHIEVED? The Case Against
Eleni Papadopulos-Eleopulos1 Valendar F. Turner2 John M. Papadimitriou3 David Causer1
1Department of Medical Physics, 2Department of Emergency Medicine, Royal Perth Hospital, Perth, Western Australia; 3Department of Pathology, University of Western Australia. Continuum, 172, Foundling Court, Brunswick Center, London WC1N 1QE., GB
Tel: 44+ 171 713 7071. Fax: 44+ 171 713 7072. Email: continue@dircon.co.uk
________________________________________