suite
CJ: It's disconcerting!
EPE: And that’s not all. According to Harold Vamus, Nobel Prize winner and director of the National Institute of Health, there is IT in normal cells, just like in bacteria. We also know that among the chemicals necessary for the culture medium, some have the property of causing normal lymphocytes to reverse transcribe. If they are leukemic 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 found almost everywhere. In the 70s it was discovered in leukemic tissues, embryonic tissues, and in the majority of animal and human placentas. This is important to note because Gallo's H9 line is a leukemic line and because Montagnier's ME photos are taken in umbilical cord cultures. Let's be careful. See for example the group of retroviruses classified as "type C": they are found in mammals, fish, snakes, worms, tapeworms, pheasants, quails, partridges, turkeys, field mice, agouti, insects... But this is precisely in this group that Gallo and Montagnier decided to place HIV. Without unanimous approval because officially HIV still wears many other disguises. See also this study conducted by O'Hara and his colleagues at Harvard in 1988. They examined photos of lymph nodes from 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: Question of percentage. 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 came first, the chicken or the egg. This is an essential point in our argument, so I hope that I will be able to make myself clearly 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 retrovirus and nothing else = particle having 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. Don't ask me why, but that's how it is! In its place we have a collection of disparate data such as photos outside the density gradient, traces of TI in crops or band 1.16 of the gradient... None is proof by itself of the existence of a retrovirus. 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. Furthermore, 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 the nature, on the other hand the origin of viral proteins. The antibody reaction does not tell us about one or the other. Why would this protein come from a particle rather than from the planet Mars? Antibodies are just waffles that bear 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 produce these antibodies by repeatedly infecting them with HIV. But they needed pure HIV for the rabbits to make specific antibodies. They should therefore have isolated HIV before making the first attempts at isolation. Once again, this doesn't make sense!
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 anti-HIV antibodies. Before we even begin to talk about antibodies directed against the proteins of a virus, we must prove that the proteins in question are indeed the constituents of a particle that resembles 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 chasing 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 when we use antibodies is that there can be two kinds: Specific ones, produced by HIV alone; they react with HIV and nothing else. Non-specific ones, produced by other agents or stimuli, which react with these agents, of course, but which will also react with HIV. In this 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 the reaction is due to? In fact, there are three scenarios: all the 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 to decide? It's simple: you are going to test a whole range of people: patients who have AIDS, patients who do not have AIDS, healthy people. In the same experiment, at the same time, you take HIV as the arbiter to judge the type of antibodies. If antibodies appear when there is no HIV, they are non-specific.
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 denied having used the French virus for his version of HIV, he displayed much more confidence than in his initial communication. He claimed to have provided "clear" evidence that HIV was the cause of AIDS. He had not changed his mind in 93. Let me quote his words during a television program entitled THE PLAGUE: "The irrefutable proof which convinced the scientific world that this virus is the cause of AIDS comes from us. Everything we know today about the virus comes from this laboratory, largely thanks to Mika Popovic. As well as the development of a sensitive, operational screening test. 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 is happening: To convince themselves that they have, in their cultures, the proteins of a virus they call HIV, researchers use antibodies from the blood of their patients. This is the first step. After that, they close their eyes and say, "OK, if these proteins are HIV proteins, then the antibodies are anti-HIV antibodies." They use the same chemical reaction to tell who reacts with what. However, there is no question that an antigen/antibody reaction will give you the identity of one of the constituents, even if you know that of the other from the start. This is precisely why you need “baseline calibration” as an arbiter. What makes the difference between testing and culture is technology. In the test the patient's blood is deposited on proteins extracted from the H9 cell line or other. 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 declared HIV positive. In Western Blotting, the number and type of proteins that must react for the test to be declared 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 no information to answer this question, and I think we never will. It would be necessary to follow groups of healthy people over several years, the only difference being that one of the groups is made up of HIV-positive people and the other of HIV-negative people. We would see who develops AIDS and who does not. The trouble is that it would be very difficult for HIV-positive people and their doctors not to believe that sooner or later they will become very ill and possibly die of AIDS. This state of mind is likely to completely bias the results of the experiment. And that 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: Let's still assume that the experiment is done blindly. 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 in risk groups. In a twist, Gallo and his colleagues discovered a test that predicts a tendency to suffer from a number of diseases that have come to be grouped under the name AIDS. This does not prove that the link between all these diseases is a retrovirus. It will never be proven until we prove that HIV exists. To do this, it must first be isolated, then used 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 can very well be in a bank at the time of a hold-up and not be the thief. More information is needed to prove causality. In any case, currently you can be diagnosed with AIDS without you 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 IT and the particles they found would be produced by the diseased cells they cultured. It's also possible that it was produced by the reagents they added to the cultures. Finally, it must 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 of the viral or even retroviral type. But in the context of HIV, what really matters is that there is at least one that provides evidence that it is retroviral. Aside from this, the possibility that the IT and the proteins in management come from an endogenous retrovirus still remains 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: Let's imagine that you culture the lymphocytes of an AIDS patient. You have mixed a few H9 cells with all the chemicals required for the culture to produce HIV. GOOD. You find something. Is this “something” what makes your AIDS person different from other people? What would it be like if you found exactly the same thing in people without AIDS? Therefore, to ensure that what you have found - and which you call HIV - is only present in people with AIDS (and therefore must be dealing with AIDS), you must 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.htmlemail :
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:
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