CJ: So the HIV antibody test is really the same procedure that used to prove the existence of HIV in cultures from AIDS patients in 1984?
EPE: Yes. And also by the French in 1983. And by Gallo and his colleagues to prove the existence of HL23V in the mid seventies. Our group find it intriguing that any scientist could regard antibodies reacting with proteins as proof of viral isolation. Is an antibody joined to a protein a virus? What would you expect to see under the electron microscope? A particle with a core and knobs?

C/J: How can that be?
EPE: Because empirically such people are more likely to develop the illnesses we classify as AIDS. In fact, there is evidence published in the Lancet that a positive test also predicts increased mortality from diseases which are not classified as AIDS. 31. But what the test don’t do, or at least there is no proof that they do, is prove HIV infection. Or even less that HIV infection is the reason people develop AIDS. You may not appreciate that the only evidence HIV causes AIDS is these tests. If the test are unproven for HIV infection then there is no proof that HIV causes AIDS . 3-5,26,32-34.

EPE: It’s the same test. Can you see what’s happened here? The HIV researchers have used some antibodies in the patients’ blood to convince themselves that some proteins in their cultures are unique constituents of a particle which they say is a retrovirus and call HIV. That’s the first thing. But having done that they’ve then turned around and said, "OK, if these proteins are from HIV then the antibodies must be THE HIV antibodies".

So they’ve used the one and same chemical reaction to prove which each reactant is when in fact there’s no way an antibody reaction can tell you even what one reactant is even if you know the other to start with. That’s why you need a independent gold standard adjudicator. As far as actually doing the test is concerned, the difference from cultures is that the patient’s blood is mixed with proteins extracted from H9 or other cell cultures and put either all together in a test tube or separately at discrete spots along a thin paper strip. The first is called ELISA and the second the Western blot. If these proteins react with the blood, and in the Western blot the number and type of reacting proteins required to produce a positive test vary all over the world and that’s yet another huge problem, then the patient is reported HIV positive.

CJ: So the HIV antibody test is really the same procedure that was used to prove the existence of HIV in cultures from AIDS patients in 1984?
EPE: Yes. And also by the French in 1983. And by Gallo and his colleagues to prove the existence of HL23V in the mid seventies. Our group find it intriguing that any scientist could regard antibodies reacting with proteins as proof of viral isolation. Is an antibody joined to a protein a virus? What would you expect to see under the electron microscope? A particle with a core and knobs?

CJ: Then is it fair to say that the HIV antibody tests are useless?
EPE: No, they’re not useless. There is no doubt being in a risk group and having these antibodies is not a good thing.
CJ: How can that be?
EPE: Because empirically such people are more likely to develop the illnesses we classify as AIDS. In fact, there is evidence published in the Lancet that a positive test also predicts increased mortality from diseases which are not classified as AIDS . 31 But what the test don’t do, or at least there is no proof that they do, is prove HIV infection. Or even less that HIV infection is the reason people develop AIDS. You may not appreciate that the only evidence HIV causes AIDS is these tests. If the tests are unproven for HIV infection then there is no proof that HIV causes AIDS. 3-5,26,32034.
CJ: What about a positive test in people who are apparently healthy and not in any risk group? Should they be worried?

EPE: There is no data to answer that question and I think it would be impossible to ever obtain that data. There would have to be a an experiment comparing matched groups of healthy people with and without these antibodies. In other words, follow people with a positive test over a period of years and see who developed AIDS and who did not. The trouble is it would be very difficult for most people knowing they are HIV positive, as well as their physicians, not to believe that sooner or later they’re going to get very sick and eventually die of AIDS. And that mindset may greatly effect the results of such an experiment. From both sides.

CJ: What do you mean from both sides?
EPE: I mean that patients’ health will be affected knowing they are HIV positive and their physicians will feel compelled to offer treatments with drugs given in the belief they are necessary to kill a virus the patients do not have.
CJ: The drugs themselves might be harmful?
EPE: Well AZR, the original and still most widely used drug is certainly well known for its toxic effect and in fact some of these effects mimic AIDS.
CJ: What if we did this experiment, and we did it blind, and found that the HIV positives were more likely to develop AIDS than the HIV negatives? What would that tell us?

EPE: On our present data that would mean the same it means in the AIDS risk groups. Gallo and his colleagues serendipitously discovered a test which for some reason predicts a tendency to get sick from certain diseases that are lumped together as AIDS. But it doesn’t prove that the link to all these diseases is a retrovirus. That can never be proven unless HIV is proven to exist by isolating it first and then used to validate the antibodies as HIV antibodies. Even then, you can’t say HIV causes AIDS just because it’s present in AIDS patients. Association doesn’t prove causation. You can be present at a bank robbery but not be the robber. You need other data to prove causation. In fact, according to the CDC AIDS definition, you don’t even need to be HIV infected to be diagnosed as having AIDS.
CJ: That sounds really crazy.

EPE: It’s written down in the literature. Under some circumstances the CDC AIDS definition requires a patient to be diagnosed as a case of AIDS even if the patient’s antibody tests are negative. 35.
CJ: What about the RNA tests. The PCR and viral load and like?
EPE: That’s another huge subject but I can say just one thing. All these tests rely on matching a piece of the patient’s RNA or DNA to a test piece of RNA or DNA deemed to originate from a particle called HIV. You can think about this like the rabbit antibodies. There’s another bottle on the shelf and the label on this one reads "HIV RNA". But if a retroviral particle hasn’t been isolated and purified and shown to be a virus, how does anyone know where this piece of RNA comes from? The HIV experts themselves say that there are about one hundred million distinct HIV RNA in every AIDS patient. 36 With that much variation one would think that a virus is the most improbable source for such RNA. I mean, how can a virus have that much variation and still be the same agent? Still make the same proteins and induce the antibodies? Still perform all the same tricks?

CJ: Tell me Eleni, if there is virus where do all the things Montagnier and Gallo found come from? I assume you do believe they did find something in their cultures?
EPE: Of course they found something. They found many things. All the things we’ve discussed. And your question is fair. In our view it is possible the RT and particles could be some reaction produced when cells from sick people are cultured. Or the result of the chemicals introduced into the cultures. We know that both normal and pathological processes can be associated with the cultures. We know that both normal and pathological processes can be associated with the appearance of retroviral-like particles.

There’s absolutely no doubt about that. What exactly are all these particles? Well, some may be no more than pieces of disintegrating cells. Other s certainly look more uniform and might conceivably be Viral-like or even retro-viral-like but in the context of HIV what really matters is proof that at least one of these varieties of particles is a retroviral particle. Even if we had that proof, the RT and the particles and proteins could all come from an endogenous retrovirus.

CJ: What’s an endogenous retrovirus?
EPE: Unlike the case for all other infectious agents, normal human DNA contains retroviral information which did not get there following a retroviral infection. The cell was born with it. So amongst all our DNA there are stretches made up of some retro-viral information and that may sit there maybe all your life until something happens. The DNA starts to make RNA and hence proteins, and this may go even further and lead to the assembly of endogenous retroviral particles. They’re called endogenous because they’re not something that got in from the outside. Like HIV is supposed to. Something that gets in from the outside is called exogenous.

Long before the AIDS era everyone knew that in animal cells endogenous retrovirus production could occur spontaneously. You make a cell culture and do nothing and do nothing else. Just leave it on the bench for a few days or maybe a few weeks and then one day it starts to produce retroviral-like particles. They seemingly come out of nowhere and the process can be significantly accelerated and the yield of particles increased, sometimes million of time, by conditions which induce cellular activation, the same conditions which are obligatory to obtain what is called HIV from cell cultures. Interestingly, up until 1993, neither Gallo nor Fauci who is another well-know HIV researcher, 37 accepted that humans contain the DNA to make endogenous retroviruses but now it’s accepted that endogenous retroviral DNA forms about 1% of human DNA. For the record, that’s about 3,000 times larger than what the experts claim is the size of the HIV genome. And what’s more, new retroviral genomes can arise by rearrangements and recombination of existing retroviral genomes.

CJ: So HIV could be endogenous retrovirus?
EPE: There are many explanations for the laboratory phenomena held up as proof for the existence of HIV. We went into all these in a very long article we wrote for Continuum magazine last October. 38
CJ: Can you tell endogenous and exogenous apart?
EPE: No. Endogenously produced retroviruses are morphologically and biochemically indistinguishable from exogenous retroviruses.

CJ: If HIV is an endogenous virus, why would AIDS patients produce such viruses when we don’t?
EPE: Because the patients are sick. In fact they are sick before they ever develop AIDS. So their cells are sick and their sick cells find themselves in the right condition in cultures to be activated. That’s what’s needed to produce endogenous virus and that’s been known for decades. Either the agents to which the patients are exposed induce the right conditions or the culture conditions play a part. Perhaps a major part. I don’t know which contribution is the greater but that might have been sorted out a long time ago if the first HIV researchers had included a few control experiments.
CJ: What are they?

EPE: When you do a culture of say lymphocytes from an AIDS patient with some H9 cells and all the chemicals which are added to make the culture produce "HIV", you really don’t know if what you find is the difference that sets AIDS patients apart from everyone else. What if you were to find exactly the same thing in similar patients that don’t have AIDS? So, to convince yourself that what you find and call HIV is present only in AIDS patients and therefore might have something to do with AIDS, you must use controls. They’re experiments run in parallel with your main experiment conducted exactly the same way using exactly the same materials. The only difference is the one variable you’re chasing.
CJ: Could you explain that further?

EPE: A control would be a culture of cells form some patients of the same age and sex and environmental exposures who are sick with diseases like AIDS but not AIDS. Even better if the cells came from patients who have low T4 cells and who are oxidized. 3, 32 AIDS patients have both these abnormalities but they’re not the only patients to have them. And one must also not forget to add the same chemicals to all cultures. We already know that one of these chemicals causes reverse transcription in normal lymphocytes. Now, if you did all that you might well find that lymphocytes from men in New York who were sick with non – AIDS diseases also develop particles and RT and antibody reactions when cultured. That would mean that one would have to be very cautious interpreting that data as being something special to AIDS.

CJ: There weren’t any controls?
EPE: This is yet another problem with so much AIDS research. Hardly any one uses controls and when they do they’re often the wrong type.
CJ: Is it possible we’ve got AIDS back to front? You hinted at this before. Could the patients or the cultures be responsible for what is called HIV and not the other way around?
EPE: Right. Having AIDS may just be a prescription for developing those abnormalities. Retrovirologists themselves have argued that retroviruses may arise as the result of a disease and not vice versa. Getting cause and effect the wrong way around is not new to Medicine. The Nobel Prize has even been awarded under such circumstances.

CJ: It’s almost time to finish up. I have several more questions. First, how long have you and your colleagues held the view HIV may not exist?
EPE: Ever since the first publication on HIV. In 1983.
CJ: So it’s not something you recently came to?
EPE: No.
CJ: Have you published these particular arguments? I mean in a scientific journal?
EPE: Yes. In my first paper on AIDS in 1988. There I put forward a non-viral theory of AIDS and I also included some of what we’ve talked about today.
CJ: Where was that published?
EPE: In Medical Hypotheses. 3
CJ: Not a well known journal?
EPE: It is a well known journal of ideas. There the discussion on HIV isolation is not as frank as we’ve had today but back then it was virtually impossible to question the existence of HIV. It was important to be subtle in order to get into print. Even so, it tool a few years for that paper to be published. Initially I submitted it to a much more prominent journal but it was rejected. Twice in fact.
CJ: Which journal was that?