Eleni: No, the only way to prove that is to have, you know, these studies. There are many reports where they say, you know, here it is one person and another, their case is reported as being due. Let’s have one example about that. In New York, I mean, AIDS first was diagnosed there and one of the aims… I think it’s 1991. By 1981 they had only eleven cases of AIDS which was heterosexually acquired, which was claimed to be heterosexually acquired. Now, that really I think is sufficient to tell us that it can’t be.
Stuart: Sorry, was that 1981?
Eleni: I think it was 1991, sorry.
Val: No, it was about 1990, 1991.
Eleni: In fact I was looking today. I wanted to write it down and I can’t find the paper, but it was ten years after AIDS was first diagnosed in the city. The cumulative number of AIDS cases which was claimed to have been acquired by heterosexual AIDS by men was eleven.
Stuart: Anal intercourse has been around forever or for as long as we know. Why is it then that the AIDS condition didn’t appear in homosexual men in large numbers until the eighties?
Eleni: Not only homosexuals. As we said, you know, this is not only homosexual practice, you know. It is practised by everybody. We don’t know what it was before.
Val: We don’t know what happened before. We don’t know that gay men didn’t get these diseases before. We don’t know… all we know is that they got it in 1981.
Eleni: We do know that there are much higher frequencies now for sure, that is certain, that they have much higher frequencies now that they…
Stuart: Kaposi’s sarcoma was a very rare disease before which only applied to… only really affected very old people.
Val: That’s not true. There’s plenty of data to show that there are cases… in fact one estimate is 20 per cent of cases of Kaposi’s sarcoma diagnosed in Europe and in America from 1900 till the beginning of the AIDS era would have been classified as AIDS had AIDS definition been around then. So no, we reject that assertion that it didn’t happen. What we didn’t know about, of course, pre-AIDS, was the number of gay men who developed these diseases. We probably don’t even really know how many of the diseases developed because we’re looking harder now. We know a little bit but we certainly don’t know whether many were in gay men because being gay was something that was not broadcast before the late 1970s, eighties. It was a social change in the way… people’s behaviour, if you like. People were no longer closeted.
Eleni: But with Kaposi’s sarcoma, you know, this is a malignancy which is… people have nearly normal life span. Even in gay men now, gay men with Kaposi’s sarcoma live longer than gay men with infectious diseases, with opportunistic infections. Even in 1981-82, both the patient and the doctor had problem diagnosing Kaposi’s sarcoma because, you know, they were thinking…
Val: The true incidence of Kaposi’s sarcoma pre-AIDS and the true incidence in gay men is totally unknown, so we’re looking at evidence of absence. It’s not evidence of… how does the saying go? Absence of evidence is not evidence of absence. But even we would agree that there was an increase in these cases because there were so many of them, that they could not be hidden, even if people were trying to hide them. So we would agree that there was an increase. Whatever the level was before in gay men, it was a lot higher in the 1980s. And you want to know how does one explain this?
Eleni: Could be, you know, because of higher sexual activity. Another reason could be that, you know, in these cities they became… gay men from everywhere round the world were going to America.
Val: To meet each other.
Eleni: To meet each other. It was there where they had the freedom to express themselves because, you know, in Europe it was not; certainly, in Asia they could not.
Val: And in Africa they certainly couldn’t.
Eleni: And in Africa they could not. So, you know, it is a combination of many factors which led to the true and apparent increase in these diseases in the gay community.
Val: For which there was little prior knowledge – epidemiological knowledge.
Eleni: Does that make sense or does not? Please ask.
Stuart: I still have trouble, I guess, coming to terms with the idea that something as noticeable as AIDS, something as observable as AIDS, was not picked up beforehand when there had been communities of gay people in areas like San Francisco, for example, for a lot longer than just the eighties or the seventies and eighties.
Val: We don’t really know; we’re guessing.
Eleni: We don’t know but, you know, Johnson and… what’s their name, who studied…
Stuart: Masters and Johnson.
Eleni: Masters and Johnson. They say, you know, that really the practice of passive anal intercourse, you know, not only of gay people, but the practice of passive anal intercourse, it really increased much more in the seventies.
As I said, the drugs, they’re there too. We cannot avoid two significant changes. I’ll say three because… most people say two but I’ll add the third one. The first is, you know, that for the first time gay men had reasons to be happy because they were not any more suppressed the way they used to be before, and when you have freedom you try to take opportunity of it. Then they had… unfortunately drugs came into the scene, which they never had them before, and then the third is – my addition is – that they came together. Gay men from everywhere were travelling to San Francisco or to Los Angeles and to New York, so all things together, to me, at least to me, make sense. I don’t know if they, you know, make sense to others, but to me…
Val: I don’t think you can… I mean, you can’t make any sense out of this without at least mentioning the fact that there is evidence that gay men at this period of history were exposed to high volumes of semen. Now, this is not meant to state that they were exposed necessarily to any more semen than any other groups practising sexual relations, but in absolute terms what counts is how much semen, in our theory, at least of our theory, our toxic theory, is how much. What the dose was. One doesn’t have any basis for comparison really from previous times, but there is evidence that gay men were having many partners, sometimes up to a thousand a year in some cases. This would seem to indicate an unusually high exposure to semen; one could postulate more possibly than the human body had been exposed to in times past – not on an individual basis of course, but en masse, as Eleni has alluded to; the fraternity, if you like, the fellowship of being gay.
I mean, this is no reflection on gay people or the gay movement. We’re only interested in the scientific issues and if it turns out that in fact exposure to large volumes of semen is a factor in inducing the oxidative stress which we postulate is a major etiological factor in the development of these diseases, then so be it. I mean, one cannot walk away from this.
Eleni: But, you know, if it is proven… because this is another thing with the theory. All right, the theory is not proven but one thing which has been proven is that AIDS patients are oxidised. That is something which nobody can deny.
Stuart: How is that determined?
Eleni: It has been determined by measuring the cellular thiols.
Val: By taking blood or cells and working out how much reducing substance is in them.
Eleni: Right. The other thing which cannot be denied… our theory postulates that the phenomena which are called HIV are induced by oxidative stress. That was postulated in… from the very beginning once I came in contact… in 1984 I postulated that the phenomena which are called HIV are induced by oxidative stress. Now today, again there is ample proof that HIV can be induced by oxidative stress in the petri dish. You put oxidative stress or substances or radiation which produces oxidative stress, you have HIV.
Val: We didn’t stress this at the beginning. We mentioned that the oxidative stress is capable of inducing pathology but we didn’t say that in fact it also induces the very phenomena which people interpret metaphorically, if I may use that term again, as HIV. In fact, the theory predicts this and it’s basic standard retrovirology. It’s not as new as it sounds. It’s knowledge which has been gained since 1911.
Eleni: Only then they were not called… you know, they did not know that really all these substances… they knew that if you put radiation, if you put carcinogens, you’ll induce retroviruses. What they… nobody apart from me, may I say so …
Val: She said modestly – modestly…
Eleni: They did not see the relationship between all these substances which… and I claim… I don’t say that I see but I claim that the relationship is oxidative stress. Now, what we know now… now it is called that and we know – there is ample evidence – that if you put oxidising substances or radiation or you radiate your petri dish, you produce the HIV phenomena. On the other hand, if you put reducing agents, you’ll inhibit the HIV phenomena. So really what is important today to me, as far as I’m concerned, is even if we disagree on what causes AIDS, you know, with most people, when it comes to the principal and the most important fact, that is, how can we prevent and how can we treat AIDS, I think the evidence from our quarter and – call it the opposition. I don’t call them opposition, but…
Val: The HIV/AIDS protagonists.
Eleni: The HIV theory and their HIV theory. We have to admit the evidence from… you know, the experimental evidence from there and the theoretical evidence from here all point to one thing: that HIV, in inverted commas, and AIDS can be prevented and reversed or treated with reducing agents. And I think at this point we all have to agree.
Val: And when you encompass the HIV phenomena with the pathology, the theory has the attractive quality of being economical and explaining many things with one simple statement which we all seem to believe is one of the properties of a good theory. The other important thing is that surely there is now enough evidence around against HIV as being the theory of AIDS to make it mandatory as a public health issue, if nothing else, for this to be discussed and debated in proper scientific terms by scientists in open forum.
Eleni: Apropos of public health issue, now, people are…
Stuart: Can we move on to the public health issue on the next tape, please.
Eleni: Apropos of the public health consequences of our theory and of the HIV theory, usually when we talk to people about our non-HIV theory of AIDS, people get a little bit upset and usually without knowing what we are saying, they say, “Oh, you’re one of the Duesberg mob”. That is Peter Duesberg who, like us, thinks that HIV does not cause AIDS, but there is a big difference between Peter Duesberg and us. In fact, Peter Duesberg… we came at about the same time, at exactly the same time, to this conclusion but from completely different points of view.
There are many differences between Peter and us, one of which was at the beginning he did not say what was the cause of AIDS and now he says that the cause of AIDS in all the AIDS risk groups is drugs and that as far as safe sex is concerned, he is of the opinion that there is no need to worry about condoms, just to put it… we are not of the same view. In fact we think safe sex is of extreme importance. That coincides with the HIV theory of AIDS as far as public health is concerned and, again, as far as drug users are concerned, in fact we go one step further: we not only say that needles should not be shared, we say that needles should not be used or even oral drugs because in our view it is the drugs which cause the abnormalities and not needle sharing. Also needle sharing could have an additional effect by transmitting infections such as hepatitis B and… I don’t know what else.
Val: Isn’t it also important to stress the differences in perspective between Duesberg and us as far as HIV is concerned?
Eleni: Peter does believe that HIV exists. He believes that the HIV antibody test, a positive HIV antibody test proves HIV infection but he says that if you test people who… for example, if you take haemophiliacs who test positive and those who test negative and you follow them up, you’ll find out that both groups will develop AIDS with nearly equal frequency. We do not agree with that.
Val: This is not a study, this is a postulate. Peter Duesberg has postulated that to prove or disprove the HIV theory, one way would be to conduct a study of two groups of haemophiliacs differing only in their seropositivity in their serostatus, that is with HIV positive or negative, follow them up for a reasonable period of time, several years, and see what happens as far as AIDS disease incidence occurs. He predicts that both groups will develop AIDS at the same rate.
We do not share that view. Because we believe that HIV antibodies, whatever that may mean, is a non-specific marker for the propensity of developing AIDS, we predict that in fact the haemophiliacs who are positive will develop AIDS at a greater rate. And thus this proposed study by Duesberg will not prove or disprove the HIV/AIDS hypothesis.
Eleni: Really, from the public health point of view, we are different from Peter and we are very much in agreement with the HIV theory.
Val: Except we probably wouldn’t recommend mass testing of people for HIV antibodies for any reasons.
Eleni: That’s for sure. In fact, maybe there are much better markers than HIV antibodies for the development of AIDS in the AIDS risk groups.
Val: There are. Not, “We believe…” There are better markers.
Eleni: We do believe there are better markers, you know, and more standardised better tests, more specific, more reproducible, more everything, easier to do.
Stuart: What sorts of things are you talking about here?
Eleni: For example, in haemophiliacs it is known that, you know, 98 per cent of haemophiliacs who develop AIDS test positive for hepatitis B. This, you know, is an easier test to do. I don’t know about expense but most probably it’s less expensive.
Val: There’s also the breast cancer…
Eleni: It won’t be really that… psychologically it won’t sound that bad than when you’re told that you have a positive HIV test.
Stuart: We’ve looked at possible ways of oxidative stress being the cause for drug addicts, for gay men and for haemophiliacs. What about people who have got AIDS through blood transfusion?
Eleni: First of all the number of people who get AIDS from blood transfusion is very limited. The people who get blood transfusion… the fact that they get blood transfusion means that they are sick, to begin with. The people who get blood transfusion hardly ever develop Kaposi’s sarcoma but they usually develop opportunistic infection and these opportunistic infections are nothing new. So, really, if somebody has the time and the money to conduct a study in people who test positive and people who do not test positive, it will find out that maybe… or if we look for these diseases before AIDS, maybe we’ll find out that the frequency is…
Stuart: They get the opportunistic infections but the key point is that something has affected their immune system to make it so they cannot compete with those infections.
Eleni: The disease they have, the drugs they had… because as I said, the fact that they have this blood transfusion, they are sick. They are treated for this. In America I think 20 per cent of people who get blood transfusion get blood transfusion related to cancer. Now, people who have cancer… first of all cancer will reduce your ability to fight infectious diseases. The chemotherapy and the radiotherapy, they are both known to induce opportunistic infection.
Val: In fact, in the AIDS definitions within arbitrary time limits, you’re excluded, or used to be excluded, as an AIDS case because you’d had something which was known to induce the same conditions. The whole problem with transfusion is one does not know what happened pre-AIDS. Don’t forget that all these AIDS diseases are… none of them are new. You would expect them… these diseases occur every so often in people who are otherwise healthy. I mean, I’ve seen it myself.
Eleni: In fact the first person who has been reported… it was a child who has been reported as having AIDS due to transfusion… if one goes and looks close… in fact the (Inaudible) I think to say that we do not know if this child has AIDS because of the blood transfusion or because he was premature and he really was prone to develop AIDS. In fact he did not have AIDS. Clinically he did not have AIDS.
Stuart: What case are we talking about now?
Eleni: It’s the first case which was reported of HIV and AIDS acquired through a blood transfusion.
Val: You see, one of the problems here is that apart from the fact you don’t know what the statistics were before AIDS came along, you don’t… we all know of people who say that they know someone who knows a case of AIDS that occurred after blood transfusion, but when you try and get the details, they’re often very dubious. They’re clouded in obscurity. And given that the disease has occurred before anyhow, that a lot of people who get given blood transfusions are, as Eleni says, sick, subject to other forms of therapy which themselves can cause these diseases, and given the fact that AIDS has consumed many diseases for itself by definition, one has to ask the question: is there anything different apart from HIV, serostatus if you like, about blood transfusion recipients than there ever was ever before? We don’t know. We doubt it.
Eleni: No, not only we doubt it, I don’t think it’s new, I don’t think it’s anything new.
Stuart: But we would have expected to see the same pattern in blood transfusion patients after screening of blood if there wasn’t the problem?
Eleni: Yes, there is evidence for people who have received blood which was screened to be negative, the recipient developed AIDS and seroconverted and the donors remained for years sero negative and healthy, and this is CDC data.
Stuart: But that would… you couldn’t tell… unless you knew what other risk factors those people were exposed to, those specific cases wouldn’t necessarily help you?
Eleni: No, this is CDC data and they excluded every other single risk factor. In fact they said, there it is, we have, you know…
Stuart: What about the cases of the famous AIDS babies in Queensland where they were able to trace the source of the blood to someone who also became sick with AIDS?
Val: We don’t know these cases. We can only comment if we saw the data. This is one of the problems, finding out the data, finding out what really happened. I mean, people put these cases up as if finding a case like this proves the whole HIV/AIDS hypothesis. I can tell you of cases where a man and a woman are married and live together and one gets melanoma and the other one gets melanoma. Now, does that prove that melanoma’s transmitted? You cannot use these cases to prove your hypothesis. Hypothesis can only be proved really by injecting pure HIV into human beings and see what happens. I mean, obviously it’s unethical to do that but, I mean, you have to… at some stage we have to agree what criteria we will accept as proof.
Eleni: Apropos of that, when Montagnier first isolated HIV from haemophiliacs, he said… commenting, he said the only way to prove that HIV is the cause of AIDS is to have an animal model. Even today, ten years after, we have not got an animal model.
Val: But they do… there are… they’ve infected chimpanzees that cost, what, $50,000 each and they’re all healthy.
Eleni: Doesn’t matter how much they cost. They have injected them long, long ago and they’re still healthy. There is no animal model available.
Val: This isn’t necessarily an argument that proves HIV can’t be the cause of AIDS, not at all, but I mean, at some stage if we were debating this with a scientist, we would have to agree on what we would accept as being a chain of events that would be a causal link, and you certainly can’t use one case of someone getting AIDS from a blood transfusion, given all the other constraints, plus the fact that 85 per cent of cases reported to the CDC only are actually subsequently shown to be AIDS. 15 per cent are over diagnosed. I mean, that surely must apply on average to blood transfusion recipients as well. We suspect that there is not really… if there’s an increase in the number of cases of AIDS, in inverted commas, in blood transfusion recipients, it’s probably due to the fact that people are looking for it or due to the test.
Stuart: My understanding of the data, and I haven’t got comprehensive… I haven’t got detailed data to put to you, but my understanding of the data is that there was a short period of time when people whose only risk factor was blood transfusion became sick with AIDS or became HIV positive, and once the testing was introduced, then that number has now dropped to zero, dropped back to zero.
Eleni: But today nobody tests transfused patients. They tested them when they thought it was due to it and now nobody tests transfused patients.
Stuart: But if someone gets sick or shows any symptoms or anything like that, then they are tested and at that stage…
Eleni: No, they are not.
Stuart: I thought they would be exposed to testing through giving blood themselves.
Eleni: If somebody gets blood transfusion and develops septicaemia or develops tuberculosis, even if he dies from septicaemia or from tuberculosis, they will be just people who have died from TB or have died from septicaemia. They are not going to be AIDS patients.
Stuart: If someone was dying from tuberculosis in this hospital, would they be tested for AIDS?
Val: Probably not. The problem… I say probably because CDC have recently added pulmonary tuberculosis, for reasons unknown, to their list of AIDS indicator diseases. So up until the beginning of this year, I can confidently say no, and I know from talking to my colleagues here that patients who are not dying of pulmonary tuberculosis but who could be very sick are not tested for HIV, not at all.
Eleni: Or even for septicaemia, even dying from septicaemia which, you know…
Val: And recurrent pneumonia is an AIDS defining disease. I mean, we see people who have pneumonia twice in a year. They don’t get tested for HIV. I mean, it’s a very biased testing, very biased indeed. And don’t forget at the background of all this is this problem of it being a non-specific marker. It might be that all people who are destined to die become HIV positive. It might be a marker for impending death from many causes, like wrinkles or superannuation problems. You may laugh but, I mean, in logic there is no reason why it shouldn’t be. We only think of it as a virus because we’ve been programmed to accept the fact that this must be the case.
Eleni: In fact really, you know, this is I think a very good point because the only relationship which… or the only evidence we have or is presented as being… the only data which is presented as supporting the HIV theory of AIDS is the relationship between the antibody tests and AIDS. There is no other evidence.
Val: Yes, that’s right.
Stuart: What you are saying is that that test is actually a truism?
Eleni: Exactly.
Val: It’s a tautology. It’s a loop. Self-referencing.
Eleni: In fact that is why we decided to really look, to have a close look at the antibody tests.
Val: See, initially we… as I was saying the other day before the interview, we decided that we didn’t get anywhere by knocking HIV. The responses of the referees were mainly pejorative remarks about us from one of the medical journals we submitted it to. As I said to you before, we postulate this to be because of the attractiveness of the germ theory of disease, because, you know, it’s nice and people will have a little agent which causes disease. If you get rid of that agent, you get rid of the disease. So we decided, well, everyone understands the tests. The man in the street understands the implications of the test. The clinical doctors… you know, the general practitioners and specialists who treat these patients relate well to the test. Let’s look at the test. Let’s see if the tests really mean what they say they mean, and we produced this huge article about the tests which we’ve referred to.
So every time we get away from that and forget that we’re actually talking about a whole lot of non-specific stuff, then we’re really not entitled to talk about HIV. Scientifically we’re not allowed to talk about it. It’s best said as… every time you say to us, what about people who are infected with HIV or have AIDS, you’re talking about people who have antibodies to certain proteins which are stuck in western blot strips. That’s what you’re really saying. You’re not entitled to say any more than that because there is no proof of any more than that.
Eleni: And you don’t know what these antibodies… I mean, AIDS patients have antibodies to everything you care to mention.
Val: Yes, I can vouch for that because I had to type a list of the anti antibodies once in one of the papers and I got tired. I must have typed anti something thirty times. And I suspect they’ve got antibodies to substances which we haven’t tested for. I’m sure that’s the case, and antibodies to things they would never normally come into contact with showing the cross-reacting problem. So I mean, each test can’t be specific when you find them in mice and…
Stuart: You’ve called for a scientific debate about this issue. What kinds of opportunities have you had within your local medical community here in Perth to debate and discuss these issues?
Val: Well, I think we’ve probably had opportunities but we haven’t been terribly pushy. I mean, we could have been a lot more pushy, but that’s to be quite…
Eleni: No, we are not pushy because from… shall we say from the beginning, we are in very good relationships, shall we say, a very friendly relationship with all the immunologists and the people who look after… with John Armstrong, you know, who is considered to have been the first person to have shown HIV in AIDS patients. We’re on very good terms with all of them, but from the beginning we agreed to disagree as to what causes AIDS, and we’re continuing to do so.
Val: I think we have been… I know that we’ve been regarded as an embarrassment to some people for our views, which is fine, but it’s the fact, and it’s an unpopular view. I mean, I don’t know whether people think we’re crazy, but…
Eleni: We may be considered as an embarrassment and maybe it’s nothing, but I never had any problems of getting help, apart from experiments. We cannot collaborate in… we did collaborate once.
Val: We did have a little bit, but I mean, I don’t know. I don’t think I’m paranoid but I just think there’s an unwillingness to embrace our ideas. And if there’s an unwillingness, then obviously there’s not enthusiasm to do the experiments. The medical superintendent of the hospital…
Eleni: But you cannot blame them. Somehow I don’t… not somehow. I don’t blame them.
Val: We understand them, that’s all right. They don’t believe this stuff.
Eleni: We are putting so much work on this, on our theory, outside. I mean, we never got any money, we didn’t get any help. We work a lot. We spend our weekends, our nights, our everything, doing…
Val: And if we’re right and they’re wrong, if that… there’s no doubt we both can’t be right. I mean, there’s no middle ground in this. I mean, toxic is not the same as infectious. Then we will naturally… it’s… when you’ve got points of view which are completely opposing, it would be almost – in human nature – [impossible] for one side to help the other, in my view. The medical superintendent’s been quite helpful in at least allowing us to sort of talk to journalists and newspapers and…
Eleni: No, everybody’s been… immunologists and everybody, I mean, they don’t believe us but if you go to them for help… if I go and ask, you know, something, if I discuss their findings, they don’t mind it at all.
Val: One of the immunologists has just agreed to allow us to use some data from one of his patients in a paper we’re writing at the moment. So I mean, they are…
Eleni: They are very helpful and, as I said, on the other hand I don’t blame them that they don’t believe us because… how do you say?
Val: They have to unbelieve themselves to believe us.
Eleni: Not only that, not only to… no, it is to come to see what we are saying, to be able to criticise or to discuss what we are saying someone has to spend a lot of time and effort to do it.
Val: That’s true. There’s a lot of prior knowledge needed on this.
Eleni: You need so much.
Val: But let’s get on with the question. The other things we’ve done…
Eleni: But this is important because, you know, you can’t blame them that they don’t believe us because to believe us or to criticise us, they have to do an enormous amount of work and they have not got the time.
Val: It’s probably not as important to them as it is to us because they’re very busy people. I mean, we’re busy people but they’re busy in different ways. The other things we’ve done…
Eleni: I spend my life…
Val: Other things we’ve done to get noticed, we did present… about a year ago Eleni and I presented a short talk on this in Sydney at one of the college meetings, but it was to a group of people, emergency physicians who really couldn’t expect to be a full bottle on this and who, quite frankly, I don’t think believed a word of it. I’ve corresponded with a couple of people, AIDS experts within Australia, and we haven’t really had much joy out of those people. I mean, I won’t name them but they’re well known. One person was very polite and commented on things which were sort of out of date but when pressed did not answer the specific questions which were asked.
We’ve done some funny things. We tried to get Elton John interested in providing money for this at one stage by writing to him, or at least to his publicists, but we didn’t get anywhere with that. We’ve approached a few newspapers in Sydney.
Eleni: No, we did not approach them; they approached us.
Val: No, I approached some through my uncle who’s a retired journalist. The fact that rather ironically, when the Biotechnology article was popularised through the London Sunday Times and newspapers from everywhere approached us, we were sort of tongue tied. We didn’t quite know what to say because we do prefer the scientific debate rather than…
Eleni: No, it’s not that we don’t know what to say and how to say it. It’s that we don’t want to have a debate on TV, radio or any other popular media because we think that neither side can gain by having that kind of debate, and certainly the patient cannot get… it will put the patient in a turmoil. So the only way this problem can be solved… I mean, we think there is a problem. The other HIV people do not think there is a problem, but the only way this problem can be solved is through the scientific media, through scientific journals.
Val: Yes, and the short answer is that if enough experts or para experts, people close to the problem, people treating patients, even some patients themselves, I suppose, sense that all is not well with the HIV/AIDS hypothesis, then this debate will happen and will happen properly, but there’s no way that we can get up and convince twenty experts they’re wrong and change course.
Eleni: I think the only way to solve the problem is to be able to convince the HIV people that there is something wrong.
Val: But we have to convince them first that there might be something wrong so they debate it.
Eleni: If the patient realises that, then it will be a big problem for everybody.
Val: We think we’ve got the science part of this right, our view, but we haven’t got the politics part right and we don’t even know whether that’s our game.
Eleni: Certainly politics is not my game.
Val: None of us are experienced in this sort of thing.
Eleni: And John Papadimitriou and even you are not.
Val: No, I’m not experienced. We’d probably get done on a television…
Eleni: And we don’t want to. I don’t want to be…
Val: We talk about writing a book but we haven’t done it yet.
Stuart: If there was to be the opportunity to do one set of experiments that would advance your case, what would that set of experiments be? What would you like to do to be able to firm up your case experimentally?
Val: Well, to tell you the truth, we can’t tell you the answer to that question. We know the answer to that question but we’re not prepared to tell you in case someone else does the experiments before us.
Eleni: That’s not true.
Val: That’s exactly how I feel. These experiments can be very easy and if positive, they would be utterly devastating to the HIV/AIDS hypothesis, but I’m not prepared at this stage to tell you what they are, but I assure you we have them. All we need is some money, and not very much money, to do them. We’re planning one. Do you want to add anything to that, Eleni? I’ve told the truth as I see it.
Eleni: Experiments are not that easy. We don’t need that much money, that is true. I mean…
Val: We need some money.
Eleni: Certainly we need some money. I mean, we are very… John and I… we’re all… AIDS is not our main work. We are busy doing other things.
Val: Earning a living.
Eleni: Earning a living. AIDS is our… I was going to say our love; shall we say…
Val: Obsession.
Eleni: Obsession; is our scientific obsession, but we have not got the time and even the expertise to do the experiments. We can design them but, you know, when it comes to actually practically
doing them, I mean, for sure I haven’t got the expertise. So we need money to employ people to do the experiments and to have the right equipment, to have everything. We do need money but not money… not even a very small proportion to… I mean, infinitesimally small proportion comparing to what is used today.
Val: And this would be basic scientific research.
Val: A little bit more about blood transfusions.
Eleni: I discuss that in my first paper but I just can’t find where I had it, because I really said… because it’s a very, very… millions of people are transfused annually in America and the number of AIDS cases in transfused patients is really insignificant. As we said before, these people, you know… the reasons that they are getting the blood tell… they’re getting blood because they’re sick, and for sure some of the diseases, if not all, and the treatment which is used for them will induce the diseases which today are called AIDS. That has been going all the time, so we can’t say that in blood transfused patients… in fact nobody will say that the clinical picture in blood transfused patients is different today than it was before the AIDS era. The only difference we have is that when these persons are tested, the ones who are… many are not, but the ones who are tested test positive for HIV.
Stuart: We’ve been talking about AIDS and the acquired immune deficiency syndrome but we haven’t really spoken about the immunodeficiency characteristic of AIDS. I’m wondering what you think about that? Does the oxidative stress account for the immunodeficiency or do you see immunodeficiency as a significant factor in all this? What is your view about immunodeficiency?
Eleni: Immunodeficiency in AIDS really is a decreased number of T4 cells as determined by the use of antibodies, specifically raised against T4 cells. Now, the fact that when blood from an AIDS patient is tested or from a person who is at risk of developing AIDS, fewer T cells bind these antibodies is interpreted as being proof that the T4 cells in those individuals are killed – are destroyed. As far as we are concerned, the fact that fewer antibodies, or shall we say fewer cells, bind antibodies direct against T4 cells is not proof that the T4 cells are being killed.
Val: Especially being killed by HIV.
Eleni: By HIV or by any other agent. To us this proves that these cells do not bind the antibody and is not due to cell destruction. In fact there is evidence to show that this is the case. We still have not published that but we’re going to publish it in the future.1 That is one side. The other side is that we do not believe the T4 cells decrease… because according to the HIV theory of AIDS, HIV destroys, kills the T4 cells and the destruction of T4 cells or the decrease in T4 cells leads to the development of Kaposi’s sarcoma and opportunistic infections, all different kinds of diseases which are called AIDS. In our view, T4 cells play no role in the… there is no relationship between T4 cells… put another way, there is no relationship between the T4 cell number and the development of either Kaposi’s sarcoma or other neoplasms or opportunistic infections.
Val: In fact, if we go back to the example of Kaposi’s sarcoma, about the CDC view that HIV is neither directly nor indirectly the cause of Kaposi’s sarcoma, some data from this study is that you can get Kaposi’s sarcoma in the absence of HIV and also in the absence of immune deficiency. So, as far as Kaposi’s sarcoma is concerned, it is now not due to HIV and it is not always associated with immune deficiency.
Eleni: No, it is agreed now, you know, and this is one thing which is agreed and is still the HIV theory.. nobody questions. To me that is… you know, if you do not have any other evidence, the fact that even the CDC today admits that Kaposi’s sarcoma is not related either to HIV or to immune deficiency, this questions the HIV theory of AIDS. And they were forced to admit it. There are two reasons. One is that Kaposi’s sarcoma was appearing only in gay men. Now, the only way to get by this is either to admit that AIDS is not caused by HIV, the different groups have different etiological agents, or to say that Kaposi’s sarcoma is caused by a different agent, but HIV, never HIV, no T4s or immune deficiency plays any role. The thing is… but now today we have evidence that not only Kaposi’s sarcoma but pneumocystis carinni pneumonia, the other…
Val: The large group of indicator diseases.
Eleni: …can appear in the absence of HIV and T4 cell decrease in gay men.
Val: So these are HIV negative, immune deficiency negative AIDS cases.
Eleni: You can’t say immune deficiency negative. You can call them immune deficiency negative, all right?
Val: And that more or less wraps up AIDS for two of the diseases. I mean, not all cases but it happens. They are the exception to the theory which means the theory must be re-examined.
Eleni: On the other hand, you can have people with chronic shortage of T4 cells, they never develop opportunistic infections.
Val: Just summarise the evidence about the fact that there’s no evidence that HIV kills T4 cells.
Eleni: Nobody has proven either in-vitro… there is no evidence either in vitro or in-vivo that HIV kills T4 cells. Without going through all the evidence, suffice to say that in 1985 or ’86, I don’t know the exact date, Zagury and Gallo – Zagury is one other well known HIV expert – they have proven that you cannot get decrease in T4 cells in the petri dish unless you put another chemical which they are using and which is used in all the AIDS cultures, is called phyto haemogglectonin. * But if you have phyto haemogglectonin by itself without HIV, you’ll get the same effect: you’ll get a decrease in T4 cells. Now, last year – was it last year? – Montagnier’s publication… they say now that the HIV kills T4 cells by a process called apoptosis. Montagnier found out that when he has HIV and phyto haemogglectonin, PHA, he gets destruction of T4 cells.
Val: …by this mechanism, apoptosis. It’s a morphological and biochemical description. It’s a process which is well recognised.
Eleni: It’s a description of killing. Now, but if he has PHA and he says, “Incredibly”. It must have been a translation from French. He said, “Incredibly, when we had only PHA and not HIV, we’re still seeing the same phenomena”. So, this is obvious to any scientist. If you have HIV by itself… if you have only HIV and you… HIV… now, let’s admit that this HIV exists. So if you put in the petri dish HIV and you don’t put PHA in, nothing happens to the cell. The cells are happily living forever after, maybe forever. They don’t… you know, the cells can’t live forever after, but they live… nothing happens to them. If you put PHA and HIV, you get cell destruction but if you put PHA by itself without HIV, you can still get cell destruction. So it is obvious what causes the destruction of T4 cells in the petri dish is not HIV.
Val: The other problem with HIV and T4 cells is that there should be a demonstrable proper temporal relationship between the two. That is, the HIV theory is that you…
Eleni: You don’t have to go to… these are the experiments, you know, which…
Val: I know, but it’s just… I wanted to introduce the New York data on drug users, about…
Eleni: Not only drug users, gay men and everybody. Now, if you go to… sorry, Val.
Val: No, you carry on.
Eleni: No, you better.
Val: There’s data from drug users in New York which show that the risk of seroconverting is whether you’re immune deficient before you seroconvert. In other words, if you prospectively study a large group of drug users, you find that one of the risk factors for actually becoming HIV positive is whether you are immune deficient before you’re seroconverted, not the other way round. This is just not on.
I mean, if the theory is that HIV infects T4 cells and kills them – and this is what the theory is, although the HIV protagonists do not know how HIV kills T4 cells, and we doubt whether it actually does kill them, it just sort of changes them in some way, because they are low. We’re not saying they’re not low. This shouldn’t happen. I mean, this is the wrong… this is the cause before the effect. It’s not on.
Eleni: You know, instead of having first HIV and then T4 decrease, to have HIV you need T4 decrease. This is a good, prospective, well-designed study.
Val: Studied over many years.
Stuart: But couldn’t that be explained by if your immune system is low, then you are more susceptible to infection, including infection with the HIV virus?
Eleni: But then we don’t have HIV. But then why do you need HIV? If you have to be first immune deficient and then you develop HIV, then you don’t need HIV because…
Val: You don’t need HIV to become immune deficient.
Eleni: Not only that you don’t need HIV to become immune deficient, but you don’t need HIV to develop all the other infectious diseases, because if immune deficiency… and you have first immune deficiency and then you have HIV, why you shall have HIV and then the other infectious agents? Why all these infectious agents don’t come in parallel? HIV cannot have priority. All the other infectious agents will be equally as…
Val: Well, the theory goes HIV, immune deficiency, then the diseases. I mean, HIV has factored itself out.
Stuart: But what I guess I’m saying is that it can be more complex than that, that you can have a kind of… if you’re infected with the HIV virus, once you’re infected with it, it affects your immune system but if your immune system is low to begin with, then maybe you’re more susceptible to getting infections. A certain number of people are exposed to the virus and only a certain number of those get… actually get infected with it.
Eleni: That is true, not only with…
Stuart: But more people would get infected who are immune deficient.
Val: That could be true but that’s not the explanation for AIDS.
Eleni: Not only that is not the explanation for AIDS, it’s the fact that why should… then why do you need HIV? You know, that’s the question. Why do you need an intermediary? You don’t need an intermediary. If you have the immune deficiency, and that’s what they think in this prospective study, it’s not one case. Here it is, a prospective study, a large study, and here it is they say “We don’t have it. The only way you can get HIV seroconversion is to have immune deficiency, and never the other way round”. Not first HIV and then immune deficiency. Now, that is one.
Secondly, is the fact that if you have first immune deficiency and if the diseases which are called AIDS are due to an immune deficiency, then why do you need the intermediary? Why do you need HIV? You don’t need HIV. We have to really stretch it then. I mean, you can assume anything you want. You can put any hypothesis you want but to me it is logical because all the other viruses… you know, it’s not only HIV which induces immune deficiency. Epstein-Barr virus induces immune deficiency, cytomegalovirus induces immune deficiency – all the infectious agents, not only viruses, induce immune deficiency. Then why HIV has all this… why do we make this virus… why do we give all…
Val: Why do we make so many exceptions?
Eleni: It’s not just the exceptions. I mean, we give to HIV so many qualities and so many…
Val: That’s right, including its continental preference; its subgroup preference.
Eleni: And trying to avoid the immune deficiency changes – because that’s the theory, that HIV changes to avoid immune deficiency. It’s a very clever virus. I mean, we never had anything like this today. As I said, you can stretch the HIV theory to no end and really now it is stretched because Montagnier says that… that’s what we did not mention because Montagnier now says that HIV is not sufficient.
Stuart: That brings in cofactors?
Eleni: That brings in cofactors, but if the cofactors can do without HIV, and that is all the evidence everywhere, if the cofactors… if you can’t have HIV unless you have PHA, and PHA can do the same thing which is attributed to HIV without HIV, why do you need HIV there?
Val: The other thing, Stuart, is that if you accept HIV as being a respectable, properly isolated, to use an Australian term, dinky-di virus and that it can cause AIDS, if you like, then how do you account for the fact that in the consortium study which was published in JAMA, I think, wasn’t it, by Lundberg et al in 1988, using the least stringent criteria for diagnosis, only 79 per cent of AIDS cases are infected with HIV?
