Eleni: In fact, not only that, but let’s be fair to Gallo because Gallo repeatedly said that finding reverse transcriptase and particles is not proof of the existence of a retrovirus. It’s not proof of isolation of a retrovirus in the culture and even of its detection. The only thing which Gallo considers as proof for the existence of a virus in individuals is to find antibodies which react – antibodies in the sera of people – which react with the proteins which are found in the test tube.
Stuart: And you have problems with the antibody theory as well?
Eleni: Yes. In fact, that is our main… one of the main themes in our…
Val: Could I just add here, speaking as an outsider in a sense, that the term “virus” is used interchangeably. It’s very important for people who listen to this tape to realise that the term “virus” is used in two different ways. When electron microscopists look at these particles, they use the term “virus” in a morphological sense; that is, they describe what they see. When an ordinary person uses the term “virus”, they think of something like the flu or a cold, something which has associated with it the ability to infect an individual and then pass the same infection on by means of this agent. Now, it’s fair to say that strictly scientifically, before you can use the term “retrovirus” in the sense that it’s an infective exogenous agent of disease, that you have to have proof that the latter occurs. And it’s unfortunate that the term is used interchangeably. Does that come across to you?
Stuart: Yes, it strikes me that you’re talking about the difference between what they’re actually seeing in the dish and what’s actually making people sick. But people are getting sick. There is no question that there is something that is making people sick, and we’ll come to what you think it is in a moment. But, in looking at the cellular material from people who are sick or who are infected, to use the generally accepted term for what’s happening here, are you not seeing a combination of things when you look at them – electron microscope or petri dish or whatever – which is different from people who are healthy?
Eleni: No, you can see the same combination of things, you know, in a petri dish even if people are healthy. That’s one.
Stuart: But you’re not… you wouldn’t get the antibody reaction?
Eleni: No, the antibody reaction you won’t get with a healthy person – although there are many healthy people, you know, which… in fact, 10 per cent… with the most stringent criteria they’re using to define a positive test, 10 per cent of healthy people test positive. So there are many healthy people, or people who are not at risk of developing AIDS, who test positive. Now, the other thing is: the fact that AIDS patients test positive, they have a positive antibody test, does not mean that the antibody which is in these people is really an HIV antibody. The antibody can be directed towards many other infectious and non-infectious agents which the AIDS patients suffer from. Then it can cross-react with the so-called HIV proteins.
So, we don’t have proof that really the antibodies which react with the HIV proteins… let’s say the proteins or the particles there, they are HIV, you can’t define by definition, you know – just because you find a reaction you [can’t] say that that is a reaction due to antibodies or due to infection of that person with HIV.
Val: Perhaps we need to explain in a little more detail what the AIDS antibody tests actually are because this must be of interest in the clinical dimension, because people go to doctors and have AIDS tests.
Eleni: How can you determine a proper test? How can you evaluate an antibody test?
Val: The basics of it are that it is believed that foreign material injected or getting access to the body causes the body to make proteins called antibodies which react with these and are supposed to neutralise their effects. In the case of HIV, to do the test you need to have two things. You need what they call HIV and you need some blood from the patient and these are reacted together and the ensuing reaction is somehow measured.
Now, the source of HIV is not, as you may imagine, a pure suspension of millions of tiny little retroviral particles. It is, in fact, a number of proteins derived from cultures of tissues from AIDS patients with other added chemicals – the petri dish we referred to before – in which some purification or separation has taken place by means of ultra centrifugation.
Eleni: Or filtration.
Val: Or filtration. Now, we have to assume therefore that the proteins that are obtained by this methodology are in fact specific for HIV, and there is no evidence… there’s no data to support this. In fact it’s admitted by the AIDS experts themselves that 80 per cent of the proteins obtained in this manner are in fact cellular and non-viral.
Eleni: The only reason that they are called HIV proteins is because they react with AIDS patient sera, but you can’t have that as proof that they are HIV. First, we have to prove that they are HIV and then you have to look at the reaction. You can’t go the other way round, you know, like Gallo and Montagnier, you know. You find that this protein reacts with AIDS patient sera and, because they react, they’re HIV.
Val: Just to continue in that vein, the preparations are not pure and, even if they were pure let us postulate, then if we look at the particular proteins which are believed to be specific for HIV, the important proteins, then there is data which is discussed in our Biotechnology paper that for each one of these important proteins, there is evidence that indeed these proteins are not specific for HIV.
Now, if we assume these proteins are specific; that is when you react the patient’s blood with these proteins, that you’re dealing with proteins which come from a unique agent, that is HIV, that still does not prove that the antibodies present in the patient’s blood were made in response to the foreign stimulus, HIV, because antibodies by their very nature – and there’s no disputing this fact – may cross-react with many other proteins, other antigens.
The only way to prove that the antibody-antigen reactions that are seen in these tests mean the presence of a particular agent, in this case HIV, is to verify the tests in parallel with a gold standard, that is another independent, not related to antibody antigen reactions, way of determining the presence of HIV. And in the case of HIV this has to be the isolation of HIV itself. There’s no work has ever been reported that this has ever been done. In our Biotechnology paper we go into this fact and we also explain why, in our opinion, if this was ever attempted, there would be considerable problems in achieving this end.
Stuart: What does this say about the clinical usefulness of the tests?
Val: We say, as a succinct summary of the situation as we see it, that the relationship between the antibody tests, the so-called HIV antibodies, and the virus is completely and utterly unknown because of this gold standard problem.
Eleni: Now, if you want to use the antibody tests as a marker for future development of AIDS, then that’s all right. But you cannot say because you have a positive antibody test, you prove the existence in the patients of HIV. As long as you take that into consideration, as long as you don’t say a positive antibody test is proof of HIV infection, it’s all right.
Val: And in this regard, it’s useful to give a couple of examples of this that people will understand. It’s well known that if you get an attack of glandular fever, for example, which is a disease most people have heard of, then the doctor can do a test on your blood to see whether you’ve been infected with the putative agent of this condition. The test that the doctor actually performs – that he orders and is performed in a laboratory – is a test to detect antibodies which react with the red blood cells of sheep. Now, this is a well known test, it’s called the Paul-Bunnell test. It’s ordered every day in surgeries all around Australia and it works. But one cannot say from this information that people with glandular fever are infected with sheep red blood cells or that sheep red blood cells are the cause of glandular fever.
The other example we often use is the example of syphilis. One of the syphilis antibody tests which predicts the likelihood, the propensity, to develop syphilis in individuals, is where they have antibodies to ox heart proteins. And this is used as a screening test, if you like, for syphilis. Again, no one is postulating that patients with syphilis are infected with ox heart or that ox heart is the cause of syphilis. So, it’s important to always examine what you think a test is telling you and what you really are entitled to know.
Eleni: And to interpret… how you’re interpreting. It’s the difference between what the actual test tells you and how you interpret it. If you want to, you know, use the so-called HIV antibody tests for a prediction of AIDS, that’s quite all right.
Val: It’s quite all right in the high risk groups.
Eleni: Exactly. You have to be very, very precise here. It’s quite all right in the high risk groups. But the same test in the population at large doesn’t say anything, even about the development of AIDS.
Val: And the reason we can say that is because there is no data on the predictive value of these tests in otherwise healthy people, and it would be now very difficult to obtain this data because persons who are told they are positive believe that they are infected with a lethal human retrovirus for starters and secondly, they may be treated with drugs as a result of this which in turn may make them sick for other reasons. It’s almost an experiment that one cannot do at present. It’s terribly important to get this point across: that it’s fine to use the tests as a marker in high risk groups but to turn around and say to a healthy individual that “You are infected with a human retrovirus, HIV, on the basis of these tests” is not scientifically allowable.
Eleni: Not even a healthy… even a non-healthy… even an AIDS patient, you can’t tell him, because the test is positive, he is infected with the retrovirus, unless you have proof that these tests indeed mean the presence of a retrovirus which, to date, we haven’t got.
Stuart: There is a great deal of testing of healthy people, particularly through the blood transfusion service, where blood is tested routinely and very, very few cases of positive findings are emerging in those studies. So it would be highly indicative if there were… if it was positive, that there was something else there, especially if you could do the test again in a week’s time and find that it was still positive.
Eleni: Let’s continue with the example which we already gave with syphilis. If you test normal people, blood donors, for antibodies to ox heart, you hardly find any one of them testing positive, but if you go and test IV drug users who are not infected with the agent which causes syphilis, you find about 20 per cent of them testing positive, although they don’t have the infectious agent – 20 per cent of them will test positive. So testing normal healthy blood donors does not prove anything about the specificity of the HIV antibody tests. What you have to do is to test sick individuals who you know they are not at risk and they never develop AIDS.
If you look in the literature, you’ll find out that many of these groups of people, including people with lupus erythematosus, people who have organ transplants, a high per cent of them have positive HIV antibody tests, but that does not prove that they are infected with HIV.
Val: I think it’s important to emphasise this point about specificity in relation to testing healthy blood donors, because we know from our correspondence with the authorities in Australia that the specificity of the HIV antibody tests is verified by testing five thousand healthy blood donors. Now, you would not expect to find healthy people making antibodies to anything new or different. That’s what health is all about. But the way the specificity is defined, defined as the number of negative tests in people who do not have HIV infection, you will conclude, erroneously, that these tests are highly specific as an artefact of the way you’ve selected the population you test for specificity on.
In America there was a study called the Sentinel Study which is at odds and supports our view that in fact people… we don’t know how healthy these people were but they were in hospital but they had everything else excluded that was vaguely AIDS related, even from the point of view of being people who’d had car accidents, because…
Eleni: Gunshots.
Val: Gunshots… and it depends which hospital they looked at. I think there were twenty-six hospitals looked at and they found antibodies in somewhere round one per cent to around 1.6 or 1.7 per cent.
Eleni: More than that, 1.7 per cent I think it was.
Val: But this was interpreted as proving that HIV is prevalent in this particular population rather than the obvious, that is, that the antibody tests are non-specific.
Stuart: You also argue some specific problems with the western blot test which is used to confirm cases when the Eliza test indicates that a person is positive in the first place.
Eleni: Well, in addition to the fact that nobody has proven the specificity of the western blot, although it’s been considered to be 100 per cent specific, there is no antibody test or any other test used in medicine, I’ll say, which is 100 per cent specific. Yet, the western blot is considered to be 100 per cent specific without ever its specificity being determined. So that is really a big problem with the western blot. But, in addition to that, there are many other problems associated with the western blot. One is that the western blot is not standardised. Every single laboratory, major laboratory, in the USA uses a different criteria for interpreting western blot. So it depends where you’re going – in which laboratory your test has been done. In one laboratory you may be called positive; in the other laboratory you will be called intermediate or negative.
Val: Indeterminate.
Eleni: Indeterminate. In Africa and in Asia the tests are not routinely performed. AIDS is defined only on clinical grounds, but when a test is performed the criteria used in those continents is completely different to the criteria used in Europe and the United States. So it is really impossible to come to any conclusion in regard to the relationship between a positive for western blot – doesn’t matter what it means – and the development of AIDS because there are no standard criteria.
The second problem is that the test is not reproducible. In the same laboratory, the same blot could give different results from one day to another and, certainly, the same blood – we do give one example in our paper – in nineteen different laboratories gave completely different patterns, because the western blot is read as a pattern – bands. Each laboratory gave a different pattern.
Stuart: But in all cases, close enough to be, say, all positive or all negative?
Eleni: It’s not close enough. Depends where, you know… what criteria you are using.
Val: Let’s just expand on the western blot. The western blot is a technique for actually visualising the individual so-called HIV proteins in a strip – a little strip of nitrocellulose. You can look at it. Various reagents are used to colour the bands so you can see them. They’re read by eye. The bands are the various proteins separated out according to their charge and molecular weight. Now, there are, as Eleni said, different criteria for positivity. The only thing the laboratories will agree on is that if there are no bands at all, including, which is rather intriguing, bands which do not represent reactions with non-viral proteins, the test is negative; everyone agrees. They all have different criteria for positivity. Anything that doesn’t fit either of those is called indeterminate.
Now, the criteria for positivity vary and, to make it quite simple and to bring it home, you can get on an aeroplane in one country or in one state in the United States and you can travel from Canada and you can travel back to the United States and you can even travel to Australia or you could travel to Thailand and you can be positive or indeterminate depending on where you find yourself. Now, a person may wish to know what is going on. It makes a big difference to know whether you’re indeterminate or whether you’re positive. Who can blame people for asking this question? Unfortunately, in some centres, the western blot bands are not actually reported. The judgment is made according to whoever reports them, so the clinician may not even be aware that this is an issue.
Eleni: And, in fact, you know, because we’re saying here with… in the indeterminate results. If you give people negative blood (Not recorded).
Val: The western blot is a technique for visualising the individual so-called HIV proteins. You see bands where the antigen-antibody reactions occur. It’s read visually and the proteins are accorded a place by their molecular weight and charge. For example, P41 is a molecular weight protein of 41,000. Now, in western blot reporting there are three criteria. One is positive, the second is indeterminate and the third is negative. All laboratories agree that a negative test is no bands reacting whatsoever, including, rather intriguingly, bands which do not represent reactions with viral proteins. A positive test is defined in various ways by different laboratories and an indeterminate test is one which is neither positive nor negative.
To bring this down to a thing that people will understand is that you can actually… because criteria for positivity vary, you can get on an aeroplane somewhere in North America and travel around, say, Canada and the United States, even take a trip to Thailand, and you can be indeterminate or positive depending on where you find yourself. Such a person may wish to know, not unreasonably: am I infected definitely with this lethal retrovirus or aren’t you sure? And you can’t answer in certain states, because of this conflicting data on what constitutes a positive test. I mean, we wonder when people make these pronouncements that their set of criteria is positive and the next state’s not, how do they know? How do they work this out? No one has ever explained this.
Eleni: Nobody tells you why, you know, some people consider this positive and the other people consider the other. In fact, there is no agreement, not even between two laboratories. Now, I think we already talk about standardisation and…
Val: Also this problem illustrates that one has to have the gold standard test done to sort this out. That is the only way that it can be done; there is no other way.
Eleni: This is for specificity but, you know, we still can agree. You know, even if you don’t have that, you still… before you determine the specificity… you can’t determine specificity. Before you use the gold standard, you have to agree as to what you consider are positive tests. There is no agreement what you consider a positive test, so you can’t even go to the second step to prove it is specific. And that is the problem for reproducibility. The test is not reproducible.
As we said, the test is not standardised and is not reproducible, so unless you have, you know, before you even talk about specificity, before you use a gold standard, you have to have the test… being able to reproduce the test from day to day and from laboratory to laboratory. This is not the case with the HIV antibody test. The same blood in two different days could give a different pattern and the same blood in different laboratories can give you different patterns of western blot. In fact, we have in the paper one example with the same blood being tested in nineteen laboratories and each laboratory came up with a completely different pattern of western blot.
Val: We also have examples of… in the reproducibility where tests that were known to be positive were occasionally negative.
Eleni: And the other way round, you know, in the same laboratory.
Val: These are not just any laboratories. These are in reference laboratories. This data is from reference laboratories.
Eleni: The best laboratories. Apropos of indeterminate western blots… in fact not indeterminate. For example, let’s go with people who are given HIV negative blood… negative testing, completely negative, the western blot pattern completely negative. You give them and…
Val: What Eleni means is you transfuse patients with blood known to be HIV western blot negative.
Eleni: Negative. And then you test them again after their transfusion and you find that 40 per cent of them have an indeterminate western blot, 30 per cent of them have a p24 band, this protein, p24, which Montagnier considers – you know, the Pasteur Institute which are today accepted as being the first to have isolated HIV – p24 as the most specific protein or band to HIV. In fact up… we don’t know what are the criteria in France now, but up till 1987, the p24 was considered proof of HIV presence in people.
Val: This is rather a chilling statistic, because there were a lot of people tested in the early days of the so-called… of the epidemic, the AIDS era, especially haemophiliacs who were tested back in the mid-eighties…
Eleni: Not mid-, before.
Val: Well, the tests only started in 1984 but they haven’t been tested since. Maybe some of them would not be classified as positive. I mean, I’m sure some of them at least would be classified as indeterminate if they were retested and had the same band patterns as they did then. Some of them didn’t have a western blot. Some of it was done on the other antibody test, the Eliza. The important thing also about p24 is that we definitely know that this is the case for Montagnier because Eleni actually has met Montagnier and discussed this. I mean, that’s just a little aside to make it interesting. But there’s no doubt about it that they believe this.
There’s a fascinating study from – is it Russia? – where patients have had blood… their own blood taken from them, removed and then irradiated and then put back, and I’m not sure of the percentage…
Eleni: The blood was negative, the people tested before it was reinjected, and yet, when the people were reinjected with their own blood which was irradiated, after that they tested positive for the p17.
Val: And in a similar manner there’s some data from experiments done in mice where, if you take the blood from a healthy mouse and inject it into another unrelated healthy mouse, they produce antibodies to these HIV proteins. And how one can claim that these are specific for HIV is a complete mystery as far as I’m concerned.
Eleni: The mice are not infected with HIV. That is accepted. Yet, you know, when they’re injected with blood… in fact when they’re injected, mice which are used as a model for lupus, when they’re injected with foreign blood – blood from other mice – they test positive to the two most specific HIV proteins, that is p24 and p41. So this raises questions certainly to us. These pose questions regarding the specificity of the antibody tests.
Val: In regard to this, this is one of the most frustrating aspects of the work, especially the Biotechnology paper, is although the paper which is quite long – it’s about ten thousand words – has a lot of data in it, all in a similar vein to what we’ve been discussing about the tests, we’ve never had any scientific criticism. As one of our commentators has said, none of the big shots have ever attempted to answer the issues that we raise.
Stuart: Why do you think that is?
Eleni: We do not know.
Val: We don’t really know. We don’t know whether they just haven’t read the paper. They certainly must know about it; it’s well publicised. It’s in a very well known journal. They choose not to deal with these very fundamental issues. I mean, I can’t imagine anyone listening to this not wanting to know answers to these questions. These are reasonable questions and people have a right to know about the answers.
Stuart: And are these refereed journals that…
Eleni: Certainly. Biotechnology is a sister journal of Nature which is… they’re both extremely…
Val: Top class.
Eleni: They’re considered to be some of the best journals.
Stuart: What about the people that they’ve sent your work to to be checked before it gets published? Have they not taken it up at all?
Eleni: They’re reviewers. The reviewers did make…
Val: You mean taking it up as an issue to propagate our views, you mean? We don’t… reviewers are always anonymous. We don’t know who they are. If they have, then we certainly don’t know about it. But it was done in the United States, not here.
Eleni: No, we sent it to the United States. We don’t know where the paper was reviewed. We don’t know who the reviewers are or where they’re coming from. And we did make a lot of changes to the paper. We sent in fact to the journal about three revised manuscripts. We had to change it again and again before it was published. We don’t want to antagonise people. We’re just putting scientific questions. In fact we really love to have scientific exchange, not personal, not political, not anything unrelated to scientific questions. In fact we really… I mean, I will love to have any criticism, even if somebody proves to us that what we’re saying is rubbish, we will be more than willing to accept it if we are proven that way.
Val: Absolutely. We want to keep the debate scientific. In fact, it would be nice in this interview to just paraphrase what John Papadimitriou said about how we regard ourselves. That is that we do not regard ourselves as AIDS experts; we are not AIDS experts. All we have done is taken the hypotheses that are put up by the AIDS experts and using their own data, we point out the inconsistencies in what they say. And we would like to know what their response is.
Eleni: Not only the AIDS data but the AIDS data and in addition the data presently available since 1911…
Val: 1911, when Roux started all this.
Eleni: Right, in relation to retrovirology in general. So it is discussed in view of the presently available data as well as the data in retrovirology in general. We are not… we never have seen… I mean, I never have seen an AIDS patient. I mean, I’ve seen people I know but not…
Val: Should we just, in anticipation, mention the PCR because in private discussions people say that our criticisms of Gallo’s and Montagnier’s isolation methods are now outdated because we have the polymerase chain reaction data, and this is such an exciting new development in molecular biology that people don’t often think about it critically what it actually means. Eleni, you can explain this better than I.
Eleni: I think suffice to say here that the Pasteur researchers, and not one, many, do not believe that HIV infection can be defined in terms of molecular biology because they say that there are many problems, you know, including the fact that no two HIVs have been isolated which are the same. The specificity of the polymerase chain reaction never has been determined. Even if the specificity is determined and reproducibility and everything else which is required with the tests, even if they are all set out and shown to be proper, and even if all HIVs were one and the same, you still can’t define it because finding… with a polymerase reaction you can detect only a very small part of what is called the HIV genome. But finding a small part of the HIV genome does not mean that the whole genome is there because the genome for retroviruses is… most of the retroviruses are defective. That is, you have one bit but you don’t have the rest. So finding one bit… and in fact they say that about 99 per cent of the HIV genomes are defective. So finding many bits of positive PCRs does not mean that the HIV is there.
Val: So although it’s attractive to think you’ve found a tiny piece of this genetic material of a virus that we don’t believe has been properly demonstrated, this is not – given the nature of retroviruses, that they can arise from pre-existing information that we all have – you can’t equate these two phenomena.
Eleni: In fact today, you know, there is evidence, of course presented by others, that even the normal human genome has HIV sequences.
Val: That’s referenced in the Biotechnology paper.
Eleni: And since then we had more information. So, you know, finding a bit of what is called HIV genome in an AIDS patient does not prove that that person is infected with HIV.
Stuart Reid: I wonder if we could turn to what you think is actually causing the condition that we know of as AIDS or AIDS related condition?
Eleni: In our view, as I said, again this is a hypothesis which has to be proven, is that each AIDS risk group has a different set of causes of HIV… sorry, of AIDS. You know, each group, although the disease appears to be caused by the same agent, in fact it doesn’t even appear because the set of conditions which are called AIDS in one AIDS risk groups are not the same with the set of conditions which are called AIDS in another AIDS risk group.
Although some of the diseases overlap, for example, you know, most of them don’t. Kaposi’s sarcoma is a disease. In fact, the disease for which the HIV hypothesis has been put forward, is exclusively restrained to gay men. So how can you know… if HIV was the cause of AIDS in all AIDS risk groups, then we know viruses produce the same disease – doesn’t matter in which person they are – all AIDS risk groups would have had Kaposi’s sarcoma.
Val: I think this is another point that needs to be emphasised from the clinical point of view. That is, if you take the gonococcus which causes gonorrhoea, it causes urethral discharge and cervicitis in those it affects, but it also has other spectrums. It can cause arthritis, it can cause meningitis, it can cause myocarditis, but these diseases occur in all people who get them. The people who get it in Sydney get the same diseases, the same spectrum, as people who get it in Perth. It would be a very curious pathogen that actually had a preference for one part of Australia or one city. And yet, HIV, which ties up a number of diseases in fact shows preference for which continent it’s in, because it’s different in Africa from it is in Europe and the Americas… in America, in North America…
Eleni: In fact, there is no relationship, hardly any relationship, between what is called AIDS in Africa and what is called AIDS in gay men in Australia or in the United States or Europe.
Stuart: What sort of differences are there?
Eleni: For example, the main and the most specific, shall we say…
Val: Just to carry this statement on, not only does it show continental preferences, it shows preferences for which group you’re in, as Eleni has said. This is an important point, that if you’re a gay man, you get a different subset of diseases from if you’re a haemophiliac, for example. Haemophiliacs almost never get Kaposi’s sarcoma, so the epidemiology which is often thrown up as showing that HIV is the cause of AIDS in fact is inconsistent, it’s unusual.
Stuart: Couldn’t that just be that people who are haemophiliacs die before they get Kaposi’s sarcoma?
Eleni: No, no, no, because, in fact, of all the AIDS risk groups who test positive, haemophiliacs live the longest.
Stuart: My other point (Inaudible).
Eleni: They live the longest. In fact, the rate of AIDS in haemophiliacs is much, much lower. This is another point. Thank you for mentioning it. I mean, if HIV causes the disease, then once you are infected, the rate of disease development should be the same in all the AIDS risk groups. In fact, if anything, in haemophiliacs it should be much higher than in gay men because gay men to start with are healthy, whereas haemophiliacs are born with a disease, they are abnormal, at least in one respect, compared to gay men. Yet AIDS in haemophiliacs, the rate is much lower than the gay men.
But again about… because you ask me, you know, in what respect it differs… again, because we start with Africa. As I said, the more specific and principal clinical syndrome or diseases of AIDS in gay men is PCP and Kaposi’s sarcoma. Now, pneumocystis carinni is a ubiquitous organism, it exists everywhere in all continents. Yet, African AIDS patients never develop pneumocystis carinni pneumonia. They do have Kaposi’s sarcoma but Kaposi’s sarcoma existed in Africa for ever, and in fact…
Val: Kaposi’s is interesting because it’s recorded in one of the ancient Egyptian papyruses, the Ebers papyrus which dates to 3,500 years ago, long before the time of Christ. So we can say with certainty about Kaposi’s sarcoma that it did antedate in Africa AIDS by a long time.
Eleni: Not only that, but it was very extensively studied in the 1950s and sixties because it was… like, in gay men now, there it affected young individuals, it was very aggressive. But all the studies… and they were looking really… they were looking to find out an infectious agent, to correlate Kaposi’s sarcoma with an infectious agent. In fact, that was the reason that they went… it was done by non-African doctors and they still could not. The conclusion was that Kaposi’s sarcoma is not caused by an infectious agent in Africa but by some either environmental or other agent. We don’t know what.
Val: And in fact in that regard, it’s interesting to note that the official view now from the CDC in America is that Kaposi’s sarcoma in gay men is no longer caused by HIV.
Eleni: Not caused by HIV, is not associated. Not only is not caused… it’s not indirectly caused by HIV, but it is not associated with HIV. In fact, they had to admit that because in the other AIDS risk groups, Kaposi’s sarcoma doesn’t exist.
Val: So it’s almost come full circle. Kaposi’s sarcoma was the reason the HIV hypothesis was originally put forward, and now it’s dissociated. So one wonders whether those gay men who only have Kaposi’s sarcoma as one of their AIDS diseases should be declassified.
Eleni: But to me as a physicist, in fact that was one of the… we wrote a lot of papers on Kaposi’s sarcoma, and to me the fact that the HIV hypothesis was put forward to explain Kaposi’s sarcoma, and its prediction is admitted now to be erroneous, is sufficient to question the HIV hypothesis as a whole.
Stuart: Just looking at that situation of there being Kaposi’s sarcoma in Africa, wouldn’t the alternative hypothesis regarding that though be that AIDS was around in Africa and was indicated by Kaposi’s sarcoma?
Eleni: No, because as… there are many reasons of that. First of all, Kaposi’s sarcoma existed forever and if Kaposi’s sarcoma was caused by HIV, now… and it was concluded it was not an infectious agent, doesn’t matter what, but if it was… let’s assume it was caused by HIV, then why was Kaposi’s sarcoma and thus AIDS and HIV restricted for so many decades in the African continent when, you know, there was plenty of relationship… or how do I say, there was plenty of travel or people being…
Val: There was the slave trade; that’s plenty of travel.
Eleni: No, I mean, you know, in the… say the fifties and sixties, you know.
Val: I see. You mean in recent times?
Eleni: In recent times. You know, there was plenty of opportunities for the virus to travel to Europe and to America.
Val: And also if this is the case, that Kaposi’s sarcoma in Africa has always been AIDS, why does Africa have a population problem?
Eleni: Yes, exactly, you know, because if AIDS existed there, you know, for so many years in AIDS and HIV, and if AIDS is such a…
Val: In fact, in Africa it is said that the incubation period of AIDS is actually four years versus ten years in the west, so even more so.
Eleni: We should not have left one African by now, we should not have had one African, but, you know, it’s not. In fact, there are so many hypotheses, many people including Gallo… I think Gallo was the first one to hypothesise that HIV somehow appeared in Africa. Nobody went to say that HIV was present there as far back as the 1940s and fifties or sixties even. And secondly, now many people are trying to… they change their mind and we don’t believe any more that HIV originated in Africa.
Val: The other important thing is that modern studies where tests have been done on Africans, because it’s a study because tests aren’t usually done in Africa, have clearly shown that if you take the WHO clinical case definitions, only about half of the people who fulfil that definition of AIDS are in fact HIV positive.
Eleni: Not even half… in Zaire 27 per cent of women who fulfil the WHO definition test positive for HIV.
Val: So what have the others got? As one of the commentators has said, is this AIDS by definition? You tell us.
Eleni: The thing is… as I said, pneumocystis (Inaudible) is the best example, you know. It is everywhere. If anybody, Africans should have the pneumocystis pneumonia and yet there are not African AIDS patients with pneumocystis pneumonia. What we have in Africa is diseases which existed forever in Africa. There is nothing different today than it was a hundred years ago.
Val: And the only difference is they just happen to have antibodies, some Africans, against the proteins in the western blot strips.
Eleni: That is not new. They have had that forever but we do not know; we are testing them now. Again, Gallo, when he did the Uganda study in 1973, he had some blood and they tested that and they count 67 per cent of children tested positive for HIV, western blot positive.
Val: And he was puzzled by that.
Eleni: And he was puzzled by that and he said, “Why then we don’t have AIDS”?
Stuart: Could we turn now to the actual mechanism of oxidative stress in AIDS. How is it that oxidative stress actually leads to AIDS?
Val: The answer to that is: we don’t know specifically how each episode of oxidative stress in a particular individual causes a particular disease.
Eleni: But we know that oxidative stress will lead to pathology. I tried in my theory because I thought that there is not an infectious agent which causes the AIDS. I had a big problem because, say, by 1983 AIDS was diagnosed in gay men, in haemophiliacs, in drug users, so if it was not an infectious agent, how could all these groups have… which was assumed then and even I do not know the diseases are different… it can be caused by… what would be the cause, what would be the relationship between all this… what would be the common denominator in all these groups? And the conclusion which I came to was that they all must be subjected to oxidising agents by either a common oxidising agent or different oxidising agents.
Stuart: What sorts of oxidising agents?
Val: If you look at the risk groups, the obvious choices are… in the gay men is semen or some constituent of semen, sperm or cellular material or something contained in semen.
Stuart: Is there evidence that there is oxidising material in semen?
Eleni: Oh yes, that is everywhere.
Val: In fact, yes, we could go on about that, but the short answer is yes, there’s plenty of evidence. The use of certain drugs, at least in the early days of AIDS, by the gay community was prevalent. The use of nitrites in particular which we’ve described particularly in our paper on Kaposi’s sarcoma was practically ubiquitous, and these are certainly potent oxidants. I mean, that’s how they work.
That’s the standard pharmacology, chemistry. Of course, so in this group there are two contenders. As far as haemophilia is concerned…
Eleni: It’s factor 8 itself. Factor 8 and most probably the proteins which are there. The way factor 8 is made, the other proteins will be oxidised as well. But, again, for factor 8 to produce its biological effect, you have to make it a strong oxidant. If you reduce it, its biological potency is destroyed. They have that and in addition they have many… then we have the drug users. The drugs they are using again are not only nitrates, because some of them all use nitrates but even the drugs which are used for intravenous injections, they’re again oxidising agents.
And on top of all this, the three AIDS risk groups are subjected to many viruses and infectious agents which again when in the body… the only way to survive, they have to take reducing equivalents from the body for them to survive. So in the body they will oxidise. All these viruses which these people… you know, the gay community have a lot of infectious diseases – suffer from a lot of infectious diseases. And in fact they are treated then for these infectious diseases again with oxidising agents. So you build up a lot of factors which maybe each separate will have no effect, but when they all come together, they add up, you know, they’ll have a synergistic effect which will culminate in pathogenesis.
Val: I mean, when you get to specifics, it’s difficult, as I said initially, to predict which person is going to get what disease, but we know that AIDS patients have reduced cellular and plasma thiols, that’s the sulfhydryl groups – which is an indicator of the oxidation/reduction status of the body. It’s known that certainly innate lymphocyte functions which are measured by immunologists and which they refer to as … in immune terms are impaired by the cell being oxidised, and that these can be reversed by giving the opposite of an oxidation reagent, that is a reducing agent.
Eleni: Not only the function of the T cells but even their survival depends on the redox state. If they’re relatively oxidised, the function will be diminished. If you oxidise them even more, they will die. They can’t survive if they are strongly oxidised.
Val: The other factor in the equation of course is that… I shall preface that by saying that therefore this theory that Eleni expounded in the early 1980s is not an infectious theory of AIDS; it is a toxic theory of AIDS. And as with all toxic substances, what matters is firstly the nature, but secondly the dose, and one would find support for this hypothesis by exploring in one group whether the dose of whatever oxidant we’re dealing with is somehow related to the development of the AIDS phenomena, the AIDS diseases, for example, and there’s certainly support for this in the gay community.
Eleni: Yes, I think this is a very good point. It’s not homosexuality as such which will lead to AIDS, even if there is proof that semen contributes to the development of AIDS or causes AIDS or nitrates contribute or cause AIDS or all the other agents act synergistically. Say, for example, that only semen and nothing else, you can exclude everything else, that semen is the cause. It is not being gay men who are practising homosexuality which will be, shall we say, the cause or which will lead to the development of AIDS.
Val: Any situation where people are exposed to a large amount of sperm, including women. Women who practise anal intercourse, for example, we would postulate would have a higher than normal incidence of the AIDS diseases.
Eleni: But not even who practise anal intercourse – this is a hypothesis – but women who are promiscuous, it is a known fact – this is not a hypothesis – have a much higher frequency of cervical cancer which has been shown to be related to the dose of semen.
Stuart: I mean, being promiscuous isn’t necessarily related to the amount of semen, to the dose, is it? Someone can be promiscuous by having ten partners over ten years or twenty partners over ten years as opposed to one partner, but one partner can give, you know… having sex more frequently would give more semen.
Eleni: Sure. It’s not the frequency or not the number of partners you have. In fact, there is good evidence that for AIDS from Amsterdam, Professor (Inaudible) and his colleagues, they have shown that there is a direct relationship between the number of episodes of passive anal intercourse and the development of HIV seropositivity and the development of AIDS. The same has been shown by the MAC study, that is the multi-centre AIDS cohort study in America. So it’s not really the number of partners you have but the number of…
Val: The dose of the oxidant.
Eleni: The dose, shall we say, of… it’s not promiscuity, it’s…
Stuart: But that’s not the case with the cervical cancer you were talking about… using as a parallel though, is it?
Eleni: Yes, it is, because, you know, shall we say, the nuns… nobody says that nuns… you know, there are no nuns who develop cancer… there are nuns who may develop cervical cancer but women like, shall we say, prostitutes, they develop a much higher frequency. Now, there you have two things. This is the easy way to find out because most probably some woman, you know, on the street, you know, who is not promiscuous, who is only with her husband, maybe she develops it because of that, but we don’t know because of the other causes of cancer.
Val: Unfortunately the word “promiscuous” has changed meanings, hasn’t it? It’s supposed to mean having a diverse number of partners. Obviously there’s an association between promiscuity and dose of semen, but it’s not a linear relationship, I suspect. We need to be specific. We need to talk about the amount of semen. Promiscuity is a loose association. In fact, at this stage it’s probably interesting to speculate how one can almost disprove the HIV/AIDS hypothesis with the data on passive anal intercourse.
Eleni: Yes, sure. Some of the best evidence against HIV in fact comes from epidemiological studies in gay men. From the beginning, from the very beginning, before 1983 when HIV was said to be isolated, there was evidence that the only sexual act directly related to the appearance of AIDS in gay men was passive anal intercourse. In fact, even in 1984 Gallo presented evidence that… in fact I just have it here. You could read it.
Val: Yes. In fact Gallo himself wrote in 1984, and I quote:
Of eight different sex acts, seropositivity correlated only with receptive anal intercourse.
That was in the Lancet in September 1984, written by Goerdhart et al.
Eleni: Goerdhart was the principal author. Now, since then the data… in fact the best…
Val: Shall we just develop that, because if receptive anal intercourse…
Eleni: No, but let’s see. There is much … since then data from everywhere appeared which supports exactly… similar data appeared everywhere. The best will be from Amsterdam where they have in fact two very, very good studies which have shown exactly the same thing, and the multi centre AIDS cohort study in America where they have shown that the only sexual act directly related to the development of AIDS is passive anal intercourse.
Val: Is that AIDS or seropositivity or both?
Eleni: No, sorry, seropositivity… to development of seropositivity, and recently they have also shown that the only sexual act directly related to the progression of AIDS is again passive anal intercourse.
Stuart: That could also be compatible with an infectious theory, given that that is a passage into the bloodstream that is…
Eleni: No, it can’t be, sorry, because, say the heterosexual… because we are told, you know, that HIV and thus AIDS is sexually transmitted. Now, we know… with gay men it’s different because some gay men practise both passive and active sexual acts, but with the heterosexuals it’s always… the woman is always passive and the man is always active. So if it is only the passive partner who develops the disease or who becomes HIV seropositive and who develops a disease…
Val: And whose disease progresses.
Eleni: And whose disease progresses, how we can… in this partner the woman cannot transmit it to the man.
Stuart: But it’s a physical difference with the walls of the vagina as against the walls of the rectum. You are actually physically getting the virus transferring through the…
Eleni: No, we are not talking about how the virus is transmitted. We are talking that here it is only the passive person… you know, doesn’t matter if it’s vaginal or it is anal intercourse, right?
Stuart: I see, yes.
Eleni: So it is only the passive person, even if the woman practises anal intercourse which many women do. This is not a practice which is a sexual act which is practised only by gay men. There is evidence now that a significant percentage of women practise anal intercourse, so it’s nothing new. We can’t condemn gay men for that. But it is only the woman can get infected and can get a disease. The men never can get infected, never can get diseases, so it is like pregnancy: only women can get pregnant. The men cannot get pregnant.
Val: And it can’t be transmitted.
Eleni: Cannot be transmitted sexually.
Val: It can be acquired by the passive partner but how does the active partner get it?
Stuart: So are you saying that there are no cases at all of people who have only been the active partner getting AIDS?
Val: There’s no scientific proof of this but we’ve had discussions with…
