by John Lauritsen
13 June 1987
NIH, Washington, DC
[This is the full interview with Duesberg. It was published in the New York Native, 6 July 1987, as “Saying No to HIV: An Interview With Prof. Peter Duesberg, Who Says, ‘I Would Not Worry About Being Antibody Positive'”. It was reprinted in Christopher Street, Issue 118, December 1987.]
The hypothesis that Human Immunodeficiency Virus (HIV), the so-called “AIDS virus”, is the cause of AIDS may have been dealt a death blow by an article that appeared in the 1 March 1987 issue of Cancer Research: “Retroviruses as Carcinogens and Pathogens” Expectations and Reality” by Peter H. Duesberg. The Duesberg article broadly reviews the putative role of retroviruses (such as HTLV-I) in causing leukemia or other forms of cancer, as well as the role of HIV in causing AIDS. Duesberg concludes that it is far from proven that retroviruses play any role whatever in causing cancer, and that the claim that HIV causes AIDS is equally unfounded:
It is concluded that AIDS virus [HIV] is not sufficient to cause AIDS and that there is no evidence, besides its presence in a latent form, that it is necessary for AIDS.
According to Duesberg, the cause of AIDS is still unknown, and HIV may be regarded as a nonpathogenic, opportunistic infection:
It seems likely that AIDS virus is just the most common among the occupational viral infections of AIDS patients and those at risk for AIDS rather than the cause of AIDS. The disease would then be caused by an as yet unidentified agent which may not even be a virus.
I interviewed Prof. Duesberg on June 13, 1987 at the National Cancer Institute (NCI), which is part of the National Institute for Health (NIH) located in Bethesda, Maryland. He was there on sabbatical, doing research. In the week before the interview I had a number of telephone conversations with spokespeople for the Centers for Disease Control (CDC) and the NCI.
I first talked with Chuck Fallis, an information officer at the CDC. I posed the question: “What evidence is there that HIV is the cause of AIDS?”, and asked whether he had read the Duesberg article. He asked for spelling of name, date and name of publication, etc., said he might have heard of it, but could not remember what he had heard. I again posed the question: What is the proof that HIV is the cause of AIDS. Fallis said he couldn’t answer that question, but would have one of the epidemiologists call me back.
Fallis called back about two hours later, and said that he had gone “on a real wild goose chase trying to find someone who could answer your question”. I said I was amazed, that every day the CDC asserts that HIV is the cause, and I assumed that anyone there could easily answer the question of what proof there was. Fallis said that they couldn’t answer the question there — referred me to the National Cancer Institute, which I called.
At the NCI I talked to Florence Karlsberg, a press officer, and asked: What is the proof that HIV is the cause of AIDS?
She replied, “They say it is”.
Asked who “they” were. She replied, “Dr. Gallo”. I repeated my question. She said she would have to get back to me.
Karlsberg called back the next day with a statement on Duesberg’s paper from a Dr. Wm. Blattner, an epidemiologist at the NCI. The statement struck me as having an abusive tone, and as being unresponsive to most of the points raised in the Duesberg article. She said she could not send it out, but could only read it; she would not say whether it would be published or not.
I asked whether the NCI intended to publish a reply to the Duesberg article. Would a letter or article would be submitted to Cancer Research? Her reply was, “We have not received many requests to reply do Duesberg’s article.”
I responded that I thought, in the interests of Free Enquiry and scientific dialogue, a major, written, public statement, by an eminent scientist, should be answered by a written, public statement.
Two days after I interviewed Duesberg, she called back again to say that the Blattner statement would be made public, and that I would be sent a copy.
The interview with Prof. Duesberg took place in the living room of a large stone house on the grounds of the NIH in Bethesda, Maryland. I began by asking background questions. Peter Duesberg came to the United States about 20 years ago from Germany. He is Professor of Molecular Biology at the University of California in Berkeley. It is because of his interest in retroviruses, on which he is an authority, that he became involved in questioning the “AIDS virus” etiology.
* * *
JL: Which argument, out of the many that you muster in your article, most strongly persuades you to disbelieve in the hypothesis that HIV is the cause of AIDS?
PD: A couple of things. The first is the consistent biochemical inactivity of the virus. The virus is consistently latent. It infiltrates or infects very low numbers of cells, as few as 1 in 100,000. In order to hurt somebody, in order to kill, in order to be pathogenic, a microbe has to do something — and that includes all microbes, viruses and bacteria alike. A virus has to make proteins, RNA, DNA, in order to have an effect.
JL: So when you talk in here about the extremely low titers of the virus…
PD: Biochemical latency. It is biochemically inactive. The titre is just one expression of that. Titer means how many particles are manufactured. But you could even see a situation where you don’t even make the particle because maybe one of the genes that are needed to form a particle are missing, but you could still make other components. You could make other viral proteins — the preliminaries, or whatever. Any of those products could be made without having all genes available, and it could be pathogenic or toxic. But none of this is found. Even in patients who are dying from the disease, the virus is almost undetectable, while RNA synthesis is essentially not detectable.
JL: So at this rate it would be impossible to deplete T-cells.
PD: That’s one of the points I’m making. Since T-cells are regenerated at a rate of approximately 3-4% a day, a T-cell on the average has a half-life of approximately a month. There are some so-called “memory cells” which may live for years and years and even a lifetime, and some that have a turnover of only a few days, but the average T-cell is said or assumed to be half a month. The T-cells that you have today — a month later half of them are gone and replaced by other T-cells.
So that is one of the key arguments, and there is no exception to the rule that pathogens in order to be pathogenic have to be active. And that is something that I didn’t even think through until it became obvious from research on HTLV-1 and leukemia, as well as on the AIDS virus [sic]. We had stretched the virus factor from initially animal work, where we forced high titers and high viral activity by injecting new-born animals in the laboratory before they were immune-competent, before they could make antibodies. Then you can artificially generate high titres. Then in certain animals, not in all, you can get leukemia or other diseases. But the human viruses, and the same retroviruses in wild animals, mice, chickens, birds whatever, or monkeys, are essentially never seen in these diseases. They are never seen at high titers. So, under those conditions, the viruses are bound to be nonpathogenic. They are latent and cannot do anything. It is exactly the same way with bacteria and other viruses.
Most people are carrying the Epstein Barr Virus, or herpes, or Cytomegalovirus (CMV). All of us contain pneumocystis carinii [the protozoan that causes AIDS-associated pneumonia]. Tuberculosis used to be endemic. It is no longer that everybody has it, but many, many more have the bacterium than get the disease. It’s even true for diseases like leprosy. The leprosy mycobacterium is also quite endemic in Africa, but very few get the disease. But in every case where there is disease, the viruses, the bacteria, are biochemically active. They make proteins, they make RNA, they replicate, and then the ultimate expression is that the titer goes up. A lot of viruses or bacteria are made, and then you have locally a high titer of virus or bacteria production.
JL: All right, so then the inactivity and the low concentrations …
PD: The low level of infiltration — very few potentially susceptible cells are ever infected, and those that are infected don’t do anything. The virus just sits there.
JL: And then there was another main argument…?
PD: The so-called latency period of the disease, the time it takes between infection and the development of symptoms of the disease. That also is a very suspicious signal that the virus is unlikely to be solely the direct cause as they claim. Viruses and bacteria alike are most toxic or most pathogenic before they induce immunity. In fact, in the case of viruses that is the only weapon we have of prevention, via so-called vaccination. We infect with a variant strain, and if antibody is formed, the show is over for the virus. The virus may still be latent in the body — in most cases it isn’t — but if it is, it is very difficult for the virus to strike against cellular immunity. That’s how we survive.
JL: I’ve found that they often use the latency argument to get around weaknesses in their theory. For example, I asked them at the NCI what explanation they have that for eight years this epidemic has been confined almost entirely to two risk groups: homosexual and bisexual men or intravenous drug users. I said that a truly infectious disease would not stay in boxes, compartmentalized. And they said, “That’s only because of the long latency period.” And they said the period could be from two years to more than nine years.
PD: Fifteen, I’ve heard. Well, when you stretch the latency period, that’s always an indication that you make room for something else to happen. But the latency period in viruses is a relatively clear situation. The most effective time for the virus to be pathogenic is right after infection and before it induces antiviral immunity. Then you are unprotected, then the virus can grow. That’s when you get your symptoms, your pathogenic symptoms. If your body has never seen that virus before and has no antibody, and you are susceptible to that virus and get infected, then you get fevers and symptoms of disease. The virus can replicate. That’s when it would be likely to be most pathogenic. Then you develop antibodies. Then usually the show is over. Either you wipe it out completely. Or, in the case of retroviruses, because of their very benign nature as parasites — they do not kill cells that they infect, unlike all other viruses — they are the most benign viruses that we know — they can remain in the cell in a latent form. And what can happen in some cases, like the herpes virus, is that years later the latent virus can come back again, cause zoster and blisters. But again then, when it is pathogenic, the virus is active. But in the AIDS cases it is not that way. Even after eight years of latency HIV remains as latent as it was before. And then, when AIDS is diagnosed, they say that now it’s possible for the disease — but, the virus is not doing any more than it had done before when there were no symptoms of the disease.
JL: I found it very striking that in your paper you use the phrase, “viral immunity”, whereas the government scientists would say simply “antibodies”. If I understand their position, it is that they do not believe that the body can make antibodies by which it can defend itself from the virus. But from what you say, that is not true.
PD: I think they say that perhaps because they want to sell a vaccine. And I think there is no need for a vaccine. Unless, of course, you know that the virus is really the cause, and then to prevent the original infection. But the diagnosis is based essentially on the presence of a vaccine, the virus-neutralizing antibody. Gallo, Weiss, and people from the CDC have published papers in which they show a neutralizing product, and that also implies cellular immunity. That’s a little harder to prove. We don’t only make cellular antibodies, we also have a T-cell involvement even to make cellular antibodies. And the antiviral immunity is apparently so effective that they can never come up with a virus titer. So I think that the one thing AIDS patients or those who have the virus do not need, is a vaccine, because that’s how we diagnose. And it’s very effective. It’s so effective that the titer is undetectably low. It takes a very expensive laboratory to activate the virus and grow it in cell culture.
JL: Now we have the testing phenomenon, where it appears that people, perhaps in the near future, will face denial of freedom, loss of civil liberties, on the basis of a test for antibodies which is not even accurate. If someone’s future were jeopardized — occupation, marriage, or some other way — by being positive in the antibody test, could such a person demand to be tested for the virus itself?
PD: To test for the virus itself is much harder. You could activate the latent virus in vitro. That’s what they do. But this doesn’t say anything about the virus’s possible role as a pathogen in you, because no one has ever seen the virus become active in a person. That has yet to be described in a single paper. So I think it’s a gross injustice to discriminate against anyone on the basis of having antibodies, which used to be called vaccination. That’s the one thing we have to offer against viruses, those vaccinations.
JL: And there are these creeping changes in terminology, where now the media are using “HIV infection” as almost a synonym for having AIDS.
PD: Yes, the majority of antibody positive persons have no symptoms of AIDS, because it’s only if you look at the so-called high risk groups, which are promiscuous male homosexuals or intravenous drug users…
JL: Now, I think a point of your paper is that some populations, in which substantial proportions are antibody positive, are at basically no risk for AIDS, whereas in other groups, such as homosexual men or intravenous drug users, being antibody positive indicates a certain risk for AIDS. And that this is an argument against HIV’s being the primary etiologic agent.
PD: Absolutely. I think something else has to happen — they call it a “co-factor” — or AIDS is caused by something that has nothing to do with the virus.
JL: Do you think that the cause or causes of AIDS may not be a microbe at all? It that feasible?
PD: It is quite possible. I think from what we know about it, it is quite possible. One thing that they all agree on, even those who are the most ardent supporters of the viral hypothesis, is that cellular contacts are necessary to transmit the disease. The classical definition of a virus is a cell-free infectious agent — that is to say you can transmit the disease without exchanging cells, and without even exchanging microbes. That would be a classical transmission of a viral disease. That is, so-called partial contacts, like sneezing, or drinking out of the same cup, or whatever, should be sufficient to transmit the disease. They all insist that AIDS cannot be caused that way. You have to have sex, or you have to exchange needles — in other words, you have to exchange infected cells. And once you admit that you have to exchange human cells, you have not excluded anything. That’s the most you can exchange between two living things. That’s what you have to exchange to get babies. You cannot exchange more. You can do an organ transplant — that’s just more than one cell. This doesn’t exclude anything. That’s what I’m saying. And it certainly doesn’t prove that AIDS is caused by a virus.
JL: Is it possible that a toxin or toxins might be the primary cause of AIDS?
PD: Yes. It is entirely possible.
JL: One of the viruses that Gallo discovered some time back was in his opinion linked to leukemia. But it does seem that leukemia has other causes. For example, following the atom bombing of Nagasaki and Hiroshima, there was an epidemic of leukemia. What role did the virus play at that time?
PD: I spent more time on this topic in my paper than I did on AIDS. I don’t think the HTLV-I virus had any role at all in this case. In experimental animal models such viruses can have a role in causing leukemia. It is only an indirect cause — namely by inducing so-called “hyperplasia”, or an overdose of certain cells, and that can only be accomplished by forcing or generating very high titres of the virus. And that in turn is only possible by infecting an animal before it is immune-competent. And in the human cases, the human viruses have never been found in high titers in anybody. The number of infected cells is incredibly small. And then the tumor that comes out of it, so-called “leukemia,” is always monoclonal — this is to say, it came from one single infected cell . And they go through many generations through the so-called “latent” period.
Gallo says in his latest article in Scientific American that the latent period is 40 years. So you go through — if a month is the half-life of a T-cell — you go through 400 generations of T-cells. And you have 10 8 or 10 9 or 10 10 at any given time. So you’re looking at ten to the 10th, 12th, or 14th power — 10 12 approximately T-cells — out of which one becomes leukemic. After 40 years. And yet you say the virus was responsible for it. Well, that is just bizarre. In vitro, this virus, or any other retrovirus, has never caused a malignant transformation. So, I think there’s not even a chance that HTLV-I has anything to do with it. I don’t think even indirectly, because there’s never a high virus titer.
JL: It reminds me of a science course I took, where we went through pre-Copernican astronomy. At the time, for theological reasons, they believed that everything revolved around the earth, but their observations didn’t always accord with that. And so they talked about “epicycles” and “retrograde planetary motion” — a planet would be going along, and all of a sudden they would have to make it do a flip flop or a somersault, in order to bring their observations into line with their theory. And somehow the latency period seems to fill the same function. No matter how absurd the contradictions are, between their theories and the facts, they think they can overcome them by extending the latency period.
PD: It’s a double-edged sword. On the one hand, they say it takes that long latency to develop the disease, but then they cannot say why it wouldn’t do anything during that latency period that it does eight years later, without changing its biochemical properties. They keep saying it activates some unknown cell to make some unknown toxin, but I haven’t seen any evidence for this.
JL: With reference to Koch’s Postulates, I think you made the statement at one point that the only evidence that HIV is necessary for AIDS to develop is that approximately 90% of people with AIDS have viral immunity, meaning antibodies. Now the test apparently is more likely to give a false positive than a false negative.
PD: That’s right.
JL: Even if it were accurate, and both tests together gave you a stable figure of 10% of people with AIDS who did not have HIV antibodies, it still seems to me that Koch’s First Postulate has not been satisfied.
PD: Well yes, you are right about that. If you could actually prove that those who are antibody negative and have AIDS are really virus free and have never seen the virus, that would kill the hypothesis right there. But then they might argue that in some cases the antibody is so low that it’s hard to detect. Individuals respond differently to different antigens, and it could be that this antigen or antibody happens to be such that it’s not reacting to the test, so it would be a false negative. They could argue that way. You could go for more direct evidence, like looking for a virus, which you almost never find anyway, and start cultivating cells, and if that is negative — they say that up to 50% of that test are negative anyway — you could go further and look for pro-virus, which is the DNA form of the virus. And there, so little DNA is made that even with the most sensitive methods you cannot detect it in more than 10% or 15% of the AIDS patients.
So it’s essentially almost impossible to say for sure that this is a total negative, because even those who are positive are so difficult to demonstrate. And it’s indirect — an antibody test is indirect. And you could say about polio or influenza virus, or measles, or many other viruses we have antibodies for, you will never find a virus particle at all, because the virus has been eliminated by the antibody. And you could argue it might be the same with the AIDS virus, the titer is so low. Although these viruses are so benign, and so kind-hearted if you wish, that they actually never kill cells. Therefore the body can afford to keep them on for a long time. In fact, chickens, mice, and humans contain as we are now a lot of endogenous retroviruses which never do any harm. They are not easily detected because they are always latent.
JL: Some people have questioned if there really is any such thing as AIDS — an acquired form of immune deficiency that is new. Some people have said that this may be a phony construct. Some call it a condition, emphasizing that one doesn’t know what it is caused by, and that it may be the result of some kind of trauma which may not be from infectious causes at all. How would you characterize AIDS?
PD: Well, that is a difficult question, and I agree with much of what you just said. AIDS is not a disease entity, like poliomyelitis or liver cancer or lung cancer or something that is a definable entity. AIDS is a condition which includes so many parameters that it’s almost inconceivable to define a simple pathogen as the cause, considering the diverse patterns of the disease. It’s very difficult to come up with something that could explain all of these things, such as immune deficiency, pneumocystis carinii [pneumonia], Kaposi’s sarcoma, lymphoma, interstitial pneumonia, meningitis, encephalopathy, “slim disease” (which is just losing weight), diarrhea. All of these things are said to be due to this one little virus, which is latent all the time. What else? I think just being antibody positive and sick is almost the definition of AIDS nowadays. To be antibody positive and have any of these things, that’s called AIDS. So how could you possibly find an agent that would explain all of these things.
JL: And immune deficiency is not new. I or anyone else could become immune deficient just by ceasing to eat protein, or by taking a large amount of cyclosporin or cortisone or many other drugs, or by living to be 98 years old. And the question is, why is it “acquired”.
PD: Yes, I think the “acquired” thing is pretty weak. Let’s take just immunity against the virus as one example. It doesn’t fit the definition. If AIDS patients are immune deficient, why can they all make antibodies? That alone is paradoxical.
JL: Perhaps they have “selective immune deficiency”?
PD: Selective? Against what though? Against Kaposi’s? And then others get diarrhea. Meningitis? Slim Disease? I share your skepticism too. That’s why I think it’s also very difficult to come up with a definition.
JL: Your article starts out with a quotation from Sherlock Holmes: “How often have I said to you, that when you have eliminated the impossible, whatever remains however improbable must be the truth.” My question is: What do you think is or are the causes of AIDS?
PD: Well, that’s a difficult one. I can only say that, considering that cellular contacts are required — they all insist on that — we haven’t excluded anything. But I would be very doubtful that any virus could fill the bill, because it would have to have an acute virus expression at the time of the disease. Likewise with bacterial infection. I doubt that it could be a known virus or bacterium, because the viruses are simply not seen, and most of the known bacteria respond to antibiotics, which I’m sure have been tried and have not been effective. So I really wonder what it could be.
JL: Well, if we looked upon AIDS as a condition, it may not be necessary to have the same cause for homosexual men as for intravenous drug users or for Africans.
PD: Absolutely. And in Africa I don’t think anybody knows what kind of AIDS exists, or whether AIDS exists. In the case of the drug users I could well see that an injection of toxin — and the drugs are impure, no one knows where they come from — is hell for the immune system. And also medical injections — streptomycin or penicillin are also not good on a regular basis. They are immunosuppressive themselves. Perhaps it is a simple question of lifestyle.
JL: Exactly. Environmental or toxic factors.
PD: But I’m really just guessing here, and I think this is where more research should be done, to see what other possibilities there are, what else could be responsible for it. What could drugs do, what could contaminated drugs do, what could injections do? Whatever they inject — heroin, speed, whatever it is? What could those things do to the system, either in animals or in humans? Rather than concentrating always on the virus.
JL: Of course it’s not your obligation to come up with an alternate hypothesis. It’s quite enough to have falsified the “AIDS virus” hypothesis, which in my opinion you have done.
PD: Yes, I think so too. In fact, I’m getting more confident about it.
JL: There doesn’t seem to be much information about the characteristics of people with AIDS. I only know of a 1982 CDC study of the first 50 homosexual men with AIDS. Obviously the study is out of date, and it was totally unacceptable by the standards of professional survey research. However, it indicated that all of these AIDS patients were heavy users of recreational drugs Most of them used half a dozen different drugs regularly. And furthermore, they had had one venereal disease after another, sometimes simultaneously, always treated with antibiotics. Looking at that profile — this is not backed by recent hard data, but according to the PWAs I have spoken to, and doctors who have treated many AIDS patients, almost all AIDS patients pretty much fit this profile — I think it would be surprising if such people did not become seriously sick from their lifestyle.
PD: I would be surprised too. The number of contacts, the things they take. You wonder how they could do it.
JL: Other viruses seem to be activated too, don’t they? The Epstein Barr, CMV, herpes, hepatitis viruses? Could these also play a role in causing AIDS?
PD: Well, it has been claimed lately that these are co-factors — that one of these viruses would activate the others. HIV could activate cytomegalo, and cytomegalo could activate HIV. But I don’t think any of the concepts will help very much, because if you have 90% of the AIDS patients — in fact, much of the population — positive for most of these viruses, then that factor would already be there. All you need would be HIV, and that would register in the population as it is now as a single factor. The co-factor hypothesis would only make sense if both agents were there. And then you would look at somebody who gets them both. But if one of them is essentially endemic, and the other shall we say is new now (the “AIDS virus”) — I don’t think so myself, but let’s say that would be the other one you would need — then you would develop the disease as soon as you got that rare one, because the other one was already there. So I think that hypothesis is not going to work either. And again, even if it were true, then you would expect that virus at least to be active in the pathological phase of the disease. And that’s not true either.
JL: CDC officials have been making statements recently to the effect that, of those people who are seropositive, who have HIV antibodies, 30%, 40%, 50%, 80% will go on to develop AIDS within the next five years or so. What would your comment be on that?
PD: Well, this is what I would call biased sampling. I mean that may be true for some of these cohorts, where they take selective groups of highly promiscuous male homosexuals who also use drugs, in San Francisco or New York. Perhaps then. They come up with annual numbers of 1%, 2%, 3%. I’ve seen up to 5% in some cases. But if you look at average virus positive people, of which they say that there are one or two million in the United States alone, certainly you don’t see that they all come up with AIDS. According to Gallo’s dogma, they would all have been infected in the last 10 to 15 years, when according to them the virus was first introduced into the country. Given the latent period of 5 years (which they keep stretching, but assume that were true), we should be catching up with the disease. So if all of them would develop the disease, we should have within five years one to two million AIDS fatalities. And even with all of the stretching of the disease that they do — if somebody dies of diarrhea and is antibody positive, I’m sure he registers as an AIDS fatality in the statistics — they haven’t come anywhere close to that. It’s very biased statistics — they look at cohorts that are at very high risk and ignore the others.
JL: You raised the point that they have changed their definition of AIDS several times. First of all they changed it so that if somebody is seronegative — even if they have AIDS, they don’t have AIDS.
PD: I have heard that too.
JL: And now they are expanding the definition so that someone who suffers from emaciation or some other thing — if they have antibodies they can now count as AIDS. But how can we track the phenomenon, the condition or whatever, if the definitions change all the time?
PD: In papers now they are treating meningitis, encephalopathy and so on as expressions of AIDS. And some things they call ARC [AIDS-Related Complex], whatever ARC is.
JL: It becomes rather mystical.
PD: I agree, the whole thing.
JL: Now, let’s go into some of the problems of free enquiry, of having a free and open discussion. It seems that it has become difficult for people to dissent from the government viewpoint. Do you understand what motives might lie behind what seems like the total unanimity of public statements on AIDS?
PD: I can only speculate on that. At the NIH it is a political structure — it is very much linked to the administration. It is not like a university that is just involved in research. It’s like the Defense Department, that has to prove itself. High-ranking NIH officials have to justify their position by solving a disease problem. And AIDS fits right in. They can say, “We have defined the disease and are about to solve it.” The Director of the NIH needs someone like Gallo, to say “This is my hero. Gallo needs all the support he can get and the recognition.” So it becomes an autonomous system, which is not what good science is supposed to be. In good science, you want to find out what’s really going on and are challenging in all directions. In good science, 99% of the experiments are negative — they don’t turn out the way you might want them to turn out. And that is not something you can advertise, that an experiment is negative. The NIH very much depends on favorable publicity.
JL: What response has there been to your article? I know it’s still kind of new.
PD: I get a lot of reprint requests. That shows there’s some interest. I get a lot of comments from people who say it’s good scholarship. I have not got one comment yet saying it was just a piece of trash, that nothing was right in it. A lot of people call me and say, “Don’t quote me to him,” or “Don’t quote me to Gallo or say that I called you, but I really liked your piece.” I have not heard from any of those who are essentially the targets — like Gallo, or like [Harvard’s Drs. William] Haseltine and [Max] Essex or [the Pasteur Institute’s Dr. Luc] Montagnier — saying, “You were completely wrong on this or that point.” They haven’t responded.
Of course there are always some people who are dissatisfied, but some of those who have called me are respectable scientists who have nothing to lose or gain, one way or another. And so, I would say the article has been fairly well received — even enthusiastically received. I’ve received a couple of dozen letters — the very extensive kind you never get anymore. A number of scientists support me, some came to me spontaneously, including members of Gallo’s lab. And so I think that the article made a point.
JL: I notice that in your acknowledgements you thank 17 scientists for “critical comments or review” of your manuscript, and Robert Gallo for “discussions”. Now, starting with Gallo — I assume he doesn’t agree with you — does he intend to publish a reply to your article?
PD: I don’t know. I went to lunch with him, I saw him in Stockholm two weeks ago, we talked a little and he said, “I was in Japan in a meeting and there were these people waving your review and saying the virus was not the cause, and I had to tell them it was not true, that the virus absolutely was the cause.” And I asked, “What else did you tell them, Bob?” And he said, “With friends like you, who needs enemies?” Well, he said that laughingly — but a direct reply? I haven’t heard from him. I think their policy is to freeze me out and try to ignore it.
Of the 17 scientists that you acknowledged at the end of your article, would you say that they are in substantial agreement with your paper?
PD: With the exception of Gallo, yes, they are.
JL: Well, if they had had any specific criticisms, either factual or analytical, wouldn’t they have communicated them to you?
PD: That is exactly what I expected. They are certainly not hesitant otherwise. If something were off, they would have said so, and I have not had such comments.
JL: How prestigious is Cancer Research? Is it a major medical journal?
PD: Actually, they chose me, I didn’t choose them. It is the foremost journal in cancer research, the oldest one, the most traditional. The Perspectives in Cancer Research, under which my article appeared, is by invitation. It had to be reviewed, and I think it was reviewed three times.
JL: And to date there has been no written response to your paper?
PD: Not that I know of.
JL: Among the people who share your misgivings about the HIV etiology — have they submitted letters or articles to other medical or scientific journals?
PD: I don’t know of anyone who has — in writing. In discussions, yes — many questions have been raised. Some people just say, “I am disgusted by this time” or ” I am a scientist, I need public relations, I don’t want to get involved.” But I haven’t seen anything written. There is almost a consensus. There used to be some degree of competition only a couple of years ago — people with other viruses trying to claim that their viruses were responsible — but they have been outlobbied somehow.
JL: I think that’s a good way of putting it. Now, tell me about the recent Third International AIDS Conference. Were any of these ideas discussed there? What was your impression of the conference?
PD: I only went once. It was so crowded, and they wouldn’t take any questions from the floor. Some of the questions were at least touched upon, like the long latency period: Why does it take so long? Why is the virus not active? But the possibility that HIV may not be the cause, or that other factors may be necessary, were not addressed in any significant way. And I could see why not. Because this was not a meeting for the exchange of minds. It was made-up minds that were projected. It was like the theatre.
JL: I had heard that Dr. Sabin [the scientist who developed the oral vaccine for polio] attempted to give a press conference, but I don’t know the details.
PD: I think he did give a conference. He told me over the phone that something like 50 reporters surrounded him and asked him his opinion — but what exactly he said, I don’t know. Over the phone he reiterated some of the points that we had discussed about ten days ago in his office.
JL: Does Dr. Sabin agree that HIV is not a very good candidate as the primary cause of AIDS?
PD: Well, he read my paper and found it very persuasive or very convincing. And he agreed with me on many points, but perhaps not on all. But I think his main interest is more, “Should this disease, this question, get the priority that it is getting?” He says it is clearly not the number one health priority in this country. Then also he questions that the virus is solely responsible for it.
JL: On the numbers involved — I’ve heard it said that in the United States about 1000 people die every single day from smoking cigarettes. And so this would mean that in a month more people have died from smoking cigarettes than have died from AIDS…
JL: And in this sense, the only way that AIDS can be considered a true epidemic, a health catastrophe, would be if the CDC’s projections were right — more than a quarter of a million AIDS cases in the U.S. alone within the next four years.
PD: Well, that’s prophesy. In science you’re supposed to analyze what happens now, what happened in the past. Prophesies, predictions are not very good science. I mean, you can say that today somebody died in a space shuttle, and tomorrow five die in a space shuttle, and you can extrapolate to predict that by the year 2000-something, everybody will have died in a space shuttle. That’s essentially what they’re doing now.
There is always a self-limiting step to disease, or we wouldn’t be around. Life is now 3 billion years old, or 4 billion. We wouldn’t be around if we were that fragile. And AIDS mortality seems to be declining. They might say because the therapy is better, patients last longer. But it certainly doesn’t look like what they always extrapolate. And of course diagnosis, under the present definition wasn’t possible until 1984, until the antibody test was developed. [Note: The Food and Drug Administration, in licensing the antibody test, specifically states that it is “inappropriate” to use it as a diagnostic for AIDS.]
It always reminds me of a talk by an expert on Epstein-Barr virus epidemic in Africa — she showed those hot spots there on the map of Africa, and then the next slide was the distribution of doctors in Africa, and the two coincided perfectly.
JL: That appeals to all of my prejudices against doctors. Perhaps I shouldn’t say this. When I was in school — I attended Harvard — we were studying psychological testing, and they told us that for many decades records were kept of the IQs of all Harvard students, and that the IQs of those in the Medical School were far below those in any of the other graduate schools or the College. The medical students had IQs about one standard deviation below students in the Law School or the College. Of course Harvard would be one of the foremost medical schools in the country, and so they would not be stupid in absolute terms. But my impression of physicians is that they tend to be arrogant, wealthy, and on the whole, not very bright.
PD: Well, I think to say “bright” is deceptive. They are selected that way. They get good grades. But I don’t think they are selected to be very original or very nonconformist. To get into medical school they have to have straight A grades. And those are the guys who please the teachers and do everything well, which is a certain type of intelligence. But it’s not the type who skips classes and sits back, like Einstein, and comes up with a new idea. It’s not the nonconformist — that type is not selected for the MD now. And the field of public health is really dominated by MD types. The basic researchers, the bench people, are given that virus, which is already said to be the cause of AIDS, and are told to do their biology on it. I think what’s really needed is not the bench work on the virus. We know almost more than we need to know about that virus by now. What we need to know is what really causes AIDS.
JL: That leads into the question of treatment — such things as AZT. In New York I know one person who’s in a terrible dilemma. He knows many other PWAs in New York, who have told him that, according to the grapevine, AZT is poison — that most patients treated with AZT feel worse, contrary to the propaganda, and that there are terrible side effects.
PD: It is a poison. It is cytotoxic.
JL: His doctor has insisted that he must go on AZT. Considering that, according to you, it’s not by any means proven that HIV — or for that matter any virus — is the cause of AIDS, what is the good of giving AIDS patients this kind of treatment?
PD: AZT? Well, to put it as kindly as possible, I think it’s highly irresponsible. I could go further. Even if the virus were the cause of the disease, the only time the AZT could possibly interfere with the infection would be during the phase when the virus makes DNA. The AZT is an inhibitor of DNA. So in effect it could be like a “morning after” pill — if you knew you were infected the night before, and took the AZT, you might have a chance of hitting the virus. But it also hits all other DNA that is made. It is hell for the bone marrow, which is where the T and B cells and all those things are made. It’s hell for that. It has a slight preference for viral DNA polymerase, compared to cellular DNA polymerase, and that’s based on in vitro studies only, but that’s certainly not absolute. It kills normal cells quite, quite extensively. And considering the size of the target — the normal cells are so much bigger than the virus — even if AZT has a preference for the virus, you will hurt the normal cells no end. That’s guaranteed. That you hurt the virus is rather hypothetical. Certainly by the time a patient has symptoms of the disease, given the long latent period of the disease, and given the fact that the virus is inactive even in the acute form of the disease, I see no rationale for treating with AZT. Considering that the virus has already been in an AIDS patient for five years, and there’s no evidence that it’s making DNA at that time, I think that giving AZT is highly irresponsible.
There was a talk here two months ago, and the speaker couldn’t explain the rationale for treating with AZT. He didn’t know. So I said, “Why don’t you use aspirin?” And everybody laughed. He had no answer. He got mad at me. He is a doctor, ministering to the sick, seeing people die, and doesn’t understand the basis for it all.
JL: I understand there are almost no data on AZT. The double-blind study was prematurely aborted after only five and a half months. They have not even tracked the people from that study who are still taking AZT, so we have no idea what percentage of them are still alive. They have no data they can give you on what percentages of patients suffer from specific side effects. In effect, it’s a matter of faith that a few people claim that they feel better.
PD: There are not even any good animal studies. Later they claimed results from mice that were treated first and then inoculated with the virus. There it clearly has an effect. But that’s when you get high virus titers and you know you’re shooting up now. But five years later? There’s no basis for doing so, because the DNA is made by then. The virus is just sitting there and making RNA from existing DNA. And the drug is only going to hurt you.
JL: Backtracking to those people who are seropositive — some people, like Mathilde Krim, have stated that anyone who is antibody positive — or in her terms “infected with HIV” — must realize that he or she can never have children. I’m not sure that I would accept that. Would you?
PD: Well, there are data on this — antibody positive women who have children — and some of the babies have AIDS, but very few of them. People with virus antibodies have children — I mean, there are tribes in Venezuela where from 3 to 13% of the men and women have HIV antibodies, and they have children.
JL: They have normal children?
PD: Yes. And in Africa the same. Now, AIDS in babies is even more poorly defined than AIDS in adults, but even so, the numbers of AIDS babies is very tiny compared to the numbers of antibody-positive individuals in these populations.
JL: So one could say that, in and of itself, having antibodies to HIV is compatible with being a perfectly healthy person who could have perfectly healthy children?
PD: That is true. Absolutely. I agree with that 100% I don’t know of any evidence that this is not so. I don’t know of one paper that says otherwise. It is certainly true of all other retroviruses, human as well as animal. In fact, there is no mouse that doesn’t contain at least several hundred retroviruses — hundreds, not just one or two, of retroviruses which are not significantly different from this one, except it’s a mouse virus. You know that mice have children. Lots of them. All the time.
JL: Wasn’t it only ten years ago that the first retroviruses were identified?
PD: No, actually the first ones were identified 70 to 80 years ago. The definition of retroviruses as viruses that replicate via DNA — that came along 15, 16, 17 years ago. But retroviruses are some of the oldest viruses known.
Gallo believed in the virus-cancer program. He was searching for viruses in humans, under the assumption that if you found them they would be close to a tumor or disease. And he was successful in the first part of that. He persistently looked for viruses in humans, and he found them, like HTLV-I. So retroviruses in humans are relatively newly discovered, because the methods to detect latent viruses were developed fairly recently. But pathology, disease, or cancer caused by these viruses is extremely far from proven. In fact, there is not even one single case where the causal relationship is proven.
JL: Apparently for years researchers have been injecting fluids from AIDS patients into apes and monkeys, and the infra-human primates seem to be perfectly healthy.
PD: Yes, they act as the vast majority of humans. They make antibodies to the virus, period. That’s it.
JL: In general, the microbes that can make human beings sick — wouldn’t they also make apes and monkeys sick? Is there any precedent for that?
PD: Well, yes there is precedent. There are bacteria and viruses that are pathogenic in some species, but not in others. But in this case, we don’t know if HIV is pathogenic for anybody. The only exception would be laboratory situations where you allow the virus to take over by injecting it into an animal before it has an immune system.
JL: In your article you dispute the claim that HIV kills T-cells.
PD: The claim is that the AIDS virus works by killing the T-cells as one of the hallmarks of the disease — that the T-cells are reduced in numbers or depleted. And that again is a difficult one to reconcile with the viral characteristics. A retrovirus is a rare entity among viruses, which needs not only cellular DNA synthesis (that’s the only way AZT could possibly work, if the virus were actively making DNA) but above all it needs mitosis in order to establish or set up infection. Mitosis means cell division. A retrovirus does not infect successfully or productively a non-dividing or resting cell. So it is very difficult to reconcile the claim that the virus works by killing cells with the fact that it needs mitosis in order to replicate in that cell. You would have to write a book on programs for viruses, whereby initially the virus encourages or at least waits for the cell to divide, in order to replicate, and then once that is done, says, “OK, now I’m going to kill you in the next phase”. Which is extremely difficult. You could possibly do it with a computer program, but not with the limited genetic information that viruses act on. It is very, very small.
It is inconceivable that the same virus could first allow mitosis in order to exist, and then in the next phase kill the cell, which would in fact be suicidal for the retrovirus. Most other viruses do that. They are cytocidal. They kill cells, and they live by producing large numbers of offspring and killing, killing more cells, or by becoming latent and not doing anything. But retroviruses are different. They need dividing cells.
There is no evidence that cells are killed by HIV. The only evidence they have is that in vitro the virus activates or agglutinates cells, when they first get infected. The reason for that is most likely that infected cells in vitro, which we know are carrying the virus particles on the surface, see uninfected cells which have receptors for these virus particles that are not satisfied yet, so the two get together. Instead of just taking in the virus particles they take on a whole cell, which is full of virus particles, and the two cells fuse together. And that in turn generates a fusion of cells. And those cells that cannot go on readily to divide, might die — in vitro. But that is not specific for this virus. This happens with all viruses, particularly with retroviruses. They do the same thing. They fuse cells together. Even cytocidal viruses do that, particularly in vitro, where you can reach locally very high concentrations of uninfected cells that sit there for the virus to colonize rather than being flushed away, as they would be in vivo, where you have blood, where you have antibodies in between. The fact that these things can happen in vitro does not mean that the virus is intrinsically killing cells, which a retrovirus cannot support.
JL: I believe you are saying two things. One is that the virus infects very, very few cells — as few as one in 100,000 — and on top of that, it doesn’t even kill the cells it infects.
PD: That’s exactly right. If the virus wants to replicate, it cannot kill cells. It needs mitosis to replicate. We don’t know of any mechanism by which it could kill cells. They have no answer for that. When you ask them, they always get very evasive. “It activates a cell, which releases a factor that is toxic, that would kill other cells.” But what the factor is, and what it activates, and how it does it — that is all unknown.
JL: One comment was made, which I remember from the statement by Dr. Blattner. I had asked how HIV could cause AIDS when it only infected one in 100,000 susceptible cells, and the NCI press officer read a statement by Dr. Blattner, which was: “The mechanisms through which Human Immunodeficiency Virus brings about extensive destruction of immunological functions is unknown.” [laughter]
PD: Well, that’s great. They claim that it is, but they don’t know the mechanism!
JL: It reminds me of early Church theology, where they glorified what they called “mysteries.” Supreme holiness was associated with unknowability. But it seems they have nothing to demonstrate with regard to how they think HIV causes AIDS.
PD: It’s become dogma. They are quite dogmatic. Did you ever talk to any of them — like Haseltine or Gallo or Essex?
JL: Not yet. I have read interviews with some of them — Dr. Gallo, for example, who disagrees even with the possibility of co-factors. He believes the virus is entirely sufficient to cause AIDS. He made the statement, “If you’re run over by a truck, you don’t need co-factors.” Well, HIV does not seem to be much of a truck, does it?
PD: Not at all!
JL: I think that, back when there was still open discussion of these things, some theoreticians thought that AIDS might be an auto-immune condition. Is there any way that this concept might fit in with the “AIDS virus”?
PD: Auto-immune disease is always used when you don’t know any other explanation. That’s been the traditional standby when you couldn’t explain things. Maybe that’s so. I don’t see it. You wouldn’t lose your T-cells. You might perhaps lose those T-cells that were infected, but not the others. If it is an auto-immune disease, what is the antigen? I don’t see how the auto-immune disease could explain it.
JL: As you know, the readership of the Native consists mostly of gay men. Is there anything you would like to say to them in conclusion, on risk reduction or any other topic?
PD: I can only reiterate what has been said. Apparently promiscuity and drug use are risk factors. But I don’t think the virus is. I wouldn’t worry about the virus. Being seropositive against a virus is traditionally to your advantage; that’s beneficial. When you have antibody to a virus, you are vaccinated. They talk about making a vaccine. We are already diagnosed by the vaccine. So I think the virus is the one thing you should not worry about.
JL: So you would not regard a positive test result as a death sentence, as some of the Public Health Service officials seem to?
PD: I keep hearing that! If somebody says you are antibody positive, just say, “Fine! That protects me against anything the virus can do to me.” That would be my reaction.
JL: That’s a strong statement.
PD: To have an antibody to a virus is better than having no antibody to a virus. But I don’t think there’s a chance it’s that virus. I told Gallo that I wouldn’t be afraid to be injected with HIV. I wouldn’t mind. But, I said, “The virus couldn’t come from your laboratory; it would have to be cleaner than that.” And, of course, something else could be transmitted, something that could be the real cause of AIDS.
I would not worry about being antibody positive.