IS HIV THE CAUSE OF
An interview with Eleni
By Christine Johnson
Continuum Autumn 1997
Dr. Eleni Papadopulos is a biophysicist and leader of a group of
HIV/AIDS scientists from Perth in Western Australia. Over the past
decade and more she and her colleagues have published many scientific
papers questioning the HIV/AIDS hypothesis. This interview by Christine
Johnson looks at this work and especially her group's views on the AIDS
CJ: Eleni, many thanks for agreeing to this interview.
EPE: My pleasure.
CJ: Does HIV cause AIDS?
EPE: There is no proof that HIV causes AIDS.
CJ: Why not?
EPE: For many reasons but most importantly, because there is no proof
that HIV exists.
CJ: That seems a rather bold and incredible statement to
EPE: I suppose it is but nevertheless, that's where my research takes
CJ: Didn't Montagnier and Gallo isolate HIV? Back in the early
EPE: No. In the papers published in Science by those two
research groups, there is no proof of the isolation of a retrovirus from
CJ: They say they did isolate a virus.
EPE: Our interpretation of the data differs.(3-5)
CJ: Perhaps you should explain what leads you to this rather
EPE: I think the easiest way to begin is to ask the question, "What
is a virus?". The answer is quite simple. A virus is microscopic
particle that reproduces itself inside a cell...
CJ: Don't bacteria do that?
EPE: They may but there's a very important difference. Bacteria are
not obliged to replicate inside a cell. Viruses must. You see, what
bacteria take from the cell, or from an inanimate source of food and
energy, is all turned into the next generation of bacteria inside the
bacterial cell itself. That's also how our own cells replicate. But
viruses can't do that. The virus particle is really no more than a few
proteins strung around a piece of RNA or DNA but without the machinery
needed to replicate.
CJ: So whereas a cell is a factory, a virus is a blueprint that
must hijack a factory?
EPE: I can't better that analogy.
CJ: How does a virus replicate?
EPE: It has to get inside the cell. To do this the protective
envelope of the viral particle fuses with the cell membrane and then the
particle passes inside. Once inside, using the cellular metabolic
machinery, the virus particle is disassembled. Then, using the same
machinery, separate pieces of new virus are synthesised. Finally, all
the viral components are put together and out come the new virus
CJ: Out of where?
EPE: The virus either destroys the cell or in the case of
retroviruses the virus particles have a more orderly exit by budding out
of the cell membrane. But thatís not what happens with HIV. Unlike
retroviruses, HIV is said to destroy the cells.
CJ: Well, what about HIV particles? Are you suggesting theyíre not
EPE: To prove the existence of a virus you need to do three things.
First culture cells and find a particle you think might be a virus.
Obviously, at the very least, that particle should look like a virus.
Second, you have to devise a method to get that particle on its own so
you can take it to pieces and analyse precisely what makes it up. Then
you need to prove the particle can make faithful copies of itself. In
other words, that it can replicate.
CJ: Can't you just look down a microscope and say there's a virus
in the cultures?
EPE: No you can't. That's the whole point of putting the virus
question. Not all particles that look like viruses are viruses. You have
to prove that whatever particle you nominate can actually make copies of
itself. No replication, no virus. I'm sorry but this is an extremely
important point. No one, especially virologists, can afford to ignore
CJ: That seems to make sense. I guess it would be hard to get sick
catching a particle that could not make more of itself.
CJ: So where did AIDS research go wrong?
EPE: It's not so much a question of where the research went wrong.
It's more a question of what was left out. For some unknown reason the
decades old method of retroviral isolation (6,7) developed to study
animal retroviruses was not followed.
CJ: You better explain retroviruses before you go on.
EPE: I should. As you probably know, HIV is claimed to be a
retrovirus. Retroviruses are incredibly tiny, almost spherical particles
CJ: How tiny are they?
EPE: One hundred nanometres in diameter.
CJ: How tiny is that?
EPE: One ten thousandth of a millimetre. Millions would fit
comfortably on the head of a pin.
CJ: How do you actually see something that tiny?
EPE: You need an electron microscope. Thatís how we know the size and
shape of retroviral particles. That theyíre almost round and they have
an outer envelope covered with knobs and an inner core consisting of
some proteins and RNA.
CJ: So, if it exists, HIV is an RNA virus?
EPE: Yes. Another important point is that retroviruses do not
directly use their RNA blueprint to make more virus. According to
retrovirologists, what sets them apart from nearly all other viruses is
that retroviruses first make a DNA copy of their RNA. This DNA then
moves into the cell nucleus where it becomes part of the cellular DNA.
This stretch of DNA is called a provirus and there it sits, hibernating,
perhaps for years, until something activates the cell.
CJ: What happens then?
EPE: The proviral DNA is copied back into RNA and it is this RNA, not
the original RNA, that instructs the production of the necessary
proteins to make new virus particles.
CJ: Why are they called retroviruses?
EPE: Because for a long time biologists believed that the direction
of information flow in the cells of all living things was from DNA to
RNA, and thence to the proteins whose synthesis the RNA instructs. If we
say this direction is "forwards" then what retroviruses do first is copy
their information "backwards".
EPE: There's one more thing. One of the proteins inside a retrovirus
particle is an enzyme which catalyses this process. Not surprisingly,
it's called reverse transcriptase.
CJ: And that's it?
EPE: Well, that's why they're called retroviruses.
CJ: You mentioned the decades old method of isolating
retroviruses. How many decades are we talking about?
EPE: From the 1940s until the late 1970s. You see retroviruses were
among the first viruses discovered. Dr. Peyton Rous at the Rockefeller
Center in New York originally encountered them when he was doing
experiments on malignant muscle tumours in chickens.(8) Not that he
could actually see them. That was back in 1911. It wasn't until the
invention of the electron microscope and the high speed centrifuge that
things began to be sorted out.
CJ: What was actually sorted out?
EPE: It was these that led to the method of identifying and purifying
CJ: That's the same as isolating them?
EPE: Yes. To purify particles of any kind a scientist has to develop
a method of separating out the particles he wishes to study from
CJ: How did electron microscopes and high speed centrifuges make
purification of retroviruses possible?
EPE: The electron microscope enabled particles this small to be seen.
The other part was played by the high speed centrifuge and was extremely
important. It was discovered that retroviral particles have a physical
property which enables them to be separated from other material in cell
cultures. That property is their buoyancy and this was utilised to
purify the particles by a process called density gradient
CJ: Sounds complicated.
EPE: The technology is complicated but the concept is extremely
simple. You prepare a test tube containing a solution of sucrose,
ordinary table sugar. But it's made so the solution is light at the top
but gradually becomes heavier, or more dense, towards the bottom.
Meanwhile you grow whatever cells you think may contain your retrovirus
and if youíre right retroviral particles will be released from the cells
and pass into the culture fluids. When you think everything is ready you
decant a specimen of culture fluids and gently place a drop on top of
the sugar solution. Then you spin the test-tube at extremely high
speeds. This generates tremendous forces and particles present in that
drop of fluid are forced through the sugar solution until they reach a
point where their buoyancy prevents them penetrating any further. In
other words, they drift down the density gradient until they reach a
spot where their own density is the same as that region of the sugar
solution. When they get there they stop, all together, or to use
virological jargon, that's where they band. That band can then be
selectively extracted and photographed with an electron microscope.
CJ: And do retroviral particles band at a characteristic
EPE: Yes. In the sucrose solutions they band at a point where the
density is 1.16 gm/ml.
CJ: So, examination with the electron microscope tells you what
fish you've caught?
EPE: Not only that. Itís the only way to know if you've caught a
fish. Or anything at all.
CJ: True. Did Montagnier and Gallo not do this?
EPE: This is one of the many problems. Montagnier and Gallo did use
density gradient banding but for some unknown reason they did not
publish any EMs of the material at 1.16 gm/ml which they and everyone
afterwards call "pure HIV". This is quite puzzling because in 1973 the
Pasteur Institute hosted a meeting attended by scientists some of whom
are now amongst the leading HIV experts. At that meeting the method of
retroviral isolation was thoroughly discussed and photographing the 1.16
band of the density gradient was considered absolutely essential.
CJ: But Montagnier and Gallo did publish photographs of virus
EPE: No. Montagnier and Gallo published electron micrographs of a few
particles which they claimed are a retrovirus and are HIV. But
photographs donít prove particles are a virus and the existence of HIV
was not proven using the method presented at the 1973 meeting.
CJ: And what was that method?
EPE: All the steps I have just told you. The only scientific method
that exists. Culture cells, find a particle, isolate the particle, take
it to pieces, find out whatís inside and then prove those particles are
able to make more of the same with the same constituents when theyíre
added to a culture of uninfected cells.
CJ: So before AIDS came along there was a well tried method for
proving the existence of a retrovirus but Montagnier and Gallo did not
follow this method?
EPE: They used some of the techniques but they did not undertake
every step including proving what particles, if any, are in the 1.16
gm/ml band of the density gradient, the density that defines retroviral
CJ: But what about their pictures?
EPE: Montagnier's and Gallo's electron micrographs and every other
electron microscope picture published up until March this year are of
unpurified cell cultures. Not the gradient. Before March this year, no
one had ever published a picture of a density gradient.
CJ: Which is what we need to do to prove isolation of retroviral
CJ: Can the 1.16 band contain material other than retroviral
EPE: Yes. Thatís another reason why you need a photograph. To see
everything thatís going on. It was known long before the AIDS era that
retroviral-like particles aren't the only material that may find their
way into this part of the density gradient. Tiny cellular pieces, some
recognisable as internal structures of cells, or just cellular debris,
can band at 1.16 gm/ml. And some of this material can enclose nucleic
acids and take on the appearances of retrovirus particles.
CJ: What are nucleic acids?
EPE: DNA and RNA.
CJ: Surely though, if retroviral particles are released from cells
without disrupting the cells, it must be possible to guard against
EPE: Well it is and it isn't. Certainly the animal retrovirologists
were well aware of this problem and strongly advised handling the
cultures gently and regularly topping them up with nutrients to keep the
cells alive. So they donít disintegrate. But in the case of HIV there
are additional problems. We are told that HIV is cytopathic meaning it
kills cells. So one could hardly claim that putative virus particles are
the only things likely to be floating around in culture fluids or at
1.16 gm/ml. The other confounding fact is that in many HIV experiments
the cells are deliberately broken up by the experimenter as part of the
experiment. Knowing all this, it's a complete mystery why any HIV
researcher could have omitted the crucial step of taking an EM of a
CJ: Could it be because electron microscopy is highly specialised
EPE: It may have been in the early days but not anymore. For the past
twenty years at least electron microscopy has been used daily in most
hospitals to diagnose all kinds of diseases. Besides, there are plenty
of EMs of HIV cultures. Itís just that until this year, for some unknown
reason, there havenít been any of the density gradient.
CJ: All right. Let's talk about the pictures of the density
gradient published this year. What do we see there?
EPE: Two groups, one Franco/German (9) and one from the US National
Cancer Institute (10), published pictures of density gradients. In the
Franco/German study the pictures are from the 1.16 gm/ml band. It is
impossible to tell from which density the pictures in the American study
are taken but let's assume it's the correct 1.16 density for retroviral
particles. The first thing to say is that the authors of these studies
concede that their pictures reveal the vast majority of the material in
the density gradient is cellular. The authors describe all this material
as "non-viral", or as "mock" virus or "microvesicles".
CJ: What are microvesicles?
EPE: Encapsulated cell fragments.
CJ: Are there any viral particles in these pictures?
EPE: There are a few particles which the researchers claim are
retroviral particles. In fact, they claim these are the HIV particles
but give no evidence why.
CJ: Are there lots of these HIV particles?
EPE: No. The band should contain billions and when you take an
electron micrograph they should fill the entire picture.
CJ: So the banded material contains only a few HIV particles and
from the HIV particlesí point of view is rather impure?
CJ: Do the experts comment on this?
EPE: They say the cellular material "co-purifies" with the HIV
CJ: Tell me, the few particles they say are HIV, do they look like
EPE: They bear only the vaguest resemblance to retroviral particles.
For sure they look more like retroviral particles than all the other
particles and material but even if they looked identical to retroviral
particles you cannot say they are a retrovirus. Even Gallo admits to the
existence of particles which band at 1.16 gm/ml and which have the
appearances and biochemical properties of retroviruses but which are not
retroviruses because they are incapable of replicating.(11)
CJ: All right, but that aside, whatís the difference between these
particles and a real retroviral particle?
EPE: Gallo and all other retrovirologists, as well as Hans Gelderblom
who has done most of the electron microscopy studies of HIV, agree that
retrovirus particles are almost spherical in shape, have a diameter of
100-120 nanometres and are covered with knobs.(12,13) The particles the
two groups claim are HIV are not spherical, no diameter is less than
120nM, in fact many of them have major diameters exceeding twice that
permitted for a retrovirus. And none of them appear to have knobs.
CJ: Surely size canít be that critical? Many things in Biology
have a range of sizes. What about humans? Thereís plenty of humans twice
the size of other humans. Theyíre all still humans.
EPE: Whatís true for humans is not true for retroviruses. For a
start, retroviruses donít have to grow up. Theyíre born adults. So the
correct comparison is between adult humans. Theyíre arenít too many
twelve foot humans. In fact, the tallest human ever recorded was eight
feet eleven inches. But thereís more than size involved here.
CJ: What else?
EPE: If we assume both the Franco/German and US groups sought
particles at the correct retroviral density then the particles found by
both groups must have the same density, 1.16 gm/ml. If you measure the
major and minor diameters of the particles in the EMs they claim are HIV
and take the average diameters and for argumentís sake, assume theyíre
all spherical, then the Franco/German particles are 1.14 times larger
than genuine retroviral particles and the US particles are 1.96 times
larger. Now, to translate this into volumes, we have to cube the ratios
of the diameters. So, if we take 120nM as the upper limit for the
diameter of a retroviral particle and do the sums, the Franco/German
particles have 50% more volume than a retroviral particle and the US
particles have 750% more volume. And the US particles are five times
more voluminous than the Franco/German.
CJ: Which tells us what?
EPE: It tells us that the Franco/German and US particles must contain
50% or 750% more mass than genuine retroviral particles.
CJ: Why is that?
EPE: Because density is the ratio of mass to volume. If the volume
goes up by a certain amount, to keep the same density, the mass has to
go up by the same amount.
CJ: OK but whatís your point?
EPE: The point is that any genuine retroviral particle contains a
fixed amount of RNA and protein. No more and no less. If thatís the case
then these particles are made up of much more material than a genuine
retrovirus. Which means that if these different sized particles are
truly HIV then HIV cannot be a retrovirus. The only other explanation is
that the electron micrographs are not from the 1.16 gm/ml band. If
thatís the case then we have no choice but to redefine retroviruses and
more importantly, not to consider the 1.16 band as HIV. But if we do
that then all the research done on HIV using this band cannot be used
because this is what everyone uses as purified HIV. That would mean for
example that this band cannot be used to obtain proteins and RNA for use
as diagnostic agents to prove HIV infection.
CJ: You mentioned the particles lacked knobs. How serious a
deficiency is that?
EPE: All the AIDS experts agree that the knobs are absolutely
essential for the HIV particle to lock on to a cell. As the first step
in infecting that cell. So, no locking on, no infection. The experts all
claim that the knobs contain a protein called gp120 which is the hook in
the knobs that grabs hold of the surface of the cell itís about to
infect.(14) If HIV particles do not have knobs how is HIV able to
CJ: You mean it can't get hold of the cell to get inside?
EPE: Precisely. And if it can't replicate, HIV is not an infectious
CJ: That sounds like a serious problem to me. How do the experts
EPE: They avoid it. And the knobs problem is not something new. The
German group drew attention to it in the late 1980s and again in
1992.(15,16) As soon as an HIV particle is released from a cell all the
knobs disappear. This single fact has so many ramifications. For
example, three quarters of all haemophiliacs tested are HIV antibody
positive. And the claim is that haemophiliacs acquired these as a result
of becoming HIV infected from infusions of contaminated factor VIII
which they need to treat their clotting deficiency. The problem is that
factor VIII is made from plasma. Thatís blood with all the cells removed
which means if there are any HIV particles present in factor VIII they
must be floating free in solution. But if cell free HIV has no knobs
those HIVs have no way of getting into fresh cells to infect them.
CJ: Then how do you explain HIV antibodies and AIDS in
EPE: My colleagues and I have published several papers discussing
alternative explanations including a detailed analysis of haemophilia in
an invited paper in the 1995 special issue of Genetica (17)
devoted to the HIV/AIDS controversy.
CJ: I must confess I find it very hard to accept that
haemophiliacs have not been infected through contaminated clotting
concentrates. And I bet haemophiliacs do too.
EPE: Unfortunately that is true but perhaps I can persuade you with
one quick and simple explanation. Tell me this. If someone HIV positive
is cut and bleeds how long does the blood remain infectious? Outside the
CJ: According to what Iíve read, for only a few hours at the
EPE: And why is that?
CJ: Because HIV dries out and dies. Certainly thatís what the CDC
EPE: OK. Let me ask you this. How is factor VIII made?
CJ: From donated blood.
EPE: Right. Have you ever seen a vial of factor VIII?
EPE: All right Iíll tell you. It comes as a dry, flaky, yellowish
powder and by the time itís used itís at least a couple of months old.
Do you see the problem?
CJ: I do. If itís dry and that old any HIV in it should be long
EPE: Exactly. So how does factor VIII cause HIV infection and AIDS in
CJ: I donít know but I think I'm beginning to see why your group
is not the toast of the town. Perhaps we'd better not get diverted into
a discussion about haemophila. Why do you think until now most HIV
experts have been happy enough to regard the material at the 1.16
density as pure HIV?
EPE: I think it's premature to assume these pictures have changed
anyoneís minds about the 1.16 gm/ml portion of the density gradient
being anything but pure HIV.
CJ: Well how does your group respond to these pictures?
EPE: On the evidence provided by these pictures there is no reason to
claim that this material is pure or that it contains retroviral-like
particles let alone a retrovirus or more importantly, a specific
retrovirus, HIV. And this vindicates the position we have held ever
since the beginning. And a position we long ago put into print That
there is no evidence proving the isolation of a retrovirus from AIDS
patients or those at risk of AIDS.
CJ: OK. Let's set aside the March pictures and talk about what we
could deduce from what was known beforehand. How solid is the evidence
prior to March that HIV exists?
EPE: Sticking to particles all the evidence comes from electron
micrographs of whole cell cultures. Not density gradients. From this
evidence it can be said that cell cultures contain a large variety of
particles some of which are claimed to look like retroviral particles.
That's all. None of the particle data has been taken further. No
purification, no analysis and no proof of replication. In these cultures
several research groups including Hans Gelderblom and his associates
from the Koch Institute in Berlin who specialise in this area have
reported not just one type of particle but a stunning array of
particles.(13,19,20) This raises several questions. If one of these
particles really is a retrovirus experts call HIV, what are all the
others? If the HIV particles originate from the tissues of AIDS
patients, where do all the others come from? Which of these particles
band at 1.16 gm/ml? If the HIV particles cause AIDS why doesn't one or
several of the other particles also cause AIDS? Why don't all the
particles cause AIDS? Or why doesnít AIDS or the cultures cause the
appearance of the particles? And when it comes to HIV, the HIV experts
can't even agree what is the HIV particle. There are three subfamilies
of retroviruses and HIV has been classified by different research groups
under two of these subfamilies as well as three different species.
CJ: Where does this leave us?
EPE: We still don't know what any of the particles are. We don't have
a definite particle proven to be a retrovirus from which to take
proteins and RNA to use in tests for infection in people or to do
experiments to try and understand what is happening if there truly is a
virus causing AIDS.
CJ: All right. Let's suppose that we do have a picture of a
density gradient and it contains nothing but thousands of particles all
the right size and shape, and with knobs, to be called a retroviral
particle. Let's go over what should be done next.
EPE: The next steps are to disrupt the particles, find out what
proteins and RNA are in them, prove one of the proteins is an enzyme
which turns RNA into DNA and finally, take more of the density gradient
and prove that when PURE particles are put into a virgin cell culture
exactly the same particles made up of the same constituents come
CJ: And has this been done?
EPE: No, but perhaps I can explain things more clearly by talking
about what has been done. Some of Gallo's experiments from 1984.
CJ: Isn't 1984 a bit ancient?
EPE: No because that's when the best research on HIV isolation was
done. Those experiments are vitally important because everything
believed and taught about HIV is founded on what happened back then.
EPE: Yes every single solitary thing. Whether an HIV particle has
been isolated and therefore any claim that it exists. The HIV proteins
used in the antibody tests. The RNA used especially to diagnose children
infected with HIV and now used to measure the so called viral load. And
more. But the question is are they good enough?
CJ: Good enough?
EPE: Good enough to claim the existence of a unique retrovirus called
HIV and that it causes AIDS.
CJ: OK. Tell us about Gallo's experiments. Why was he interested
in AIDS anyway?
EPE: By 1984 Gallo had already spent more than a decade researching
retroviruses and cancer. He was one of the many virologists caught up in
President Nixon's decade of war against cancer. In the mid 1970s Gallo
claimed to have discovered the first human retrovirus in patients with
leukaemia. He claimed his data proved the existence of a retrovirus
which he called HL23V.(11,21) Now, just like he would later do for HIV,
Gallo used antibody reactions to "prove" which proteins in the cultures
were viral proteins. And not long afterwards others claimed to have
found the same antibodies in many people who did not have leukaemia.
However, a few years after that these same antibodies were shown to
occur naturally and be directed against many substances that had nothing
to do with retroviruses.(22,23) Then it was realised that HL23V was a
big mistake. There was no HL23V retrovirus. So the Gallo data turned out
to be an embarrassment and HL23V is now extinct. Whatís interesting for
us though is that the evidence used to claim proof of the existence of
HL23V is the same kind of evidence said to prove the existence of HIV.
In fact the evidence for HL23V was better than HIV.
CJ: Better in what way?
EPE: Well, unlike HIV, Gallo found reverse transcriptase in fresh
tissue. Without having to do cultures. And he published an EM of density
gradient material present at 1.16 gm/ml.
CJ: But it still turned out to be a false alarm?
EPE: Not even Gallo talks about HL23V anymore. But in 1980 he said
he'd discovered another retrovirus. It was yet more of the same kind of
data from leukaemia patients and this time he called it HTLV-I and
claimed it caused a particular rare form of leukaemia which Gallo now
calls adult T4 cell leukaemia, ATL. In fact, there are some very
interesting parallels and paradoxes between HIV and HTLV-I.
CJ: What are they?
EPE: Theyíre said to infect the same cells and to be spread the same
way. Yet unlike HIV, HTLV-I has not gone beyond where it was discovered.
The greatest prevalence of HTLV-I was reported from Africa and Southern
Japan and thatís where itís remained. Thatís longer than weíve had AIDS
and donít forget that although this virus is said to cause leukaemia,
less than 1% of persons who test positive ever develop leukaemia. Even
after forty years. But I digress. What I was about to say was that many
of the first AIDS patients had a cancer known as Kaposi's sarcoma, as
well as low numbers of the same T4 cells which are present in excessive
amounts in ATL. This was known because the technology to count the
different classes of lymphocytes came along about the same time that
CJ: HIV was hypothesised to be killing the T4 cells?
EPE: Well, this was too early for HIV but it was hypothesised that
something was killing them. Later Gallo actually went through a stage of
thinking that HTLV-I might be the culprit but that theory was a problem
because HTLV-I allegedly causes leukaemia which is far too many T4
cells. Also, despite the high prevalence of antibodies to HTLV-I in
Southern Japan, there were no AIDS cases. However, because gay men with
AIDS had such a high incidence of the cancer Kaposiís sarcoma, and
because something seemed to be affecting their T4 lymphocytes, Gallo
persisted in trying to find a retrovirus to explain it all.
CJ: What happened next?
EPE: Gallo and his colleagues did a lot of experiments which
culminated in four consecutive papers published in Science in May
1984. That was a year after the French published their paper also in
Science. Gallo's group began by culturing lymphocytes from AIDS
patients but apparently, none of the cultures produced enough reverse
transcriptase to convince Gallo that a retrovirus was present. At that
time Gallo had a Czech researcher called Mikulas Popovic working for him
and so Popovic and Gallo agreed to mix up culture fluids from ten AIDS
patients and add that to a culture of leukaemia cells. The leukaemia
cells they used in this culture had been obtained years earlier from a
patient with ATL. When they did this enough reverse transcriptase was
produced to convince Gallo and Popovic they now did have a
CJ: You mean a retrovirus would not grow in individual cultures
from AIDS patients but did when the specimens were mixed up and
CJ: Isn't that a little puzzling? How can a germ do that? Surely
if it's present in one of the specimens, as long as the cultures are
done the same way, it should grow no matter what?
EPE: You would think so.
CJ: And if you mix up all the specimens, how would you know who
had the virus in the first place? It might have come from just one
patient. Was Gallo ever questioned about this?
EPE: He was and in a 1993 television documentary said he didn't care
whether the virus came from a single patient or whether it came from a
pool of patients.
CJ: Did you not say that the leukaemic cells used in the cultures
were originally obtained from a patient with adult T4 cell
CJ: Then surely the cultures must have contained many T4
EPE: Thatís true.
CJ: If those cultures were made up from T4 cells and if HIV kills
these cells, how could a cell killing virus be expected to grow?
EPE: That's another of the problems with the HIV theory of AIDS. Even
though HIV is said to kill T4 cells and make people immune deficient,
that's what the "AID" in AIDS actually refers to, the leukaemic cell
line as well as its H9 clone which Popovic eventually produced, are both
immortal even when infected with HIV. That means rather than being
killed by HIV the cells permit what is regarded as HIV to grow
indefinitely. The H9 clone is widely used in both research and
commercially for producing what are regarded as the HIV proteins for use
in the antibody tests kits.
CJ: OK. What did Gallo actually do to prove he had isolated a new
retrovirus from AIDS patients?
EPE: If you read the first paper, what was called isolation consisted
of electron microscopic photographs of a few particles in the cultures,
not the gradient, finding reverse transcriptase and observing that some
antibodies present in a haemophilia patient as well as rabbits reacted
with some of the proteins in the cells of the cultures.
CJ: That was reported as isolation of a virus?
CJ: Is that really isolation?
EPE: No. Isolation means separation from everything else. Not just
detection of some phenomena. The only way to prove the existence of an
infectious agent is to isolate it. That's what this debate is all
CJ: Yes, but isolated or not, how do you respond to Gallo's claim
that his cultures grew a retrovirus?
EPE: Let me repeat, there is no question of isolation. Gallo did not
isolate a virus. There were no electron microscope pictures of a banded
specimen that one would expect to show nothing but retroviral particles.
How could there be? There were no EMs at all of a banded specimen. Just
pictures of cells with a dozen or so particles lying nearby but no
extraction and analysis and proof that these particles could replicate
into identical particles. But what we must ask is whether Gallo had the
proof to say he had even detected a retrovirus. In our view he did not.
And it's vitally important at this point to state that finding particles
and reverse transcriptase is not proof that a retrovirus is present.
CJ: You said retrovirus particles contain reverse
EPE: They do, in fact reverse transcriptase was discovered in
retroviruses but there's a catch. The catch is two things. The way the
presence of RT is proven and the fact that RT is not unique to
EPE: Reverse transcriptase. The existence of RT is proven indirectly.
By putting some RNA into a culture and seeing if DNA bearing the
corresponding sequence appears.
CJ: You mean the presence of RT is implied by the ability of the
culture to do this particular trick?
EPE: Yes. It's measured by demonstrating the process of reverse
transcription. Like many enzyme tests the test for reverse transcriptase
measures what the enzyme does, not the actual enzyme itself. So in the
case of RT it measures the production of DNA copied from a synthetic
piece of RNA introduced into the cultures. The problem is that RT is not
the only thing capable of doing this trick as you call it. Other
enzymes, normal cellular enzymes can also do this trick. In fact they do
it very well with the same synthetic RNA that all HIV researchers
introduce into their cultures to copy into DNA (24) and to claim their
cultures contain HIV RT and thus HIV. And whatís more, when you read the
AIDS literature, it becomes apparent that some researchers who publish
claims to have isolated HIV have done no more than detect RT.
CJ: That's quite disconcerting.
EPE: Thereís much more to RT. For instance, according to Harold
Varmus, Nobel Laureate and Head of the National Institutes of Health,
RTs themselves are also present in normal cells. And bacteria have RTs.
And it's known that some of the chemicals that are an obligatory
component of these cultures cause normal lymphocytes to reverse
transcribe. And leukaemic cells can also do the same trick unaided when
not cultured with such chemicals or cells from AIDS patients.
CJ: That's many possible reasons for RT then?
EPE: Yes and there's yet another. Remember that Gallo and Popovic
used H9 cells to demonstrate the existence of what they claimed was a
new retrovirus. But as I said before, if you trace the lineage of the H9
cell line it comes from the HUT78 cell line, a cell line which began
life in a patient whom Gallo says had a form of malignancy caused by
HTLV-I. If that malignancy is caused by HTLV-I then HTLV-I and its RT
will be in the very cells Gallo used to prove the presence of HIV.
CJ: But surely no one would search for a new retrovirus using
cells that already contained another retrovirus?
EPE: You would think not especially since a year earlier Gallo
published a paper in Nature reporting HTLV-I genetic sequences in
the cell line from which the H9 cells ultimately originated.(25)
CJ: So the evidence using RT does not look good?
EPE: The problem with RT is the same problem with all the evidence.
It's just like the particles Gallo photographed. They might be the
particles of a retrovirus, the reverse transcription might be caused by
the RT of a retrovirus but "might" is not scientific proof. You donít
construct scientific theories from what "might" be going on.
CJ: But even so Eleni, how can you dismiss particles? They're so
convincing. How can you escape the fact that no matter how widely Gallo
and everybody else deviated from the traditional method of isolating a
retrovirus, there are particles in these cultures and a lot of very
important people regard them as particles of a retrovirus.
EPE: I appreciate your point but I think particles have to be viewed
with a considerable amount of perspective. Retroviral-like particles are
practically ubiquitous. In the 1970s such particles were frequently
observed in human leukaemia tissues, in cultures of embryonic tissues
and in the majority of animal and human placentas. This is of
significance given that the H9 cell line is made up of leukaemic cells
and also because Montagnier obtained his EMs from cultures done with
umbilical cord blood lymphocytes. There's also a large group of
retroviral particles classified as type-C particles that are found in
fish, snakes, worms, pheasant, quail, partridge, turkey, tree mice,
agouti, tapeworms, insects as well as mammals. And amongst its many
official guises HIV has been described as a type-C particle, by both
Montagnier and Gallo.(26) Also, thereís an electron microscope study
reported in 1988 by O'Hara and colleagues from Harvard.(27) They
examined enlarged lymph nodes from both AIDS and non-AIDS patients and
found "HIV" particles in 90% of BOTH groups. They had to concede that
particles alone do not prove infection with HIV.
CJ: All right. Letís leave particles. What about the antibodies
that reacted with the cells in the cultures? Surely that must signify
something that ordinarily isn't present? Wouldn't this fit with a
retroviral infectious agent?
EPE: It might fit but thereís that word again. Itís simply not
possible to prove proteins belong to a retrovirus or antibodies are
caused by a retrovirus, or to claim proof of the isolation of a
retrovirus just because some things react together in a test-tube.
CJ: Could you explain that a little more please?
EPE: Again, let's not take the data any further than good science
allows. The experiments reported in the first Gallo paper tell us that
some antibodies present in a patient with haemophilia, as well as in
rabbits, reacted with some proteins in H9 cells cultured with
lymphocytes from AIDS patients.(1)
CJ: That's the data?
EPE: That's the data we have to work on. What's important is how we
interpret the data. Now, for what he called isolation of HIV Gallo
regarded the antibodies as the crucial evidence. How do we know this?
For two reasons. First, what we have already said. Gallo knew there are
particles which look exactly like retroviruses, which band at 1.16 gm/ml
and which contain RT but which do not replicate. So, whatever they are,
no matter how they arise, they can't be viruses. Second, we know because
in one of Gallo's papers he actually talks about the need to have
specific agents to identify a particle as a virus. And by that he means
specific antibodies or proteins. The Gallo hypothesis is that there is a
virus causing AIDS, it's foreign so when it infects a patient the
patient develops antibodies to the virus.
CJ: So it works backwards as well as forwards? Virus produces
antibodies and antibodies can be used to point to the virus?
EPE: No. Thatís the problem. Antibodies do not work backwards. Weíll
get to why in a minute. The important thing here is not to forget what
question weíre trying to answer. Weíre trying to define which proteins
are unique constituents of a retroviral particle. For me, thereís only
one way to do that. And itís easy. We define viral proteins exactly the
same way we define our arms and legs. Or our kidneys.
CJ: Meaning what?
EPE: My bits and pieces of anatomy are mine because they're part of
me. Either inside or outside. If one of my kidneys is diseased and has
to be removed the first thing the surgeon must do before Iím put on the
operating table is to check and make sure it's me. It's no different
with viruses. Viral proteins are the proteins that come out of particles
proven to be a virus. It's that simple. If you want to define the
proteins of a retroviral particle first you must prove you HAVE a
CJ: Antibodies are too imprecise?
EPE: Antibodies are imprecise but that's not the issue here.
Antibodies are irrelevant. You prove proteins come from a virus particle
by isolating the particle and then doing a dissection. You donít prove
proteins are constituents of a viral particle by performing chemical
reactions on what is essentially a culture soup. It has nothing to do
with it. So what if some proteins and antibodies react? There's many
reasons why these reactions might take place.
CJ: Such as?
EPE: There are many antibodies and antibodies to one thing can and do
react with other things.(28,29) Immunologists call these
cross-reactions. This is a fact of Nature and it causes problems because
an antibody reacting with a protein in a culture could just as well be
an antibody made to something totally unrelated. Quite possibly
something not even in the culture. To put it into plain language,
antibodies adopt other partners. My colleague Val Turner adopted the
term "promiscuous" to explain this behaviour. The only way to prove a
reaction you see is caused by the one antibody reacting with the one
protein is to see how the reactions compare with what you think they
signify. What we have to do is correlate the reactions against HIV
itself. Antibodies are specific to HIV if and only if they are present
only when HIV is present.
CJ: Not if HIV is absent?
EPE: One hundred percent specific means no antibodies reacting when
HIV is absent. Now, as my colleagues and I see it, using antibodies to
prove the existence of a retrovirus is the crux of the problem. This is
a very important part of our argument so I hope to get this very
important message across.
CJ: I'm all ears.
EPE: Think about what's happened so far. Thereís an old, logical,
reliable, commonsense method of proving the existence of a retrovirus.
Itís based on nothing more than the definition of a retrovirus as a
particle having a particular size, shape, appearance and constituents
and the ability to replicate. But for some unknown reason this method
has been abandoned in the HIV era. Don't ask me why but it has. In its
place we have a disparate collection of data including particles not
photographed in density gradients and some evidence for reverse
transcription either in the culture or the material which bands at 1.16
gm/ml. Neither of these are proof that a retrovirus exists in the
cultures. Gallo says so himself.
CJ: I'm following. Go on.
EPE: Then along comes the idea with antibodies. If there really is a
virus then being foreign, it should induce antibodies in people it
infects. Perhaps these antibodies are indeed specific meaning they are
made solely in response to HIV and react with viral proteins and nothing
else. OK. Let's assume this unlikely specificity is a fact and let's
make an even less probable assumption.
EPE: Let's say what's considered true of the so called HIV antibodies
is true for all antibodies. Every single antibody ever made only reacts
with what stimulated its production and with nothing else. Antibodies to
the tuberculosis germ only react with the tuberculosis germ. Antibodies
to hepatitis virus only react with hepatitis virus et cetera. OK.
We have some cultures of tissues derived from AIDS patients which react
with antibodies present in the serums of AIDS patients. What next? We
know that AIDS patients are infected with many different agents. So if
these agents, or bits of them, are present in AIDS patients, they're
also likely to be in their cell cultures. Isnít this why laboratory
workers are believed to be at risk from handling these specimens? And we
also know that despite being labeled immune deficient, everyone agrees
that AIDS patients have myriads of antibodies to all manner of things.
Including antibodies to human T-cells, the cells that make up the
cultures. If you add some antibodies from the same kind of patients to
these cultures, even if each antibody only reacts with its mate,
wouldn't you expect to see lots of reactions between lots of different
CJ: I see your point. Since all you see is reactions you canít
tell what is reacting with what.
EPE: Exactly. Antibodies react and things light up but whoís got a
finger on the switch? And for this argument we've agreed that every
antibody is directed against one agent and only reacts with that agent.
What if we bring back real life where antibodies cross-react as
CJ: I guess it's a big mess. It's difficult to tell where any
proteins or antibodies come from.
EPE: Thatís absolutely correct. And one must not confuse origins with
composition. For sure you canít prove the origin of a protein by an
antibody reaction. Why should a reaction tell you that a protein comes
from a particle any more than it comes from Mars? But you canít prove
identity either. Thatís because antibodies do not work backwards.
CJ: Are there any germs in AIDS patients that could actually react
like youíve said?
EPE: Yes. A good example is hepatitis B virus. Many, and in the case
of haemophiliacs, virtually all AIDS patients are infected with
hepatitis B virus. And HBV doesn't just infect liver cells. It also
infects T-lymphocytes. And strange as it may seem, hepatitis B virus has
a reverse transcriptase enzyme. And people make antibodies to this
CJ: OK. I get the drift.
EPE: But there's more to Gallo's experiments. For a start, the serum
that Gallo used in this experiment came from a patient with the initials
"E.T.". But ET didn't actually have AIDS. He had a condition known as
pre-AIDS. Thatís enlargement of lymph nodes in many parts of the body.
But pre-AIDS is caused by many infectious agents which are present for
example in gay men, intravenous drug users and haemophiliacs even when
there is none of what is called HIV present.
CJ: So ET might not have had HIV antibodies?
EPE: Exactly and the other puzzle is the rabbits.
CJ: Yes. I was going to ask about that.
EPE: Gallo claims he had a serum from rabbits that contained
antibodies specific to HIV. Just imagine for a moment the scene in
Gallo's laboratory. They've cultured H9 cells with lymphocytes from AIDS
patients and when they come to determine which proteins in their
cultures originate from a presumed virus they reach up on the shelf and,
lo and behold, they pull down a bottle labeled "specific antibodies to
HIV". How did they manage to get those antibodies? This was the first
paper they wrote but they already had a bottle containing rabbit
antibodies specific to a virus they were currently attempting to isolate
for the very first time.
CJ: Well how did they do it?
EPE: They say they prepared rabbit antibodies by repeatedly infecting
rabbits with HIV. But if they were preparing antibodies to HIV they
would have had to inject rabbits with pure HIV (30) which again means
they must have already isolated what they were now attempting to do for
the first time. It doesn't make sense.
CJ: Well, if they didnít inject pure HIV into the rabbits what did
EPE: At the very best, if they used a banded specimen which they and
everyone else regard as pure HIV, the evidence is that what they
injected would have been something akin to what we see in the
Franco/German and US National Cancer Institute pictures. Now any
immunology book will tell you that proteins are the most potent antibody
producing substances available. Even more so if they're introduced
directly into the blood stream. So, by injecting their culture material
into rabbits, even if they had used a banded specimen, Gallo and Popovic
would have exposed their rabbits to a multitude of cellular proteins.
The rabbits would have then produced antibodies to all those proteins
and when they added these antibodies back with the material they
injected of course there would be reactions. That's exactly what you
would expect but that doesn't make the material you inject into a virus.
And even less into a unique retrovirus.
CJ: OK. I understand what you're saying. Your argument is that,
before he had a virus, there was no way Gallo could have known there
were antibodies in patient ET or in AIDS patients or rabbits that would
specifically recognise HIV proteins.
EPE: Yes. Before he had a virus there was no way of knowing that
antibodies to HIV existed at all. Anywhere. To even begin to talk about
specific antibodies to specific HIV proteins first you have to prove the
proteins are constituents of a retroviral-like particle that is able to
replicate. And the only way to do that is to isolate the particles and
do everything else I've described. You need the virus BEFORE you go
looking for proteins and antibodies.
CJ: Well what on Earth are these antibodies in AIDS patients which
everyone calls HIV antibodies?
EPE: What my colleagues and I have been arguing all these years is
that there is no evidence they are HIV antibodies. The only way to find
out if they're HIV antibodies is to do the experiment comparing
antibodies with virus isolation. That is whatís meant by having a gold
standard. Using virus isolation as a totally independent means of
determining whether there truly are specific HIV antibodies. You can
think of HIV as being the adjudicator. If antibodies specific to a
retrovirus called HIV exist they will reveal themselves by reacting only
when a retrovirus called HIV is present. Nothing could be simpler. Now,
although you may not realise, thereís another problem. There might be
specific HIV antibodies but what if thereís non-specific HIV antibodies
CJ: I can see people getting confused. Could you please
EPE: All right. The problem using antibodies is that there could be
two types of antibodies. One type is specific meaning antibodies caused
by HIV and nothing else and reacting with HIV and nothing else. The
other type is non-specific meaning theyíre antibodies caused by other
agents or stimuli and sure they react with those agents but they also
react with HIV. If you add a personís serum to some of the "HIV"
proteins in a culture or in a test kit and see a reaction how can you
tell which type of antibodies are doing the reacting? In fact there are
three possibilities. All the antibodies might be the specific type or
none of them might be. Or there might be a mixture. All you see is a
reaction. Something changes colour. Thatís all. So how do you tell?
Simple. You test for antibodies in all sorts of patients, some with
AIDS, some who are sick but who donít have AIDS and in some healthy
people as well. But in the same experiments, at the same time, you use
HIV as the adjudicator. To judge what type of antibodies they are. And
if antibodies show up when thereís no HIV then non-specific antibodies
CJ: What about the experiment to sort out the antibodies?
EPE: The experiment, which should have been done long before HIV
antibody testing was ever introduced into clinical medicine, has never
been done. And in fact it could not have been done because to date
nobody has isolated HIV. But there's plenty of evidence that people who
all the experts accept are NOT infected with HIV do have antibodies
which react with what are claimed to be the HIV proteins. So there are
non-specific "HIV" antibodies and if some are non-specific how do you
know how many? Why not all of them? Even if itís only some how can you
tell them apart? The answer is you canít and that means that not one
single person can be diagnosed using an antibody test. It also means
that scientists must question the existence of HIV for exactly the same
reason scientists at the Sloan Kettering and National Cancer Institute
questioned the existence of HL23V.
CJ: So your argument essentially boils down to "HIV" antibodies
not arising because of or being directed against HIV in spite of the
fact that everyone calls them "HIV" antibodies?
EPE: Thatís right.
CJ: What about proof that HIV causes AIDS? Did Gallo prove that in
EPE: To be fair, in his 1984 Science papers Gallo did not make
such a direct claim. He said HIV was the probable cause of AIDS. But
even this conclusion is questionable. Even if Gallo's evidence was
incontrovertible proof he had isolated a retrovirus he only managed to
isolate it from 26 out of 72 AIDS patients. That's only 36 percent. And
only 88% of 49 AIDS patients had antibodies. And that was mostly using
ELISA, the antibody test considered the least specific. No one diagnoses
HIV infection on a single ELISA. And if the virus was present in only
36% of patients why did 88% have antibodies? I mean there were more
patients with antibodies without virus than there were patients with
virus? And there was not even a hint of proof that HIV was killing T4
cells or that having low T4 cells could cause all the diseases diagnosed
CJ: The evidence in 1984 was light on?
EPE: There was no evidence. But two years later, when Gallo was
defending the accusation he had used the French virus to discover his
version of HIV, he was much more definite about his 1984 papers. He said
they provided "clearcut" evidence that HIV is the cause of AIDS. And his
opinion was no different in 1993. Let me read you Gallo's own words from
the 1993 TV documentary, "The Plague".
"The compelling evidence that convinced the scientific community
that this kind of virus is the cause of AIDS came from us. The proper
growth of the virus came from this laboratory principally through Mika
Popovic. The development of a sensitive, workable blood test. I don't
think that we have to debate. I think the history speaks for itself"
CJ: Do the problems you see with the Gallo papers also apply to
the tests used to diagnose patients infected with HIV when cultures are
EPE: You mean the antibody tests?
EPE: It's the same test. Can you see whatís happened here? The HIV
researchers have used some antibodies in the patientsí blood to convince
themselves that some proteins in their cultures are unique constituents
of a particle which they say is a retrovirus and call HIV. Thatís the
first thing. But having done that theyíve then turned around and said,
"OK, if these proteins are from HIV then the antibodies must be THE HIV
antibodies". So theyíve used the one and same chemical reaction to prove
which each reactant is when in fact thereís no way an antibody reaction
can tell you even what one reactant is even if you know the other to
start with. Thatís why you need a independent gold standard adjudicator.
As far as actually doing the test is concerned, the difference from
cultures is that the patientís blood is mixed with proteins extracted
from H9 or other cell cultures and put either all together in a test
tube or separately at discrete spots along a thin paper strip. The first
is called the ELISA and the second the Western blot. If these proteins
react with the blood, and in the Western blot the number and type of
reacting proteins required to produce a positive test vary all over the
world and thatís yet another huge problem, then the patient is reported
CJ: So the HIV antibody test is really the same procedure that was
used to prove the existence of HIV in cultures from AIDS patients in
EPE: Yes. And also by the French in 1983. And by Gallo and his
colleagues to prove the existence of HL23V in the mid seventies. Our
group find it intriguing that any scientist could regard antibodies
reacting with proteins as proof of viral isolation. Is an antibody
joined to a protein a virus? What would you expect to see under the
electron microscope? A particle with a core and knobs?
CJ: Then is it fair to say that the HIV antibody tests are
EPE: No, they're not useless. There is no doubt being in a risk group
and having these antibodies is not a good thing.
CJ: How can that be?
EPE: Because empirically such people are more likely to develop the
illnesses we classify as AIDS.(31) In fact, there is evidence published
in the Lancet that a positive test also predicts increased
mortality from diseases which are not classified as AIDS. But what the
tests don't do, or at least there is no proof that they do, is prove HIV
infection. Or even less that HIV infection is the reason people develop
AIDS. You may not appreciate that the only evidence HIV causes AIDS is
these tests. If the tests are unproven for HIV infection then there is
no proof that HIV causes AIDS.(3-5,26,32-34)
CJ: What about a positive test in people who are apparently
healthy and not in any risk group? Should they be worried?
EPE: There is no data to answer that question and I think it would be
impossible to ever obtain that data. There would have to be an
experiment comparing matched groups of healthy people with and without
these antibodies. In other words, follow people with a positive test
over a period of years and see who developed AIDS and who did not. The
trouble is it would be very difficult for most people knowing they are
HIV positive, as well as their physicians, not to believe that sooner or
later they're going to get very sick and eventually die of AIDS. And
that mindset may greatly effect the results of such an experiment. From
CJ: What do you mean from both sides?
EPE: I mean that patientsí health will be affected knowing they are
HIV positive and their physicians will feel compelled to offer
treatments with drugs given in the belief they are necessary to kill a
virus the patients do not have.
CJ: The drugs themselves might be harmful?
EPE: Well AZT, the original and still most widely used drug is
certainly well known for its toxic effects and in fact some of these
effects mimic AIDS.
CJ: What if we did this experiment, and we did it blind, and found
that the HIV positives were more likely to develop AIDS than the HIV
negatives? What would that tell us?
EPE: On our present data that would mean the same it means in the
AIDS risk groups. Gallo and his colleagues serendipitously discovered a
test which for some reason predicts a tendency to get sick from certain
diseases that are lumped together as AIDS. But it doesn't prove that the
link to all these diseases is a retrovirus. That can never be proven
unless HIV is proven to exist by isolating it first and then used to
validate the antibodies as HIV antibodies. Even then, you can't say HIV
causes AIDS just because it's present in AIDS patients. Association
doesnít prove causation. You can be present at a bank robbery but not be
the robber. You need other data to prove causation. In fact, according
to the CDC AIDS definition, you donít even need to be HIV infected to be
diagnosed as AIDS.
CJ: That sounds really crazy.
EPE: Itís written down in the literature. Under some circumstances
the CDC AIDS definition requires a patient to be diagnosed as a case of
AIDS even if the patientís antibody tests are negative.(35)
CJ: What about the RNA tests. The PCR and viral load and
EPE: That's another huge subject but I can say just one thing. All
these tests rely on matching a piece of the patient's RNA or DNA to a
test piece of RNA or DNA deemed to originate from a particle called HIV.
You can think about this like the rabbit antibodies. There's another
bottle on the shelf and the label on this one reads "HIV RNA". But if a
retroviral particle hasn't been isolated and purified and shown to be a
virus, how does anyone know where this piece of RNA comes from? The HIV
experts themselves say that there are about one hundred million distinct
HIV RNAs in every AIDS patient.(36) With that much variation one would
think that a virus is the most improbable source for such RNA. I mean,
how can a virus have that much variation and still be the same agent?
Still make the same proteins and induce the antibodies? Still perform
all the same tricks?
CJ: Tell me Eleni, if there is no virus where do all the things
Montagnier and Gallo found come from? I assume you do believe they did
find something in their cultures?
EPE: Of course they found something. They found many things. All the
things weíve discussed. And your question is fair. In our view it is
possible the RT and particles could be some reaction produced when cells
from sick people are cultured. Or the result of the chemicals introduced
into the cultures. We know that both normal and pathological processes
can be associated with the appearance of retroviral-like particles.
Thereís absolutely no doubt about that. What exactly are all these
particles? Well, some may be no more than pieces of disintegrating
cells. Others certainly look more uniform and might conceivably be
viral-like or even retroviral-like but in the context of HIV what really
matters is proof that at least one of these varieties of particles is a
retroviral particle. Even if we had that proof, the RT and the particles
and proteins could all come from an endogenous retrovirus.
CJ: What's an endogenous retrovirus?
EPE: Unlike the case for all other infectious agents, normal human
DNA contains retroviral information which did not get there following a
retroviral infection. The cell was born with it. So amongst all our DNA
there are stretches made up of some retroviral information and that may
sit there maybe all your life until something happens. The DNA starts to
make RNA and hence proteins, and this may go even further and lead to
the assembly of endogenous retroviral particles. They're called
endogenous because they're not something that got in from the outside.
Like HIV is supposed to. Something that gets in from the outside is
called exogenous. Long before the AIDS era everyone knew that in animal
cells endogenous retrovirus production could occur spontaneously. You
make a cell culture and do nothing else. Just leave it on the bench for
a few days or maybe a few weeks and then one day it starts to produce
retroviral-like particles. They seemingly come out of nowhere and the
process can be significantly accelerated and the yield of particles
increased, sometimes millions of times, by conditions which induce
cellular activation, the same conditions which are obligatory to obtain
what is called HIV from cell cultures. Interestingly, up until 1993,
neither Gallo nor Fauci who is another well-known HIV researcher, (37)
accepted that humans contain the DNA to make endogenous retroviruses but
now it's accepted that endogenous retroviral DNA forms about 1% of human
DNA. For the record, that's about 3,000 times larger that what the
experts claim is the size of the HIV genome. And whatís more, new
retroviral genomes can arise by rearrangements and recombination of
existing retroviral genomes.
CJ: So HIV could be an endogenous retrovirus?
EPE: There are many explanations for the laboratory phenomena held up
as proof for the existence of HIV. We went into all these in a very long
article we wrote for Continuum magazine last October.(38)
CJ: Can you tell endogenous and exogenous apart?
EPE: No. Endogenously produced retroviruses are morphologically and
biochemically indistinguishable from exogenous retroviruses.
CJ: If HIV is an endogenous virus, why would AIDS patients produce
such viruses when we don't?
EPE: Because the patients are sick. In fact they are sick before they
ever develop AIDS. So their cells are sick and their sick cells find
themselves in the right condition in cultures to be activated. That's
whatís needed to produce endogenous virus and that's been known for
decades. Either the agents to which the patients are exposed induce the
right conditions or the culture conditions play a part. Perhaps a major
part. I don't know which contribution is the greater but that might have
been sorted out a long time ago if the first HIV researchers had
included a few control experiments.
CJ: What are they?
EPE: When you do a culture of say lymphocytes from an AIDS patient
with some H9 cells and all the chemicals which are added to make the
culture produce "HIV", you really don't know if what you find is the
difference that sets AIDS patients apart from everyone else. What if you
were to find exactly the same thing in similar patients that don't have
AIDS? So, to convince yourself that what you find and call HIV is
present only in AIDS patients and therefore might have something to do
with AIDS, you must use controls. They're experiments run in parallel
with your main experiment conducted exactly the same way using exactly
the same materials. The only difference is the one variable you're
CJ: Could you explain that further?
EPE: A control would be a culture of cells from some patients of the
same age and sex and environmental exposures who are sick with diseases
like AIDS but not AIDS. Even better if the cells came from patients who
have low T4 cells and who are oxidised.(3,32) AIDS patients have both
these abnormalities but they're not the only patients to have them. And
one must also not forget to add the same chemicals to all cultures. We
already know that one of these chemicals causes reverse transcription in
normal lymphocytes. Now, if you did all that you might well find that
lymphocytes from men in New York who were sick with non-AIDS diseases
also develop particles and RT and antibody reactions when cultured. That
would mean that one would have to be very cautious interpreting that
data as being something special to AIDS.
CJ: There weren't any controls?
EPE: This is yet another problem with so much AIDS research. Hardly
any one uses controls and when they do they're often the wrong type.
CJ: Is it possible we've got AIDS back to front? You hinted at
this before. Could the patients or the cultures be responsible for what
is called HIV and not the other way around?
EPE: Right. Having AIDS may just be a prescription for developing
those abnormalities. Retrovirologists themselves have argued that
retroviruses may arise as the result of a disease and not vice
versa. Getting cause and effect the wrong way around is not new to
Medicine. The Nobel Prize has even been awarded under such
CJ: It's almost time to finish up. I have three more questions.
First, how long have you and your colleagues held the view that HIV may
EPE: Ever since the first publication on HIV. In 1983.
CJ: So it's not something you recently came to?
CJ: Have you published these particular arguments? I mean in a
EPE: Yes. In my first paper on AIDS in 1988. There I put forward a
non-viral theory of AIDS and I also included some of what we've talked
CJ: Where was that published?
EPE: In Medical Hypotheses.(3)
CJ: Not a well known journal?
EPE: It is a well known journal of ideas. There the discussion on HIV
isolation is not as frank as we've had today but back then it was
virtually impossible to question the existence of HIV. It was important
to be subtle in order to get into print. Even so, it took a few years
for that paper to be published. Initially I submitted it to a much more
prominent journal but it was rejected. Twice in fact.
CJ: Which journal was that?
EPE: Thatís not important. Then in 1988 Val Turner and I wrote a
paper which directly spelt out all the problems we've discussed today.
We aimed that paper at clinicians and offered it to a journal read by
practising doctors in Australia.
CJ: No luck?
EPE: No luck.
CJ: So only the people who read Medical Hypotheses would have
known what you thought ten years ago?
CJ: You mentioned your non-viral theory of AIDS. Tell me a little
EPE: We were among the first people in the world to put forward the
idea that non-infectious factors explain AIDS in gay men and the first
to propose a non-infectious theory for all risk groups as well as a
unifying mechanism. Whatís more, our theory predicts that the factors
which cause the development of the AIDS diseases are also responsible
for the phenomena which everyone else infers as the "isolation" of a
retrovirus from AIDS patients.
CJ: How much reaction has there been to your theory?
EPE: Unfortunately very little but some research groups have
confirmed some of our predictions including our prediction that
antioxidants may be useful for treating individuals who are at risk for
CJ: Have you managed to overcome the inertia to your
EPE: We havenít had much luck in the scientific press but some gay
men and gay mensí organisations have become our greatest allies. If it
wasnít for them I think our task would be almost impossible.
CJ: If you had to nominate a single obstacle hindering the
resolution of the scientific problems with AIDS what would that
EPE: In our view the greatest single obstacle to understanding and
solving AIDS is HIV.
CJ: That would explain why your group has written so many papers
EPE: Thatís quite right. In fact weíve written a lot more papers than
weíve had published. Unfortunately, weíve only managed to get about a
dozen or so papers into print in the scientific journals. One of the
most important was a paper published in Bio/Technology (5) which
is now called Nature/Biotechnology There we said straight out
there is no proof of HIV isolation. That paper was certainly noticed but
again, no one responded to our views.
CJ: So you remained a minority?
EPE: We aren't just a minority. We are still the only people to ever
publish data in scientific journals questioning the existence of HIV and
arguing that the HIV antibody tests are not proof of HIV infection.
CJ: Eleni, why, despite everything you have explained today, do
virtually all the world's scientists and physicians appear extremely
comfortable with the very evidence you find so hard to accept?
EPE: The problem is not a matter of accepting evidence. Itís how
evidence is interpreted. The way I see it is this. Most of the
scientists and doctors who believe in HIV and that HIV causes AIDS do so
because they accept the interpretation of a relative minority of
experts. It's totally unrealistic to expect all the people who work in
AIDS to analyse the data to the degree we have. As far as the HIV
experts themselves are concerned, I don't know why they interpret the
evidence as they do. I can only speculate. Perhaps it's because pictures
are so powerful. There are pictures containing particles which look like
a virus and there's reverse transcriptase in the same cultures as the
particles. It is possible mentally to connect particles, reverse
transcription and proteins and the antibodies that react with the
proteins and make this into evidence for the existence of a retrovirus.
Especially for a retrovirologist. I suppose that is the whole problem.
We must not forget we are all subjective and we look at problems from
our own perspective.
CJ: Well doesnít the same apply to your groupís interpretation of
EPE: Certainly it does but donít lose sight of one very important
aspect of all this that is not subjective.
CJ: What is that?
EPE: The definition of a virus and the method that follows for
proving the existence of a virus. The same method that was endorsed by
the Pasteur Institute in 1973. Nobody can deny that here is a method
which constitutes absolute proof for the existence of a retrovirus. And
what nobody can also deny is that HIV has never been accorded reality
according to this method. In other words, in spite of AIDS being
regarded as one of the gravest conditions ever to afflict the human
race, no one has deemed it necessary to use a proven method to establish
the existence of the putative cause of this dread disease. Instead
everybodyís opted for a set of non-specific criteria and appear to
imagine that if you put all these together they must somehow
metamorphose into the right answer.
CJ: Doesnít that have some merit? If theyíre all clues to a
retrovirus surely the more you have the closer you get?
EPE: Certainly not. What if the true cause is something unexpected?
Or something of which you have no knowledge or cannot even possibly
imagine? In that case the more clues you have to what you are expecting,
or what you want it to be, the more likely you will be misled. It all
boils down to whether you would rather deal in probabilities rather than
facts. Thatís what I mean about being subjective. Itís like a physician
seeing a patient with fever, diarrhoea, vomiting, weakness and shock and
then declaring the cause is cholera. Sure it might be cholera but what
about the dozens of other germs that cause a similar pattern? What if
your life depended on it?
CJ: I see your point. Do you think now weíve seen whatís actually
in a density gradient, the tide will turn against HIV?
EPE: I would expect that data to be a turning point. Especially the
more people get to see or know about it. And it confirms what our group
has been saying for a very long time. In the introduction to the
Franco/German paper the authors clearly affirm that before their
pictures the 1.16 gm/ml density gradient was "considered to contain a
population of relatively pure viral particles". Thatís our point. HIV
has never been isolated and yet for the past fourteen years scientists
and biomedical companies having been using this material to obtain
proteins and RNA as if it is pure HIV. Pictures are powerful and that
cuts both ways.
CJ: What do you think should happen now to AIDS research?
EPE: I think that the traditional method of virus isolation should be
applied as urgently as possible using cultures with cells from AIDS
patients as well as suitable controls. As I said, we must find out once
and for all if there is such a thing called HIV. It's taken fourteen
years to get a mere handful of electron microscope pictures of a density
gradient and even if these had shown nothing but the right looking kind
of particle, we're still missing all the other steps which are needed to
arrive at a retrovirus.
CJ: Which steps are the most important?
EPE: All the steps are important. Establishing the presence of
retroviral-like particles in cultures, purification and analysis of
those particles, proof the particles can replicate and proof that the
antibodies in patients' blood which react with the proteins taken from
the particles are specific.
CJ: If this is not the case?
EPE: If these phenomena are also seen in control cultures, or if the
particles which band at 1.16 gm/ml are of the wrong morphology or are
not infectious, or if the antibodies present in AIDS patients are not
specific to those particles, then AIDS patients cannot be said to be
infected with a unique virus HIV.
CJ: Which means HIV could end up similar to HL23V?
EPE: That is quite possible. The proteins said to belong to HL23V
were defined in the same manner as the HIV proteins. By antibody
reactions. So, when the antibodies were shown to be non-specific, HL23V
disappeared. In the case of HL23V it was relatively easy because the
antibodies occured in so many people who were never going to get
leukaemia they were bound to be something unrelated and that's what was
eventually proven at Sloan Kettering and the National Cancer Institute.
My group thinks that scientists will eventually accept that the same is
true of HIV antibodies. You see AIDS patients are inundated with
antibodies to so many different things a few of these could easily react
with two or three of the ten proteins present in the "HIV" test. That's
all thatís required to be HIV positive. In fact, there's now ample
evidence that antibodies produced as a result of infection with the two
germs that infect ninety percent of AIDS patients react with all the HIV
proteins. I mean the germs known as mycobacteria and yeasts that between
them cause two of the commonest AIDS defining diseases. We have a paper
on this in press in the British journal Current Medical
Research and Opinion.(39) If that's the case how can anyone say
these antibodies prove infection with HIV or that these diseases are
caused by HIV?
CJ: Eleni Papadopulos-Eleopulos, many thanks you for your time
EPE: My pleasure. *
This interview, examining the very roots of the controversial
HIV/AIDS paradigm, was reviewed by scholar and international gay media
personality Prof. Camille Paglia, in her column in the US Salon magazine
October 28th: "For a superb critique of the scandalously overpoliticized
scientific research on AIDS, see Christine Johnson's long interview with
Australian biophysicist Eleni Papadopulos-Eleopulos in the new issue of
the British AIDS magazine Continuum. The American major media have
effectively suppressed long-standing questions about whether the AIDS
test is reliable or whether an HIV virus in fact exists at all."
Christine Johnson is a member of MENSA and a freelance science
journalist from Los Angeles, USA. She is the Science Information
Coordinator of HEAL-Los Angeles, is on the Board of Advisors of
Continuum magazine and copy-editor of Reappraising AIDS. She has an
extensive background in medicine, law and library research and is
motivated by a desire to find out the truth about AIDS. She has a
special interest in making the information in technical, obscure science
journals accessible to the lay public. Over the past four years she has
followed the fortunes of the Perth group and written articles critical
of the HIV antibody tests which have been published world-wide.
Christine Johnson July 1997
P.O. Box 2424
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1. Popovic M, Sarngadharan MG, Read E, Gallo RC. (1984). Detection,
Isolation,and Continuous Production of Cytopathic Retroviruses
(HTLV-III) from Patients with AIDS and Pre-AIDS. Science
2. Barrť-Sinoussi F, Chermann JC, Rey F. (1983). Isolation of a
T-Lymphotrophic Retrovirus from a patient at Risk for Acquired Immune
Deficiency Syndrome (AIDS). Science 220:868-871.
3. Papadopulos-Eleopulos E. (1988). Reappraisal of AIDS: Is the
oxidation caused by the risk factors the primary cause? Medical
4. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1993). Has
Gallo proven the role of HIV in AIDS? Emerg. Med. [Australia] 5(No
5. Papadopulos-Eleopulos E, Turner VF, Papdimitriou JM. (1993). Is a
Positive Western Blot Proof of HIV Infection? Bio/Technology
6. Sinoussi F, Mendiola L, Chermann JC. (1973). Purification and
partial differentiation of the particles of murine sarcoma virus (M.
MSV) according to their sedimentation rates in sucrose density
gradients. Spectra 4:237-243.
7. Toplin I. (1973). Tumor Virus Purification using Zonal Rotors.
Spectra No. 4:225-235.8. Rous P. (1911). A Sarcoma of the Fowl
transmissible by an agent separable from the Tumor Cells. J Exp Med
9. Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. (1997). Cell
membrane vesicles are a major contaminant of gradient-enriched human
immunodeficiency virus type-1 preparations. Virol. 230:125-133.
10. Bess JW, Gorelick RJ, Bosche WJ, Henderson LE, Arthur LO. (1997).
Microvesicles are a source of contaminating cellular proteins found in
purified HIV-1 preparations. Virol. 230:134-144.
11. Gallo RC, Wong-Staal F, Reitz M, Gallagher RE, Miller N,
Gillepsie DH. Some evidence for infectious type-C virus in humans.
(1976). p. 385-405 In: Animal Virology Baltimore D, Huang AS, Fox CF,
eds Academic Press Inc., New York.
12. Frank H. Retroviridae. (1987). p. 253-256 In: Animal Virus and
Structure Nermut MV, Steven AC, eds Elsevier, Oxford.
13. Gelderblom HR, ÷zel M, Hausmann EHS, Winkel T, Pauli G, Koch MA.
(1988). Fine Structure of Human Immunodeficiency Virus (HIV),
Immunolocalization of Structural Proteins and Virus-Cell Relation.
Micron Microscopica 19:41-60.
14. Levy JA. (1996). Infection by human immunodeficiency virus-CD4 is
not enough. NEJM 335:1528-1530.
15. Gelderblom H, Reupke H, Winkel T, Kunze R, Pauli G. (1987).
MHC-Antigens: Constituents of the Envelopes of Human and Simian
Immunodeficiency Viruses. Z. Naturforsch 42C:1328-1334.
16. Layne SP, Merges MJ, Dembo M, et al. (1992). Factors underlying
spontaneous inactivation and susceptibility to neutralization of human
immunodeficiency virus. Virol. 189:695-714.
17. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D.
(1995). Fator VIII, HIV and AIDS in haemophiliacs: an analysis of their
relationship. Genetica 95:25-50.
18. CDC. (1994). Facts about the human immunodeficiency virus and its
transmission. CDC HIV/AIDS Prevention January.
19. Hockley DJ, Wood RD, Jacobs JP. (1988). Electron Microscopy of
Human Immunodeficiency Virus. J. Gen. Virol. 69:2455-2469.
20. Lecatsas G, Taylor MB. (1986). Pleomorphism in HTLV-III, the AIDS
virus. S. Afr. Med. J. 69:793-794.
21. Gallagher RE, Gallo RC. (1975). Type C RNA Tumor Virus Isolated
from Cultured Human Acute Myelogenous Leukemia Cells. Science
22. Snyder HW, Fleissner E. (1980). Specificity of human antibodies
to oncovirus glycoproteins: Recognition of antigen by natural antibodies
directed against carbohydrate structures. Proc. Natl. Acad. Sci. U S A
23. Barbacid M, Bolognesi D, Aaronson SA. (1980). Humans have
antibodies capable of recognizing oncoviral glycoproteins: Demonstration
that these antibodies are formed in response to cellular modification of
glycoproteins rather than as consequence of exposure to virus. Proc.
Natl. Acad. Sci. U S A 77:1617-1621.
24. Weissbach A, Baltimore D, Bollum F. (1975). Nomenclature of
eukaryotic DNA polymerases. Science 190:401-402.
25. Wong-Staal F, Hahn B, Manzuri V, et al. (1983). A survey of human
leukemias for sequences of a human retrovirus. Nature 302:626-628.
26. Papadopulos-Eleopulos E, Turner VF, Papdimitriou JM. (1996).
Virus Challenge. Continuum 4:24-27.
27. O'Hara CJ, Groopmen JE, Federman M. (1988). The Ultrastructural
and Immunohistochemical Demonstration of Viral Particles in Lymph Nodes
from Human Immunodeficiency Virus-Related Lymphadenopathy Syndromes.
Human Pathology 19:545-549.
28. Berzofsky JA, Berkower IJ, Epstein SL. Antigen-Antibody
Interactions and Monoclonal Antibodies. (1993). p. 421-465 In:
Fundamental Immunology Paul WE, ed 3rd ed Raven, New York.
29. Owen M, Steward M. Antigen recognition. (1996). p. 7.1-7.12 In:
Immunology Roitt I, Brostoff J, Male D, eds 4th ed Mosby, London.
30. Francis DP. The search for the cause. (1983). p. 137-150 In: The
AIDS epidemic Cahill KM, ed 1st ed Hutchinson Publishing Group,
31. Mulder DW, Nunn AJ, Kamali A, Naklylngi J, Wagner HU,
Kengeya-Kayondo JF. (1994). Two-year HIV-1-associated mortality in a
Ugandan rural population. Lancet 343:1021-1023.
32. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1992).
Oxidative Stress, HIV and AIDS. Res. Immunol. 143:145-148.
33. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D,
Hedland-Thomas B, Page B. (1994). A critical analysis of the
HIV-T4-cell-AIDS hypothesis. Genetica 95:5-24.
34. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Bialy H.
(1995). AIDS in Africa: Distinguishing fact and fiction. World J.
Microbiol. Biotechnol. 11:135-143.
35. Fauci AS, Lane HC. Human Immunodeficiency Virus (HIV) Disease:
AIDS and Related Disorders. (1994). p. 1566-1618 In: Harrison's
Principles of Internal Medicine Isselbacher KJ, Braunwald E, Wilson JD,
Martin JB, Fauci AS, Kasper DL, eds 13 ed McGraw-Hill Inc., New
36. Wain-Hobson S. (1989). HIV genome variability in vivo. AIDS
37. Gallo RC, Fauci AS. The human retroviruses. (1994). p. 808-814
In: Harrison's Principles of Internal Medicine Isselbacher KJ, Braunwald
E, Wilson JD, Martin JB, Fauci AS, Kasper DL, eds 13 ed McGraw-Hill
Inc., New York.
38. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D.
(1996). The Isolation of HIV: Has it really been achieved? Continuum
39. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D.
(1997). HIV antibodies: Further questions and a plea for clarification.
Curr. Med. Res. Opin. 13:627-634.