IS HIV THE CAUSE OF AIDS?
An interview with Eleni Papadopulos-Eleopulos
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 virus itself.
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
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 make.
EPE: I suppose it is but nevertheless,
that's where my research takes me.
CJ: Didn't Montagnier and Gallo isolate
HIV? Back in the early eighties?
EPE: No. In the papers published in Science
by those two research groups, there is no proof of the isolation of a retrovirus
from AIDS patients.(1,2)
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 radical view.
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
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 particles.
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 that’s not what happens with
HIV. Unlike retroviruses, HIV is said to destroy the cells.
CJ: Well, what about HIV particles?
Are you suggesting they’re not a virus?
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 is 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 it.
CJ: That seems to make sense. I guess
it would be hard to get sick catching a particle that could not make more
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 that...
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
EPE: You need an electron microscope. That’s
how we know the size and shape of retroviral particles. That they’re 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
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 retroviral particles.
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 everything else.
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 centrifugation.
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 you’re 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
CJ: And do retroviral particles band
at a characteristic point?
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. It’s the only way to
know if you've caught a fish. Or anything at all.
CJ: True. Did Montagnier and Gallo not
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 particles.
EPE: No. Montagnier and Gallo published
electron micrographs of a few particles which they claimed are a retrovirus
and are HIV. But photographs don’t prove particles are a virus and the
existence of HIV was not proven using the method presented at the 1973
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 what’s inside and then
prove those particles are able to make more of the same with the same constituents
when they’re 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 particles.
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 particles?
CJ: Can the 1.16 band contain material
other than retroviral particles?
EPE: Yes. That’s another reason why you
need a photograph. To see everything that’s 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 cellular contamination?
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 don’t 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 density gradient.(5)
CJ: Could it be because electron microscopy
is highly specialised and expensive?
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. It’s just that until
this year, for some unknown reason, there haven’t been any of the density
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
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 particles’ point of view is rather
CJ: Do the experts comment on this?
EPE: They say the cellular material "co-purifies"
with the HIV particles.
CJ: Tell me, the few particles they
say are HIV, do they look like a retrovirus?
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, what’s
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
CJ: Surely size can’t be that critical?
Many things in Biology have a range of sizes. What about humans? There’s
plenty of humans twice the size of other humans. They’re all still humans.
EPE: What’s true for humans is not true
for retroviruses. For a start, retroviruses don’t have to grow up. They’re
born adults. So the correct comparison is between adult humans. They’re
aren’t too many twelve foot humans. In fact, the tallest human ever recorded
was eight feet eleven inches. But there’s 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 argument’s sake,
assume they’re 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
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 what’s 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 that’s 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 that’s
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
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 it’s
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 particle.
CJ: That sounds like a serious problem
to me. How do the experts respond?
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. That’s 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 haemophiliacs?
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 body?
CJ: According to what I’ve read, for
only a few hours at the most.
EPE: And why is that?
CJ: Because HIV dries out and dies.
Certainly that’s what the CDC says.(18)
EPE: OK. Let me ask you this. How is factor
CJ: From donated blood.
EPE: Right. Have you ever seen a vial of
EPE: All right I’ll tell you. It comes
as a dry, flaky, yellowish powder and by the time it’s used it’s at least
a couple of months old. Do you see the problem?
CJ: I do. If it’s dry and that old any
HIV in it should be long dead.
EPE: Exactly. So how does factor VIII cause
HIV infection and AIDS in haemophiliacs?
CJ: I don’t 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 anyone’s 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 doesn’t 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
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
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
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. What’s 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
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: They’re 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 that’s where it’s remained. That’s longer
than we’ve had AIDS and don’t 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 Kaposi’s 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 retrovirus.
CJ: You mean a retrovirus would not
grow in individual cultures from AIDS patients but did when the specimens
were mixed up and cultured?
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 leukaemia?
CJ: Then surely the cultures must have
contained many T4 cells?
EPE: That’s 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
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 about.
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
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
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 what’s 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: There’s 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
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
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 don’t 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,
there’s 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. Let’s 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 there’s that word
again. It’s 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
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. That’s the problem. Antibodies
do not work backwards. We’ll get to why in a minute. The important thing
here is not to forget what question we’re trying to answer. We’re trying
to define which proteins are unique constituents of a retroviral particle.
For me, there’s only one way to do that. And it’s 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 I’m 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 retroviral particle.
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 don’t 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.
There’s an old, logical, reliable, commonsense method of proving the existence
of a retrovirus. It’s 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. Isn’t 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 things?
CJ: I see your point. Since all you
see is reactions you can’t tell what is reacting with what.
EPE: Exactly. Antibodies react and things
light up but who’s 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
CJ: I guess it's a big mess. It's difficult
to tell where any proteins or antibodies come from.
EPE: That’s absolutely correct. And one
must not confuse origins with composition. For sure you can’t 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 can’t prove identity either. That’s because antibodies do not work
CJ: Are there any germs in AIDS patients
that could actually react like you’ve 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 virus...
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. That’s 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
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 didn’t inject pure
HIV into the rabbits what did they inject?
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 what’s 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, there’s another problem. There might be specific HIV antibodies
but what if there’s non-specific HIV antibodies as well?
CJ: I can see people getting confused.
Could you please elaborate?
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 they’re antibodies caused
by other agents or stimuli and sure they react with those agents but they
also react with HIV. If you add a person’s 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. That’s 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 don’t 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
there’s no HIV then non-specific antibodies must exist.
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 it’s only some how
can you tell them apart? The answer is you can’t 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"
EPE: That’s right.
CJ: What about proof that HIV causes
AIDS? Did Gallo prove that in 1984?
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 as AIDS.
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 not done?
EPE: You mean the antibody tests?
EPE: It's the same test. Can you see what’s
happened here? The HIV researchers have used some antibodies in the patients’
blood to convince themselves that some proteins in their cultures are unique
constituents of a particle which they say is a retrovirus and call HIV.
That’s the first thing. But having done that they’ve then turned around
and said, "OK, if these proteins are from HIV then the antibodies
must be THE HIV antibodies". So they’ve used the one and same chemical
reaction to prove which each reactant is when in fact there’s no way an
antibody reaction can tell you even what one reactant is even if you know
the other to start with. That’s why you need a independent gold standard
adjudicator. As far as actually doing the test is concerned, the difference
from cultures is that the patient’s blood is mixed with proteins extracted
from H9 or other cell cultures and put either all together in a test tube
or separately at discrete spots along a thin paper strip. The first is
called 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
that’s yet another huge problem, then the patient is reported HIV positive.
CJ: So the HIV antibody test is really
the same procedure that was used to prove the existence of HIV in cultures
from AIDS patients in 1984?
EPE: Yes. And also by the French in 1983.
And by Gallo and his colleagues to prove the existence of HL23V in the
mid seventies. Our group find it intriguing that any scientist could regard
antibodies reacting with proteins as proof of viral isolation. Is an antibody
joined to a protein a virus? What would you expect to see under the electron
microscope? A particle with a core and knobs?
CJ: Then is it fair to say that the
HIV antibody tests are useless?
EPE: No, they're not useless. There is
no doubt being in a risk group and having these antibodies is not a good
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 patients’ health will
be affected knowing they are HIV positive and their physicians will feel
compelled to offer treatments with drugs given in the belief they are necessary
to kill a virus the patients do not have.
CJ: The drugs themselves might be harmful?
EPE: Well 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
doesn’t prove causation. You can be present at a bank robbery but not be
the robber. You need other data to prove causation. In fact, according
to the CDC AIDS definition, you don’t even need to be HIV infected to be
diagnosed as AIDS.
CJ: That sounds really crazy.
EPE: It’s written down in the literature.
Under some circumstances the CDC AIDS definition requires a patient to
be diagnosed as a case of AIDS even if the patient’s antibody tests are
CJ: What about the RNA tests. The PCR
and viral load and like?
EPE: That's another huge subject but I
can say just one thing. All these tests rely on matching a piece of the
patient's RNA or DNA to a test piece of RNA or DNA deemed to originate
from a particle called HIV. You can think about this like the rabbit antibodies.
There's another bottle on the shelf and the label on this one reads "HIV
RNA". But if a retroviral particle hasn't been isolated and purified
and shown to be a virus, how does anyone know where this piece of RNA comes
from? The HIV experts themselves say that there are about one hundred million
distinct HIV 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
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 we’ve discussed. And your question is
fair. In our view it is possible the RT and particles could be some reaction
produced when cells from sick people are cultured. Or the result of the
chemicals introduced into the cultures. We know that both normal and pathological
processes can be associated with the appearance of retroviral-like particles.
There’s absolutely no doubt about that. What exactly are all these particles?
Well, some may be no more than pieces of disintegrating cells. 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
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 what’s 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
CJ: Can you tell endogenous and exogenous
EPE: No. Endogenously produced retroviruses
are morphologically and biochemically indistinguishable from exogenous
CJ: If HIV is an endogenous virus, why
would AIDS patients produce such viruses when we don't?
EPE: Because the patients are sick. In
fact they are sick before they ever develop AIDS. So their cells are sick
and their sick cells find themselves in the right condition in cultures
to be activated. That's what’s needed to produce endogenous virus and that's
been known for decades. Either the agents to which the patients are exposed
induce the right conditions or the culture conditions play a part. Perhaps
a major part. I don't know which contribution is the greater but that might
have been sorted out a long time ago if the first HIV researchers had included
a few control experiments.
CJ: What are they?
EPE: When you do a culture of say lymphocytes
from an AIDS patient with some H9 cells and all the chemicals which are
added to make the culture produce "HIV", you really don't know
if what you find is the difference that sets AIDS patients apart from everyone
else. What if you were to find exactly the same thing in similar patients
that don't have AIDS? So, to convince yourself that what you find and call
HIV is present only in AIDS patients and therefore might have something
to do with AIDS, you must use controls. They're experiments run in parallel
with your main experiment conducted exactly the same way using exactly
the same materials. The only difference is the one variable you're chasing.
CJ: Could you explain that further?
EPE: A control would be a culture of cells
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 circumstances.
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 not exist?
EPE: Ever since the first publication on
HIV. In 1983.
CJ: So it's not something you recently
CJ: Have you published these particular
arguments? I mean in a scientific journal?
EPE: Yes. In my first paper on AIDS in
1988. There I put forward a non-viral theory of AIDS and I also included
some of what we've talked about today.
CJ: Where was that published?
EPE: In Medical Hypotheses.(3)
CJ: Not a well known journal?
EPE: It is a well known journal of ideas.
There the discussion on HIV isolation is not as frank as we've had today
but back then it was virtually impossible to question the existence of
HIV. It was important to be subtle in order to get into print. Even so,
it 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: That’s 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 about that.
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. What’s 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 developing AIDS.
CJ: Have you managed to overcome the
inertia to your ideas?
EPE: We haven’t had much luck in the scientific
press but some gay men and gay mens’ organisations have become our greatest
allies. If it wasn’t 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 be?
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 against HIV?
EPE: That’s quite right. In fact we’ve
written a lot more papers than we’ve had published. Unfortunately, we’ve
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
EPE: The problem is not a matter of accepting
evidence. It’s 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 doesn’t the same apply to your
group’s interpretation of the literature?
EPE: Certainly it does but don’t 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 everybody’s
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
CJ: Doesn’t that have some merit? If
they’re all clues to a retrovirus surely the more you have the closer you
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. That’s what I mean about being subjective. It’s 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
we’ve seen what’s actually in a density gradient, the tide will turn against
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". That’s 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
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
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 that’s 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 today.
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
Venice, California 90294-2424
VOICE (310) 392-2177
FAX (310) 273-2972
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