DO ANTIBODY TESTS PROVE HIV
A blood-curdling interview
with Dr. Valendar F. Turner
By Huw Christie
Continuum winter 1997
Dr. Valendar F. Turner is a member of the Perth group of HIV/AIDS
dissidents. He graduated from the University of Sydney in 1969, is a
Fellow of the Royal Australasian College of Surgeons and a Foundation
Fellow of the Australasian College for Emergency Medicine. He practises
at the Royal Perth Hospital in Western Australia. Huw Christie is editor
of Continuum magazine in London. After a childhood in Tasmania,
Australia he graduated from Oxford University England in 1981. He is a
board member of the Swiss-based International Forum for Accessible
HC: Good afternoon Downunder.
VFT: Good morning Huw.
HC: The Perth Group publications (1-13) seem to cover just about
every facet of HIV and AIDS but what I want to go over again is the
HC: I'm particularly interested in trying to make this subject
plain and simple for ordinary folk who havenít read the arguments
published in the Group's papers over the past decade. Or if they have,
don't quite understand. I mean it's pretty much in your face to read an
abstract telling you Eleopulos et al don't accept HIV antibodies tests
as proof of HIV infection in anyone.
VFT: I know but that's how Eleopulos et al read the data.
HC: Could you start with an overview?
VFT: Sure. Let's consider the two words 'antibody' and 'test'. In
this context 'test' has two meanings. The first is something you do in
an attempt to indicate the presence or absence of some substance or
property. For example, does a patient have appendicitis? Or is a woman
pregnant? The second is something you do to ascertain something's worth.
For example, if you develop a blood test for pregnancy, how well does it
HC: And antibodies?
VFT: Antibodies are proteins produced by cells of the immune system
known as B lymphocytes. Not to be confused with T lymphocytes, the
immune system cells which HIV allegedly kills making people immune
deficient. The present theory of antibody production is that each B
lymphocyte and its descendants, known as a clone, elaborates one and
only one unique antibody molecule.
HC: What switches B-cells into producing antibodies?
VFT: Two things. Firstly, when a B-cell encounters a substance known
as an antigen. That word is derived from the letters of ANTIbody
GENerating. Antigens are always large molecules and are often proteins.
In fact proteins are the most powerful antigens. Even more so if they
gain direct access to the blood stream.
HC: How does the antigen get the B-cell to make the
VFT: In the old days it was thought antigens instructed B-cells in
the art of making antibodies. Like reading out a recipe while someone
else makes the cake. But that's no longer believed. Nowadays the theory
is that each B-cell already knows the recipe. But for only one type of
cake. Each is programmed to make a unique antibody. Many times over of
course but all the same. It's estimated B-cells have a combined
repertoire of about one million distinct antibody molecules. It's just a
matter of an antigen meeting up with the right B-cell. When it does
that's the key which turns the switch as you suggest. The cell divides
and produces a clone and out come the antibodies. That antibody then
unites chemically with the antigen.(14)
HC: What else induces antibodies?
VFT: B-cells can be stimulated non-specifically. You give the immune
system a belt and an assortment of B-cells go into production. For all
we know this might be quite common. The only way to find out is to test
for antibodies to everything except what you used to belt the immune
HC: What is the biological purpose of the antibody/antigen
VFT: Supposedly antibodies neutralise the untoward effects of
HC: Are germs antigens?
VFT: Yes but with some qualification. Obviously antibodies and
antigens must combine at particular places on their molecules. It's like
hugging your grandmother. Your arms are only a small part of you and
make contact only over a small part of grandma. The business end of the
antibody molecule is called the combining site and the part of the
antigen it joins on to is the antigenic determinant. There are many
possible antigenic determinant sites on each antigen and any of these
can induce a corresponding clone of B-cells to produce a particular
HC: So the antibodies produced to a germ are really a mixture of
many different molecules to many different bits of the germ?
VFT: Yes. The technical term is that the antibody response is
HC: How do you give the immune system a belt?
VFT: Let loose with drugs or infectious agents or foreign proteins,
wich all the HIV/AIDS risk groups are exposed. Of course these may act
as conventional antigens but they can also act on other B-cells. This
may produce arcane reactions. A good example is that of Epstein-Barr
virus, the virus that causes glandular fever.
HC: What's arcane there?
VFT: Somehow the virus switches on a set of B-cells programmed to
make antibodies which react with the red blood cells of horses. And
another which makes antibodies to sheep blood. But these aren't
antibodies destined for EBV itself. They're something completely
different. One wonders why we would ever need to produce such antibodies
but we can. In fact as doctors we make use of this to diagnose glandular
fever. This is an antibody test but it doesn't look for antibodies to
the causative virus. Instead it looks for the horse blood
HC: Curioser and curioser. What's the basis of using antibodies to
prove HIV infection?
VFT: The belief that because HIV is foreign it will induce the
production of antibodies directed against HIV.
HC: The theory is an antibody to a virus can only arise if B-cells
have encountered that virus?
HC: Why not infection by growing the virus?
VFT: Antibodies is technically easier and a lot quicker and
HC: And you detect the antibody by taking some blood, mixing in
some virus and seeing if the two react?
VFT: That's the theory but before we get to that let me explain
something else very important. What we can call the age old antibody
problem. Why you can't reason backwards from antibodies to germs. It
comes about because a particular antibody may also react with an antigen
or antigens that did not stimulate its production.(14-22) This can be
due either to non-specific stimulation or because antibodies
HC: What does cross-react mean?
VFT: Two different antigens may share the same business end. So the
same antibody can get hold of either antigen by reacting with that part.
Even though they're otherwise different proteins. You can also prove the
existence of cross reactions by doing a little thought experiment.
Antibodies are large proteins and can themselves act as antigens. So
that's at least two things an antibody can react with. The antigen that
produced it and the antibody to it when it acts as an
HC: Why are these phenomena a problem?
VFT: Because they spoil what would be a nice theory that when you
take a substance 'X' and discover a person has an antibody to 'X', that
person must automatically be infected with 'X'. It's scientifically
impossible to make such a claim merely from a chemical reaction.
HC: Even if it is beyond question that 'X' is a constituent
protein of a unique virus?
VFT: Yes. You may never be infected with what your antibodies react
with. Otherwise we'd have to say patients with glandular fever are
infected with horse blood. As well as sheep blood. Or AIDS patients are
infected with laboratory chemicals.
HC: AIDS patients have antibodies to laboratory chemicals?
HC: Can you name some?
VFT: Off the top of my head I can name one. Trinitrophenyl
HC: And itís not known how that arises?
VFT: Not precisely.
HC: How does one get around the antibody problem?
VFT: First by realising the problem exists. If you like analogies,
diagnosing infections using antibodies, that is, serological diagnosis,
is like trying to identify objects from the shadows they cast on the
ground. Thereís a connection but clouds, buildings, trees and so forth
all produce shadows that may look the same or similar. The way around
the dilemma involves an appreciation of both meanings of that word
'test'. According to the first meaning what we want is some method of
finding HIV in the body. HIV infection. That's what we're really
chasing. The best way to do that would be to find the actual object
itself. HIV. Prove the existence of HIV in every patient by means that
are unambiguous for a unique retrovirus.(24-25) The gold standard. Any
other way, including antibody tests, is indirect and therefore must be
validated by comparison alongside the gold standard. The second meaning
VFT: By running the two sets of data concurrently. The antibody test
and whatever you do independently to prove the existence in the person
of the virus.
HC: Virus isolation versus the antibodies?
VFT: Yes but there's more to proving the existence of the virus than
isolating a particle. After Eleni's interview (26) I'm sure your readers
must be a full bottle on this topic.
HC: I wonder! How is an antibody test for HIV actually
VFT: As you said. Take some blood from a patient, remove the red
cells and then add what's left, the serum in which the antibodies are
dissolved, to some proteins the experts claim are unique constituents of
HC: What do you see if the test is positive?
VFT: If the antibodies react with the proteins there will be some
detectable change in the solution or in whatever medium the test is
performed. It may change colour or a may precipitate form. Or there is
some other measurable effect.
HC: Things light up? That's all there is to it?
VFT: Basically. But there are refinements. For example, the ELISA
versus the Western blot. The ELISA has all the proteins mixed
together and in the Western blot you can see each reacting individually,
side by side along a thin nitrocellulose strip.
HC: How is the comparison with HIV gold standard done?
VFT: What everyone wants to know is whether the test can be positive
when there is no HIV infection. In other words, is my test a false
positive? So, what a scientist is obliged to do long before the test is
introduced into clinical practice is to determine what's known as the
specificity of the test. That's a measure of how often a positive test
turns up given HIV is known to be absent. Proven by viral isolation. If
the test is one hundred per cent specific the answer of course should be
HC: Yes. I think people tend to get confused here. Can we go over
these two words, sensitivity and specificity?
VFT: Sure. Sensitivity is a measure of how often a test is positive
when you already know what you're testing for is present. For example,
if a thousand women are pregnant, does the test diagnose them all? If it
picks 980 then it's only 98% sensitive. And is it specific, in other
words, is it ever positive when a woman is definitely not pregnant? For
example, if, from a thousand women known not to be pregnant there was
one positive test, the test would be 99.9% specific. You'd never dream
of putting a pregnancy test into practice until you'd sorted out these
HC: If we take the HIV ELISA, which is the first and sometimes the
only type of test patients have performed to diagnose HIV infection, how
is the sensitivity determined?
VFT: First let's examine the way it should be determined. The
correct procedure is to assemble say a thousand people proven by HIV
isolation to be infected with HIV and see how many have a positive
ELISA. Now the ELISA is made positive because the solution in which the
antibodies react turns cloudy and the degree of cloudiness can be
measured with a special instrument that gives out a number.
HC: Is any degree of cloudiness positive?
VFT: No because there is always some nonspecific background activity.
If you set the degree of cloudiness for a positive test very low then
everyone might be positive. If it were a pregnancy test for example,
even men could be pregnant. So you set some limit or sets of limits for
HC: How is this determined?
VFT: Here there are some very unscientific practices. Basically, a
group of healthy individuals is tested to estimate the background
activity. This will have a range of values and from this range
researchers select an upper limit which is maybe two or three standard
deviations higher than the mean value. Any reading greater than that is
defined as positive.
HC: It's arbitrary?
HC: They don't set the level according to the results of virus
VFT: No. And setting a level doesn't prove the antibodies are genuine
anti-HIV antibodies. You can't say antibodies are HIV just because
there's more of them. Higher levels might just be more of the same that
caused the lower level of cloudiness. Or lower levels might be the real
thing. The only way to prove the antibodies are a reaction to something
called HIV is first to prove you have the virus.
HC: What about the sensitivity of the Western blot?
VFT: Again, you have to set criteria for what constitutes a positive
test and then apply this to a population of known infected people. Again
there are no such data for even one of the multitude of different
criteria which are said to define a positive HIV Western blot. But, as
I'm sure you know, the sensitivity is not of prime importance to the HIV
experts because in most parts of the world the Western blot is put
forward as a means of sorting out which positives ELISAs are due to HIV
infection and which are not. What's important for the Western blot is
HC: How does one perform an experiment to measure specificity of
the HIV antibody tests? ELISA and Western blot?
VFT: Take a thousand people including AIDS patients, as well as
people who are sick with similar illnesses and laboratory abnormalities
as AIDS patients, as well as those at risk and some healthy people,
perform HIV isolation to prove none have the virus and amongst this
group see how many are antibody positive by whatever criteria you set
for each test.
HC: Why such a diverse range of individuals?
VFT: Because these tests measure antibody reactivity and you need
lots of antibodies and lots of variety to produce lots of chances of
reactions to prove that the reactivity which defines a positive test is
restricted to those individuals who are HIV infected.
HC: Well, if sensitivity of either antibody test has never been
measured against the guaranteed presence of HIV, has the specificity
ever been measured against the certified absence of HIV?
VFT: No one has ever reported an experiment performed to draw this
comparison. Not for the ELISA nor the Western blot. This is one of the
great AIDS mysteries. However, if you look at Gallo's 1984
Science papers,(27) what Gallo and his colleagues called HIV
isolation was positive in only a third of their AIDS patients. Yet
nearly three times that number had antibodies.(28)
HC: That's a huge disparity. Thatís nearly twice as many people
with antibodies and NO virus as with antibodies AND virus! Itís a much
better correlation between antibodies and absence of infection. So right
from the start it should have been obvious the test was grossly
HC: How did Gallo explain this discrepancy?
VFT Gallo didn't admit to any discrepancy in virus isolation. Instead
his group believed all the patients with antibodies were infected. They
blamed the low yield of virus isolation on failure to keep their
specimens under proper conditions.
HC: Yet the Gallo lab was considered expert in culturing
VFT: Yes over a decade of experience and nowadays it's claimed that
the blood of untreated AIDS patients is teeming with HIV.
HC: Has the discrepancy between antibodies and HIV isolation
narrowed over time?
VFT: Not in the least. If you remember our reply to Peter
Duesberg,(11) between 1992-93 several reputable, international
laboratories in the UK, Germany and the USA tested 224 specimens from
antibody positive individuals. These labs also claimed to have performed
viral isolation but like all HIV researchers, theyíre forever perverting
the meaning of that word. What they called HIV isolation was another
antibody test. This time for detecting just one protein, p24. And under
this guise Ďisolationí was positive only 83 times.(29) That's 37%.
Substantially the same rate as Gallo in 1984.
HC: Do HIV experts really refer to an anti-p24 antibody test as
VFT: Most of the time. And some report just finding reverse
transcriptase as virus isolation.
HC: Is the failure to perform the gold standard comparison the
reason why the Perth group claims not one antibody positive person in
the world is infected with HIV?
VFT: Principally on that basis we say there is no proof that one
person is infected. Yes. But the other reason of course is that no one
has yet proven the existence of HIV using the proper method. The method
based on the definition of a virus and as discussed at length at the
1972 Pasteur Institute meeting.(24-25)
HC: Which the Perth group was the first to argue over a decade
VFT: Right from day one.
HC: Nonetheless, it still seems an intrepid claim. No proof that
even one antibody positive person in the world is infected?
VFT: Look Huw you just can't put the words 'HIV' and 'antibodies'
next to each other and claim you've proved they exist. Or a virus
exists. All the test indicates is that some antibodies in
patients react with some proteins present in cultures of tissues
from the same patients. But given that information what a scientist is
obliged to do next is make the comparison with the virus gold standard.
Before pronouncing the test highly specific for diagnosing HIV
infection. In fact, do you see that the origin of the proteins used in
the tests doesn't matter? They don't have to come from HIV. I
mean we diagnose Epstein-Barr virus infection without using proteins
from the Epstein-Barr virus. Horse red blood cells are not constituents
of that virus. What counts is the correlation between certain reactions
and the presence or absence of the virus.
HC: But surely it makes sense to use proteins from the
VFT: It does because if there is a germ there is a possible
connection, forwards, between the germís antigens and the patientís
antibodies. But just because you use the germ doesn't mean you can
ignore the problem of antibody cross reactivity and everything else.
HC: So it's incorrect for scientists to say the HIV antibody tests
are better nowadays because they use purer proteins?
VFT: That's right. It doesn't follow. Even if genetically engineered
proteins are used in the test. You could take the purest protein in the
world and find a patient with an antibody to that protein. That doesnít
create an axiom that a person with that antibody is infected with a germ
containing that particular protein. This is an extremely important but
frequently unappreciated concept. In fact you could take a genetically
engineered protein and make the test worse.
VFT: Because every time you change the antigens there's a possibility
you could introduce a new antigenic determinant. All antibodies know is
how to react and there might be an antibody lurking that links up with
that determinant but whose presence bears no relation whatsoever with
whatever you're testing for. For example, lots of humans have antibodies
to things like hepatitis A and even Pneumocystis carninii. In
fact by the age of four most children have antibodies to the PCP
organism. Without ever being sick from either organism. One of those
antibodies might cross react with the new determinant.
HC: And patients are tested for antibodies despite the fact that
no one has done a gold standard comparison?
VFT: The tragedy is that these tests were introduced in the total
absence of proof of their specificity. This is a fact. The moving finger
has writ and all our tears cannot wipe out a word of it.
HC: That's from Omar Khayyam*?
HC: The Perth group has claimed that the HIV proteins and
antibodies as well as the existence of HIV are based on a circular
argument. Could you explain that?
VFT: Sure. When Montagnier and Gallo went hunting for retroviruses in
1983/84 they knew that merely finding a particle that looked like a
virus, even if they were to isolate the particle and prove it could
reverse transcribe RNA into DNA, did not prove the particle was a virus.
That's because not all particles, even those that look like viruses, are
viruses. And not everything that reverse transcribes is a retrovirus. Or
even a virus. These phenomena are nonspecific. And stringing together
reverse transcription and particles doesn't cure the problem. The only
scientific proof that a particle is a virus is purification and analysis
followed by experiments to prove particles make more particles exactly
the same. In other words, proof that the particles are infectious. These
experiments have never been done. Proof of the existence of HIV is based
on antibodies but unfortunately, picking on antibodies just added yet
another nonspecific item to the list.
HC: But Montagnier and Gallo did discover antibodies from AIDS
patients which reacted with some proteins in their cell
VFT: Yes they found a few but that doesn't prove the proteins which
reacted with these antibodies are the constituents of a virus. Or that
the antibodies were induced by contact with a virus. If you'd like
another analogy imagine this experiment. In place of the AIDS patient
cell culture someone hands you a test tube containing milks obtained
from half a dozen different animals. In other words, a mixture of
several different proteins but you don't know from which animals. Now in
place of a mixture of antibodies from AIDS patients you obtain a second
test tube containing a number of different acids. You add the mixture of
acids to the mixture of milks and produce curdles. Now you claim you've
isolated a cow. Or a goat. And not just any cow or goat. A completely
new species of cow or goat. One never seen before. There, in the
culture. And then you claim that only a particular selection of the
acids in the mixture produced that curdle. So, getting back to HIV,
proteins reacting with antibodies makes them into the HIV
proteins. But since these newly discovered proteins react with these
particular antibodies that means these antibodies must be
the HIV antibodies. It's called chasing your tail. It's not the
way a scientist should establish the existence of a virus or determine
which are its antibodies.
HC: Yet almost everyone believes these antibodies are the HIV
antibodies and they're highly specific to HIV.
VFT: True and thatís because of virtually the same circular argument.
AIDS, the clinical syndrome, usually but not always, is accompanied by
antibodies which are interpreted as proof that AIDS patients are
infected with HIV. Then the antibodies are used to prove that HIV is the
cause of AIDS. In other words, AIDS proves itís HIV proves itís AIDS.
Naturally the antibodies are specific. They and AIDS run around the same
circle. What's important for anyone in this debate to realise is that
when you pare down what the experts claim proves the existence of HIV,
it's all nonspecific phenomena including antibody reactions. That's all.
It's not isolation. No viral-like particles are separated and analysed
and then added to fresh cells to see if the exactly the same come
HC: But regardless of where these antibodies come from, doesnít
their relationship to AIDS mean something?
VFT: In the AIDS risk groups yes it does. If you have these
antibodies youíre at risk of either having or developing a number of
diseases which constitute the AID clinical syndrome. But it doesnít
prove the link is a retrovirus.
HC: Or that the illnesses are inevitable?
VFT: They may well not be inevitable. After all, we're talking
HC: All right. The Perth group has also written at length about
the global variation in the HIV Western blot. It was first presented in
the Bio/Technology paper of 1993 and Continuum published
your chart illustrating the same thing in the November 1995 issue.(30)
Tell us about that.
VFT: OK. The Western blot is a general laboratory technique for
visualising individual protein/antibody reactions. The proteins are
placed at discrete spots in a thin paper strip. In the case of HIV about
ten of them. The human operator inspects the strip and declares which
proteins react with antibodies. What you actually see is a series of
dark horizontal rectangles called bands. You'd think that if there
really were such things as HIV proteins, and that the HIV antibodies are
highly specific, then just having one band light up would be proof that
HIV is present. But according to the experts that's not the case.
HC: They say you need more than one?
VFT: With one single exception. The intriguing thing is this. Even if
one or two bands are not sufficient to diagnose HIV infection there must
still be a reason why theyíre there.
HC: Cross-reacting or non-specifically induced?
VFT: Right. Proteins in the tests lit up by part of the menagerie of
antibodies present in AIDS patients. Or maybe a few present in a healthy
person following some chance, B-cell stimulus. In fact, cross-reactions
is the explanation given by all the HIV experts for "non-infected"
Western blots. Non-HIV antibodies produced by non-HIV stimuli. But if
one or two bands in a Western blot can be caused by non-HIV, cross
reacting antibodies why can't three or four, or five or six, or all ten
bands be caused by cross reacting, non-HIV antibodies?
HC: I don't know. You tell me.
VFT: Well, a scientist must admit to this possibility. And there's
only one way to find out. Compare your favourite combination of
antibodies with HIV itself.
HC: But that has not been done?
VFT: Not only not done. Not even possible to do because no research
group has ever presented evidence for the existence of HIV according to
the proper rules.(6-13,26)
HC: What about the actual variation in the Western blot?
VFT: Another mystery. What is considered positive depends on where
and by whom the test is done. Around the world different combinations of
two or three or four of the ten possible bands are deemed proof of
infection.(31-36) In Africa you need two bands but in France, the United
Kingdom and Australia that wouldn't count. In Australia you need four
and under the US FDA and Red Cross rules you need three.
HC: This is the basis of the Group's quip about
VFT: Yes. If you're positive in New York City just get on a plane and
come to Perth. You'll no longer be positive.
HC: You mentioned an exception?
VFT: The US Multicenter AIDS Cohort Study or MACS. This excellent
study began in the early 1980s and followed the fate of 5000 gay men.
Under the study rules the Western blot could be positive with just one
band.(36) Although that later changed. But until 1990 one band was
considered sufficient to diagnose HIV infection.(31) That wouldn't count
anywhere else. Not even in Africa. So there are gay men out there HIV
infected on this basis. And perhaps given antiviral drugs as a
HC: Let me get this right. We are always conscious of our new
readers and I think this is extremely important. You're saying that even
the experts concede that some numbers or patterns of bands in the
Western blot are not indicative of HIV infection because they're caused
by non-HIV antibodies?
VFT: Yes. You can read what Anthony Fauci wrote about this in
Harrison's Principles of Internal Medicine.(22) Maybe you could print
the quote at the end of the interview.
HC: So itís definite that non-HIV antibodies react in an HIV
VFT: Yes Huw. There's plenty of examples. For instance, 30% of people
transfused with HIV negative blood develop antibodies to p24.(37) That's
regarded as one of the most specific HIV proteins and itís present in
the Western blot. And it was one way any one of those 5000 gay men could
have scored a positive test in the MACS. So some gay men are infected
with HIV on the basis of a test that turns up positive in one third of
people transfused with blood that does not even contain HIV.
HC: I find that more than a bit disturbing.
VFT: So should any man in that study. Or any person Western blot
tested before 1987.
HC: Why then?
VFT: Before 1987 anyone with a p24 or a p41 band was diagnosed
positive and thereby infected. That is, if they were ever Western blot
tested. Not everyone has had a Western blot. Some were diagnosed just on
the ELISA. The way people are in most of the UK today, except Scotland
where the Western blot is still routine. For example, in 1985, using
either p24 or p41 or both on the Western blot, Australian experts
diagnosed HIV infection in a gay man and transmission of HIV from his
semen to four women following artificial insemination. This was big news
at the time because it was said to be direct proof for heterosexual
spread. This is an oft quoted paper. In 1996 we questioned this in a
letter published in the Lancet. In light of the current
Australian criteria we asked were the man or the four women still
considered infected? In their reply the Australian experts defended the
original claim of HIV infection because all five people had progressed
to AIDS and died. They implied that the reason extra bands were not
present in 1985 was because in 1985 the Western blot was in its
HC: What's infantile about a test?
VFT: We donít know but if the test had not yet come of age, why was
it being used? But thereís two interesting points here. First, it
confirms what I said earlier. HIV researchers use the diagnosis AIDS as
proof that the antibodies are caused by HIV. The second is that if p41
and p24 were sufficient to diagnose HIV infection in Australia in 1985
and, according to the Australian experts, they were correct in these
five patients, why arenít they sufficient now? They certainly still are
in other parts of the world.
HC: What about the missing bands?
VFT: Although the WB criteria changed in 1987, apparently it was not
until the Lancet published our letter that the sera from the gay
man and one of the women were retested. On these sera the gay man and
the woman now did have four bands.
HC: How would they arise?
VFT: The band that proved difficult was the p120 band. There was a
belief that a protein of this molecular weight should be present
in the Western blot. However, it took a lot of time and experimentation
to work out how to produce one. In fact, it's impossible to have a
"viral" p120 in the Western blot because we know from the work of Hans
Gelderblom and his colleagues that HIV particles, once they're shed from
the cell, rapidly lose all their knobs, and that's where the HIV experts
claim the p120 protein is to be found. The real reason there's a p120
band in the Western blot has nothing to do with a virus. It's due to the
fact that the HIV researchers eventually found the right chemical
conditions to produce it when they prepare the Western blot strips. This
was proven in 1989 when it was shown the p120 band is no more than a
polymer of the p41 protein. We discuss this in our Bio/Technology
HC: How interesting. What other instances are there of cross
VFT: There's many more examples. Surely everyone knows about the dogs
by now? Fifty percent of 144 dogs tested in the USA in 1990 were found
to have antibodies to one or more HIV proteins.(38) But dogs don't get
HIV or AIDS so those bands can't mean HIV infection. If a gremlin had
mixed up the blood from the dogs and the men in the MACS no one could
have told the difference. There's also non-HIV infected mice who develop
HIV antibodies when they're injected with cells from similar HIV free
mice (39) and there's the study co-authored by the Australian expert Dr.
Elizabeth Dax.(40) In 1991 her group reanalysed Western blot strips, not
sera, performed in 1985 on sera originally obtained from ten intravenous
drug addicts in 1971-72.
HC: What did that reveal?
VFT: Could I read the details from one of our unpublished papers?
HC: Go ahead.
VFT: Ten persons "with potentially positive WB patterns, when the
more specific 1985 criteria were used", were traced. One patient had
died from a motor vehicle accident and there were "no lymphoreticular
changes at autopsy, and a thorough retrospective analysis provided no
evidence of either current substance abuse or HIV infection". Of the
nine living addicts, two could not be assessed clinically, seven were
not chronically ill, (one was in prison but in good health, one had been
successfully discharged from a methadone program, one was enrolled in a
methadone program, another sporadically consumed illicit drugs). "The
two former patients whose 1971-72 WB results were most strongly reactive
had current ELISA and WB assays that were negative. The immune function
parameters were inconsistent with immune suppression". Their data led
the authors to conclude, "it is possible that antibodies to a
nonpathogenic virus would have disappeared during the 17 to 18
years...followup. Although this potential cannot be ruled out, it is
more likely that the earlier results were false positives...definitive
evidence of HIV infection in the United States' addict population as
early as 1972 is still lacking".
HC: HIV antibodies can fade and even disappear over time?
VFT: Yes. Despite the fact weíre told HIV is forever here are drug
addicts who gave up drugs, started to live a more healthy lifestyle and
their antibody tests reverted to negative. And their T4s returned to
normal. And most telling of all, they were alive twenty years later to
tell the tale.
HC: And nowadays they'd be hailed as saved by the latest anti-HIV
VFT: Quite possibly. Itís worth stressing how great a dilemma these
data create for the HIV experts. If these addicts had not attracted
attention by being alive they would have died carrying a pathogenic HIV
and most likely their deaths would be attributed to HIV. No doubt that
was the official cause of death for many of their less fortunate
brothers and sisters. But since they were alive and in
relative good health this challenged the HIV theory of AIDS. So the
experts toyed with the idea of a nonpathogenic HIV. That would at least
rescue the tests. But it would also set the beginning of the AIDS era
back to 1971. And place it not in Africa but in the United States. And
make us wonder how lethal or relevant is a virus that hangs around for
at least twenty years without killing the patient. And which disappears
as the patients' health improves. So, for these particular addicts, who
turned over a new leaf, it had to be false positives. Why couldn't all
drug addicts all turn over new leaves and end up the same?
HC: Perhaps all AIDS patients? Stay well away from drugs,
including anti-retrovirals, and live wholesomely and long enough for the
antibodies, and the risk factors, to metamorphose into something
VFT: Maybe for some but don't forget AIDS patients have diseases.
These should be evaluated and treated.
HC: Why is this paper unpublished?
VFT: We wrote the paper in early 1997 and called it "A critical
appraisal of the evidence for the isolation of HIV". I'm a Fellow of the
College of Surgeons in Australia and we sent it there hoping to get the
surgeons interested. The reviewing took months and there was a lot of
correspondence. They declined to publish, not because of significant
disagreement with the science but because the editorial board considered
that debate about the existence or non-existence of HIV "would be of
little interest or use to the majority of readers of the Australian and
New Zealand Journal of Surgery".
VFT: Incredible but true.
HC: Where's the paper now?
VFT: On the Net. At the Rethinking AIDS Website (13) and also, thanks
to the most generous efforts of Robert Laarhoven, at our own Website (at
Last week Neville Hodgkinson told us that from the point of view of
getting out the message about the existence of HIV, it was the most
readily understood paper we have ever written.
HC: Getting back to Western blots, do the experts offer any
explanation for the extreme variation around the world in the criteria
for a positive Western blot?
VFT: Well thereís a couple of things that emanate from our National
HIV Reference Laboratory.
HC: What do they say?
VFT: First, it is claimed that the different WB criteria have become
more closely aligned over time.
HC: Is that right?
VFT: How can it be? In 1985 it was all p24 and p41. Whatever side
you're on, at least youíd have to say THAT was aligned. But a mere
glance at the chart shows just how aligned the WB criteria are at
present. If thatís aligned what existed sometime in the past must have
been close to anarchy.
HC: What about the different criteria for a positive test?
VFT: According to our experts itís perfectly legitimate to set the
criteria for a positive test according to the prevalence of HIV
infection in the community being tested.
HC: Meaning what?
VFT: Where the prevalence is low, as claimed for Australia, you set a
lot of bands for a positive test. In fact we have four. But in Africa,
where they claim the prevalence is up to 10%, you can get away with
less, just two. And in the USA it's sort of intermediate. Two or three
HC: Where's the problem?
VFT: First, what if I told you the Faculty of Medicine at the
University of Western Australia teaches its students to interpret chest
X rays differently in smokers versus non-smokers? Or in Catholics
and Jews? Or in different countries? So in Iceland your chest X-ray
shows lung cancer but not if you send the films to Perth. Second, the
experts regularly make assertions about the prevalence of HIV infection
but how do they know what this is? When you find out how this is
estimated it turns out to be the same antibody test. You can't do that.
You can't use an antibody test to determine the prevalence of a disease
unless you know its specificity. No one knows the specificity of the HIV
antibody tests. What the experts are doing is using a test of unknown
specificity and setting it up as judge and jury over itself. This
is the trouble with this so called AIDS science. This is the sophistry
used to determine the specificity of the HIV Western blot an
HC: Could you explain what you mean by that?
VFT: HIV researchers perform an HIV antibody test in a number of
individuals and then repeat it half a dozen times using a slightly
different technique or a different brand of test. But they're all the
same test. If the tests are positive and all match they say this proves
the test is one hundred percent specific.
HC: Repeating the result is taken as proof of what caused the
result? Unbelievable. How do they make an independent judgment as
to the presence or absence of HIV?
VFT: That isn't done. What's done is like taking a chest X ray or an
ECG on a number of different machines or in different hospitals and
claiming that finding the same thing over and over proves lung cancer or
a heart attack is truly present.
HC: So although everyone admits to interference caused by non-HIV
antibodies, no one has really sorted out the magnitude of the problem.
As the Perth Group says, things stretch as far as the possibility they
might all be non-HIV antibodies?
VFT: Yes. For example, our HIV Reference Laboratory admits that one
quarter of HIV free blood donors have one or more reactive bands on the
HIV Western blot. They concede these are caused by cross-reacting,
non-HIV antibodies. Now, the way you get your cross-reacting, non-HIV
induced antibodies is to give your immune system a few belts. And the
more belts, and the more closely spaced, the more likely a person tested
will have cross reacting antibodies. But we know that in places like
Africa this kind of thing is happening all the time. And it happens
across all the AIDS risk groups. So the very people you're testing for
HIV are those with the greatest chance of cross reacting or
nonspecifically induced antibodies. So we have this grotesque paradox.
One quarter of pristine, well fed, OZ (Australian -ed.) blood donors
have one or more HIV WB bands, and that might include four bands, but
they're not infected with HIV. But in Africa, poverty stricken,
malnourished, Ugandan subsistence farmers with malaria or tuberculosis,
or repeated attacks of dysentery, have buckets of cross reacting
antibodies but if they've got just two bands on the Western blot, not
four, they are infected with HIV. Do you know anyone who can
HC: It seems at odds with what one would expect. I know a lot of
people who would avoid even trying.
VFT: It gets even more arcane. If the our experts are right about the
Western blot criteria becoming more closely aligned over time, since the
Australian criteria haven't changed recently and since scientists seem
obliged to set the number of bands according to the prevalence of HIV
infection, one must deduce that the prevalence of HIV infection in the
rest of the world is approaching that of Australia.
HC: Which is deemed to be one of the lowest in the world?
HC: Obviously it's been made much easier to diagnose HIV infection
in Africa compared to Australia.
VFT: The World Health Organisation criteria make it much easier to
report a positive test in Africa. But that doesn't prove a positive test
is caused by HIV infection.
HC: The criteria should be the most stringent in the developing
VFT: No one knows the correct criteria anywhere in the world but
everyone does know about cross reacting antibodies. And they are what
create the confusion. It's like losing your five year old kid at the
pictures. If you had to take him to something Adults Only because your
baby sitter ran away, then it's simple. The theatre is most likely full
of adults and any kid you see is likely to be your kid. But what if you
took him to see Snow White? There's kids all over the place. You need
far more stringent criteria before you can pick out your kid. If he had
a look alike, or even just dressed the same, you'd have to set the
stakes higher still. If he had a twin brother you might need to take off
his socks and look for the mole on his foot.
HC: So using only two bands in Africa means the test is worse
quality that it is even in the West for example?
VFT: When you talk about tests you need to be careful with words.
'Quality' could refer to any test parameter. We don't know any of the
test parameters because they've never been appraised against the gold
standard. I must stress this again and again. Without knowing the
sensitivity and specificity of the HIV antibody tests it is impossible
to use the tests to prove HIV infection. But your question raises
another interesting point. When you look at the mathematics of testing
it's very easy to prove that where the prevalence of whatever you're
chasing is high even a lousy test will get it right more than half the
time. Thatís because the odds are stacked before a person even has the
test. And 10% prevalence is very high. Diabetes is around five percent
and migraine ten percent. So if one in ten Africans were HIV infected,
and here I'm talking prevalence determined by bona fide means,
not a circular abstraction based on antibodies, and the average African
could afford to pay for a test, you could just about use anything. Even
a test for Vegemite (a favourite Australian edible spread for sandwiches
made from yeast - ed.) antibodies might provide a reasonably good
prediction of infection.
HC: Antibody tests aren't done routinely in Africa?
VFT: The World Health Organisation, Bangui definition of AIDS in
Africa requires neither an antibody test nor a T cell count. I think
this is something else extremely important to stress. People may not
appreciate what the African data imply. First, no one would dream of
diagnosing HIV infection or AIDS in the West without a blood test. But
under the African definition it's OK. You can be an AIDS case just on
symptoms, for example, fever, cough and diarrhoea for thirty one days
fulfils the definition. Second, the only reason that heterosexuals in
the West are deemed at risk of infectious immunodeficiency is because of
how the African situation is interpreted. Because equal numbers of men
and women in the reproductive age group have African AIDS diagnoses and
when tests are done equal numbers have antibodies. Based on assumptions
from these parallel but potentially misleading results, an African
diagnosed under the Bangui definition, without an antibody test is
condemned to HIV and AIDS unlike anyone in the West. And under such
diagnostic rigour the example of thousands of African men and women, who
are essentially suffering from symptoms and diseases all called other
names before 1981, is held up as proof that the West is menaced by the
threat of heterosexually transmitted AIDS.
HC: Caused by the same virus?
VFT: Yes even though the antibody test used to diagnose the same
virus is read differently in Africa. And might not be positive in other
places. In fact, according to the CDC, in the United States, an African
individual with an AIDS defining diagnosis is counted as heterosexual
AIDS simply by the fact that he or she comes from a country where
heterosexual AIDS is the claimed to be the "predominant" mode of
transmission. Knowledge of actual sexual contact is not a
HC: So itís assumed an African will invariably be
HC: Could an equal sex distribution of AIDS in sexually active
adults prove sexual transmission?
VFT: It's consistent with sexual transmission but it's not sufficient
proof. Equal numbers of sexually active adults develop appendicitis or
meningitis. Or schizophrenia. Are these diseases sexually
HC: Hasn't the Perth group recently published a paper reviewing
cross reacting antibodies?
VFT: Yes. Our last paper (12) reported a considerable amount of data
showing that antibodies to the types of organisms which infect 90% of
AIDS patients may also react with all the HIV proteins. Including in the
Western blot. So, if 90% of AIDS patients are infected with either a
mycobacterium or a fungus such as Pneumocystis carinii, how it is
possible to diagnose HIV infection in such persons, or to assert that
HIV is the cause of their diseases? The paper also examined cross
reacting antibodies in relation to proof for the existence of HIV. In
fact, as a caveat, we go into great detail to explain how
virtually overnight the world's first human retrovirus, Galloís HL23V,
became extinct when its antibodies were proven non-specific.
HC: And the Perth group posits a similar fate for HIV?
VFT: When someone finally takes on the isolation or specificity
problem, they're really the same problem, we believe this is a distinct
HC: So compared to 1993, when the Bio/Technology paper was
published, there's more evidence that positive antibody tests are caused
by factors even the experts admit are non-HIV?
VFT: Definitely. The other thing that's important to remember is that
patients are highly selected for antibodies before they ever get to the
Western blot. WBs are done on people who first of all feel the need to
go to a doctor and then have sufficient antibodies to make the ELISA
react twice in a row.
HC: They're preloaded with a selection of antibodies?
VFT: Right. You see Huw, when you say someone is HIV negative, the
truth is they're not ELISA negative, WB negative. They are actually
ELISA negative either once or one out two, and Western blot not done. A
negative is not confirmed with a Western blot, only a positive. But by
choosing this particular testing strategy the HIV/AIDS experts have
maximised the chances for the appearance of cross-reacting
HC: Maximised cross reactions? Is there evidence for this?
VFT: Yes. In 1988 the US Army (41) tested over a million soldiers and
found that even in healthy military recruits, half of all the 12,000,
first positive ELISAs were negative second time around. And after a
second positive ELISA two thirds failed to react on a first Western
blot. And some first Western blots failed to react in a second Western
blot. So, what you set up with two positive ELISAs before a WB is ample
opportunity to introduce confusion caused by cross-reacting antibodies.
Snow White in a test tube.
HC: Might there be people who would test negative twice on ELISA
and then positive on Western blot?
VFT: This happens but there are little data on how often it happens
because negatives usually arenít confirmed in this way.
HC: Are any other reasons put forward to justify the
variation in the actual WB criteria?
VFT: None that I know unless of course HIV is endowed with some kind
of global navigation system. It figures out where it is and then chooses
which B-cells to engage. That skill would be extremely hard to encode in
eight or nine or ten genes.
HC: Why eight or nine or ten genes?
VFT: It may be the most studied object in the universe but the
experts still don't agree how many genes it has.
HC: In 1998 what advice would you give a patient wishing to know
about his or her HIV antibody test?
VFT: First of all, from the point of view of establishing the
presence of HIV infection, Iíd say donít have a test. Don't spread HIV
testing. You wouldnít expect a woman whoíd missed a period to have a
pregnancy test if you didnít know how well the test performed. So why
HC: What if someone, say in a high risk group wants, to know his
or her chances of developing an AIDS defining illness? Regardless of
whether HIV is the cause?
VFT: I suppose there's two ways of looking at this. What are the
chances of getting sick, which is how doctors tend to think, or what are
the chances of remaining healthy? That puts a different emphasis from
the point of view of the person. There's no doubt about the association
between being in a risk group, having a positive test and developing
certain diseases defined as AIDS. But that doesn't apply across the
board. It's only statistical. So for an individual these two variables
cannot be the whole story. Not all such people get sick and the risk
varies up to fifty times between the risk groups. So, if you put aside
the retrovirus link and all that goes along with that, you might look
around for other factors. Now, like the ultimate causes of most
diseases, some of these factors may be completely unknown and totally
out of your control. But there might be some that are not unknown and
are under your control. Maybe as simple as being in a risk group.
You could, for example, decide to get OUT of your risk group or cease
doing whatever is risky WITHIN your risk group. Remember what happened
to the drug addicts. As far as explaining the association with the
antibody tests is concerned, perhaps HIV researchers have inadvertently
stumbled across a "something wrong test", like the ESR for example.
HC: What's the ESR?
VFT: The erythrocyte sedimentation rate. It's a test widely used in
clinical medicine. It measures how fast a drop of blood falls to the
bottom of a test tube of anticoagulant solution. The rate at which red
blood cells sediment is affected by changes in the plasma in which
they've been living, especially changes caused by alterations in the
composition of the proteins. For example in inflammatory conditions such
as rheumatoid arthritis and in tuberculosis, although non-diseases such
as pregnancy also produce a high ESR. In fact, in the old days, the ESR
was used as a pregnancy test. The point is this. Our group has long
argued lack of proof for a retrovirus as the cause of these antibodies.
But nonetheless, something must stimulate their production and
understanding that this is a possibility might lead people to things
which could undo their possibly harmful warnings. If the positive test
is not caused by one of the actual diseases then maybe there are
elements of the person's life which can be changed so that the stimulus
to this warning system is turned down. Or even switched off. Again we
come back to those drug addicts. They didn't have HIV, the experts say
so, but they did have antibodies which reacted in an HIV test. Whatever
the reason, when they altered their lives towards attaining better
health, somewhere along the same road where they shook off their habit,
they shook off their antibodies. I know the experts' explanation was
that they never had "real" HIV antibodies but that, much more innocent
interpretation, presents our side of the argument. These data are
predicted by our theory. These data are a test of our theory and
our theory has passed this test. The only difference is we say there are
NO proven, "real", HIV antibodies. So, maybe just the idea that these
antibodies could have other causes might bring sufficient hope to
neutralise the doom wrought by the explanation that they must be due to
HIV. I think those of us who are not HIV positive cannot even begin to
imagine how profoundly the psyche and health of an individual is
affected by belief in the existence of a lethal retrovirus inexorably
eating at the immune system. It must take extreme valour to even
question what almost the whole of the rest of world believes to be
HC: We should study long term survivors with HIV antibodies to
delineate what factors lead HIV positive individuals towards
VFT: Or away from diseases. That would be of enormous interest and
HC: What about people with actual AIDS defining diseases?
VFT: As I said before, the diseases should be vigorously treated in
their own right.
HC: What if someone not in a risk group is healthy but
VFT: The only honest answer is that, from the antibodies point of
view, there are no data upon which to pronounce a prognosis.
HC: Why do you say that?
VFT: Because from a purely scientific point of view, to determine
whether these antibodies represent an independent hazard, one would have
to take a hundred or so healthy, no risk, HIV positive individuals and
follow them untreated for a number of years and see what happens. But
you would not be able to tell them theyíre HIV positive.
HC: Why not?
VFT: Because, as we've just discussed, patients and physicians
believe most fervently that being HIV positive is a death sentence. This
belief and the possible administration of anti-HIV drugs may themselves
produce illness. These two variables would severely confound the
HC: As a doctor yourself, what in particular would you say
patients should ask their doctors?
VFT: Request scientific proof that the antibodies present in your
body arise for no other reason than infection with a virus called
HC: What if the answer is donít worry, trust us and the tests are
VFT: Then ask how, where and when and by whom this was established.
Request citations, scientific papers, names, dates, places, researchers,
journals. Get a copy of our 1993 Bio/Technology paper or our
latest paper, or this or Eleniís interview, or some of the other stuff
Christine Johnson has written about our research, and ask that each
point is specifically answered. What you must find out is how the
specificity of your test was determined. Since all the HIV experts
declare cross-reacting antibodies affect both ELISAs and the Western
blot, ask how they know your antibodies aren't all cross-reacting. Put
that very question. And refuse to accept obfuscatory remarks and don't
be put off by big names and big institutions.
HC: What if the answer includes advice to have a viral load
VFT: Then ask your doctor for proof that the RNA or DNA used in the
test to match your RNA or DNA is a unique constituent of a particle
proven to be an infectious retrovirus. I know the experts now regard
virus particles old hat but on the other hand, they still say a particle
called HIV causes AIDS. So there has to be a direct link between the RNA
and DNA and a particle. Where is it? Contact the manufacturer of the
primers and probes and ask for the scientific justification for the
label on the bottle. And since the PCR is quite capable of amplifying
non-target sequences, how and where the sensitivity and specificity of
the test for HIV infection was determined?
HC: What if oneís told itís all too hard to understand?
VFT: It's not hard to understand. I know it takes time but basically
most of this stuff is EASY to understand. You know Huw,
Papadopulos-Eleopulos et al have spent well over a decade
behaving impeccably as scientists and all weíve really proven is that
even if you think you're right, that forms about three percent of the
answer. The issues weíve written about languish waiting for scientific
responses. The trouble is so many of us, doctors included, accept the
validity of the HIV theory and all the tests because of big names and
big institutions. In good faith I must add but nonetheless without
checking up for themselves or asking questions. Well, they're not
usually the ones told they're infected with a lethal retrovirus. So
patients must be their own advocates and thereby influence public
opinion towards the debate. Let me remind you of what Galileo said, "In
Science the authority embodied in the opinion of thousands is not worth
a spark of reason in one man".
HC: Do you ever entertain thoughts that your ideas about all this
may be totally wrong?
VFT: Yes. And if there was a scientific debate, and we were proven
wrong, we would accept it.
HC: Finally, I believe you have written a book about some of your
VFT: It's nice of you to ask. The truth is I've written a manuscript.
It's not yet a book because I'm still having a hard time doing the
rounds of the publishers.
HC: What's it about?
VFT: It's a novel. A thriller (42) set in the US and Australia. About
a biotechnology company trying to bump off an AIDS dissident because the
Chairman of the Board perceives a huge threat to company profits. The
story is woven around a Professor of Chemistry, a lady of course, and an
HIV positive haemophiliac boy with a skeptical, politician uncle. There
are several conversations and a court scene where our view of HIV and
AIDS is aired.
HC: In plain language I hope?
VFT: Thatís for the reader to judge.
HC: Dr. Turner. Thank you very much for your time today.
VFT: Thank you Huw. I hope I've managed to stir a few hearts and
minds. And if anyone out there wants to publish a highly controversial
book, please let me know. *
The Moving Finger writes: and, having writ,
Moves on: nor all
thy Piety nor Wit
Shall lure it back to cancel half a Line,
all thy Tears wash out a Word of it.
- The Rubaiyat of Omar Khayyam
According to Anthony Fauci, "the least likely explanation for an
indeterminate [insufficient bands for positive but not the complete
absence of bands=negative] western blot is that the individual is
infected with HIV...The most likely explanation is that the patient
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