THE LAST DEBATE
Reappraising AIDS Dec. 1999
Eleni Papadopulos-Eleopulos (1) Valendar F.Turner (2) John M
Papadimitriou (3) Helman Alphonso (4) David Causer (1)
There is a tide in the affairs of men, which, taken at the flood,
leads on to fortune; Omitted, all the voyage of their life is bound in
shallows and in miseries. On such a full sea are we now afloat; And we
must take the current when it serves, or lose our ventures.
-- Julius Caesar Act V Scene III
Over recent months debate has been taking place amongst the
HIV/AIDS dissident groups regarding the wisdom of taking up the issue of
HIV isolation as an argument in our fight against mainstream AIDS
science. According to some dissidents this question should not be raised
because:
- it will provide HIV/AIDS protagonists with additional ammunition
with which to discredit us;
- it makes little difference if people are being killed in the name
of a non-existent or a merely harmless virus;
- it is an "existentialist" discussion.
On the other hand, other dissidents are of the opinion that we have
no strong arguments. To quote Vladimir Koliadin, "There are many
observations…which seem to provide strong support for the official
theory and to refute dissident views. Dissidents must "not turn the
blind eye to inconvenient facts".
From the very beginning the Perth group questioned the evidence which
may well prove the most significant "inconvenient" fact to fly in the
face of all HIV/AIDS protagonists. If the data do not prove beyond
reasonable doubt the existence of HIV then, in terms of a putative
exogenous retrovirus, there can be no "observations…to provide strong
support for the official theory". This is a point from which the
staunchest of each side cannot escape. However, although our group has
long published many scientific and epidemiological reasons for
questioning the existence of HIV, we largely chose to leave the facts
speak for themselves rather than making pronouncements such as "HIV does
not exist". There were two reasons for this:
- To facilitate publication;
- To avoid a split in the group which Charles Thomas founded. Also,
we could not exclude the possibility that the HIV theory of AIDS could
be deconstructed without questioning the existence of HIV.
In 1996, when Peter Duesberg wrote a paper claiming the
Continuum prize, he directly challenged the Perth group. We then
had no choice but to openly defend our position, and we repeated the
reasons in our lecture given at the 1998 Geneva International AIDS
Conference. At present there are four reasons why it is necessary to
question the isolation and thus the existence of HIV:
- Since 1996 it has become clear that, as far as the existence of
HIV is concerned, the Group for Reappraising AIDS is divided. Some of
the best known HIV experts are aware of this fact and it is now too
late to pretend otherwise.
- There is no proof that such an entity exists. To claim the
opposite is to deny the scientific evidence. Certainly conduct an
anti-HIV debate avoiding this issue as exemplified by many in our
midst. However, in arguing against the HIV hypothesis of AIDS in this
manner one has to be content with half truths.
- "HIV" is the main obstacle, indeed, the only obstacle, in
deconstructing the HIV theory of AIDS.
- Demonstrating that HIV has no been isolated is not an
"existentialist" debate. In fact we consider this to be the strongest
argument we can muster.
If we accept there is no proof for the existence of HIV then
undoubtedly "the construction AIDS, also called HIV disease, collapses
immediately and all so called "HIV tests" are automatically unmasked as
being useless". If, on the other hand, we accept the existence of HIV,
the debate could be endless, no matter how courageously one fights and
what sacrifices one makes. In this regard Peter Duesberg’s unprecedented
contribution is a wise and timely reminder to all of us.
Why HIV isolation is necessary
The word "isolation" appears frequently in scientific papers and in
debate concerning HIV and indeed in virology in general. For example,
Montagnier’s 1983 and two of Gallo’s 1984 Science papers contain
the word in their titles as well as the text. Use of this word signals
the reader that the experimenter is claiming that the data presented
proves that a virus exists. If this is the first such report the authors
may claim to the discovery of a particular virus. What all scientists
must consider is whether the data presented as "isolation" do indeed
justify the claims.
A virus is an obligatory intracellular, replicating particle of
particular physical and chemical properties. Thus the first absolutely
necessary, but not sufficient step in proving the existence of a
retrovirus is to isolate retrovirus-like particles. That is, obtain the
particles separate from everything else. In other words, purify them.
There are many reasons for this including the following:
1. To prove that the retrovirus-like particles are infectious,
that is, the particles are a virus.
Finding a retrovirus either in vitro or in vivo is not
proof that it originated from outside, that is, the virus is infectious,
exogenous. Furthermore, Gallo was well aware of this problem as far back
as 1976 when he wrote: "Release of virus-like particles morphologically
and biochemically resembling type-C virus but apparently lacking the
ability to replicate have been frequently observed from leukaemic
tissue". In other words, it is not sufficient to claim a particle is a
retrovirus merely on appearances. To prove that retrovirus-like
particles observed in a culture are virus particles one must isolate
(purify) the particles, characterise their proteins and RNA and
introduce them in a secondary culture, preferably containing cells of a
different type than the primary culture. If any particles are released
in the secondary culture, isolate them and prove that their proteins and
RNA are exactly the same as those of the particles isolated from the
primary culture. In these types of experiments one must not ignore the
pivotal importance of proper controls.
2. To determine their biological effects.
For this one must use pure particles otherwise it is impossible to
determine whether the effects are due to the virus particle or to
contaminants. As Peter Duesberg has pointed out in "Koch's second
postulate: The microbe must be isolated from the host and grown in pure
culture", "was designed to prove that a given disease was caused by
a particular germ, rather than by some undetermined mixture of
non-infectious substances". Ironically Peyton Rous, the discoverer of
retroviruses, issued the same caveat for "filterable agents",
"retroviruses" in 1911.
3. To characterise the viral proteins.
The only way to prove that a protein is a viral protein is to obtain
it from that object, or when the object is very small, as is the case of
viruses, from material which contains nothing else but virus particles.
In the material contains impurities which also have proteins it is not
possible to determine what is viral and what is not. Only after the
viral proteins are characterised they can be used as antigens in the
antibody tests.
4. To characterise the viral genome.
As for viral proteins the only way to prove that a stretch of RNA is
viral, it is to obtain it from material which contains nothing else but
virus particles. If the material contains impurities, the impurities
must not contain RNA. Then, and only then, can the RNA and its cDNA be
used as probes and primers for genomic hybridisation and PCR
studies.
5. To use it as a gold standard.
Just because a virus or viral protein reacts with an antibody present
in a patient's sera, this does not prove that the antibody is directed
against the virus or its proteins. That is, the reaction is specific. To
determine the specificity of an antibody reaction one must use the virus
as a gold standard. Protagonist HIV experts such as Dr. Donald Francis
agree. Speculating on a viral cause for AIDS in 1983, Francis wrote,
"One must rely on more elaborate detection methods through which, by
some specific tool, one can "see" a virus. Some specific substances,
such as antibody or nucleic acids, will identify viruses even if the
cells remain alive. The problem here is that such methods can be
developed only if we know what we are looking for. That is, if we are
looking for a known virus we can vaccinate a guinea pig, for example,
with pure virus...Obviously, though, if we don't know what virus
we are searching for and we are thus unable to raise antibodies in
guinea pigs, it is difficult to use these methods...we would be looking
for something that might or might not be there using techniques that
might or might not work" (italics ours). The only way to perform
hybridisation and PCR studies is to use the viral RNA or its cDNA or
small fragments of it, as probes and primers. However, as with
antibodies which react with viral proteins, a positive result,
especially a positive PCR result, does not guarantee that what is
detected is viral RNA. To determine the specificity of the PCR the virus
must be used as a gold standard.
HIV "Isolation"
All retrovirologists agree that one of the principal defining
physical characteristics of retroviruses is their density. In sucrose
density gradients they band at the density of 1.16g/ml. Using the method
of sucrose density banding in 1983 Francoise Barre-Sinoussi, Luc
Montagnier and their colleagues claimed to have isolated a retrovirus,
that is, to have obtained material which contained nothing else but
"purified labelled virus" which now is known as HIV. Similar claims were
reported by Robert Gallo’s group in 1984. It goes without saying that if
the material was pure HIV, then all the proteins present in such
material must be HIV proteins. Instead, only the proteins which were
found to more often react with sera from AIDS patients and those at risk
were said to be HIV proteins, and the antibodies which reacted with them
the specific HIV antibodies. Since then the reaction of these proteins
with antibodies is considered proof for HIV infection. Again, if their
material was pure HIV then all the nucleic acids present in their
material must be the HIV genome. Instead, only some fragments of RNA
rich in adenine were arbitrary chosen and were said to constitute the
HIV genome. Since then, these fragments have been used as probes and
primers for hybridisation and PCR studies, including the determination
of "viral load".
The biggest problem in accepting Montagnier's and Gallo's groups
claims is the fact that neither published even one electron microscope
picture of the "pure" HIV to prove that the material contained nothing
else but isolated, retrovirus-like particles, "purified labelled virus".
In 1997 Montagnier was asked by the French Journalist Djamel Tahi why
such pictures were not published. Incredibly Montagnier replied because
in what his group called "purified" HIV there were no particles with the
"morphology typical of retroviruses". When he was asked if the Gallo
group purified HIV, Montagnier replied: "I don't know if he really
purified. I don't believe so". If this is the case then the 1983
Montagnier findings and the 1984 Gallo's finding, prove beyond all
reasonable doubt that they did not have any retrovirus much less a
unique retrovirus, and that the proteins and the RNAs which were present
in their "purified" material could not have been of retroviral
origin.
In the same year, 1997, some of the best known HIV experts accepted
that no evidence existed which proved HIV isolation and thus a "virus to
be used for biochemical and serological analyses or as an immunogen". In
that year, two papers were published in Virology with the first
electron micrographs of "purified HIV" obtained by banding the
supernatant of "infected" cultures in sucrose density gradients. The
authors of both studies claimed that their "purified" material contained
some particles which looked like retroviruses and were said to be the
HIV particles. But they admitted that their material predominantly
contained particles which were not viruses but "mock virus", that is,
"budding membrane particles frequently called microvesicles".
Furthermore, "The cellular vesicles appear to be a heterogeneous
population of both electron-lucent and electron-dense membrane
delineated vesicles ranging in size from about 50 to 500nm". Many, but
not all of these mock viruses "appear "empty" by electron microscopy".
According to the authors of these studies, one of the reasons that some
of the "mock virus" particles appear to have no core "might be that the
vesicles contain large amounts of protein and nucleic acid which are
unstructured". They showed that the microvesicles "are a major
contaminant" of the "purified" HIV. Indeed, the caption to one of the
electron micrographs reads, "Purified vesicles from infected H9 cells
(a) and activated PBMC (b) supernatants", not purified HIV.
In a further experiment the supernatant from non-infected cultures
was also banded in sucrose gradients. They claimed that the banded
material from these cultures contained only microvesicles, "mock virus"
particles but no particles with the morphology of HIV. The mock virus
particles contains both DNA and RNA, including mRNA which is known to be
poly-A rich.
No reason(s) is given, other than morphological, for why some of the
particles in the fractions from the "infected" cells are virus particles
and the others "mock virus". As far as morphology is concerned, none of
the particles have all the morphological characteristics attributed to
HIV, or even retroviruses.
The minimum absolutely necessary but not sufficient condition to
claim that what are called "HIV-1 particles" are a retrovirus and not
cellular microvesicles is to show that the sucrose density fractions
obtained from the "infected" cells contain proteins which are not
present in the same fractions obtained from non-infected cells. However,
Bess et al have shown this is not the case. The only difference
one can see in their SDS-polyacrylamide gel electrophoresis strips of
"purified virus" and "mock virus" is quantitative, not qualitative. This
quantitative difference may be due to many reasons including the fact
that there were significant differences in the history and the mode of
preparation of the non-infected and "infected" H9 cell cultures.
That the "viral" proteins are nothing more than cellular proteins was
further demonstrated by Arthur, Bess and their associates. In their
efforts to make an HIV vaccine they immunised macaques with, amongst
other antigens, "mock virus", that is sucrose density banded material
from the supernatants of non-infected H9 cell cultures. After the
initial immunisation the monkeys were given boosters at 4, 8 and 12
weeks. The animals were then challenged with "SIV" propagated either in
H9 cells or macaque cells. When the WBs obtained after immunisation but
before "SIV" challenge were compared with the WBs post-challenge, it was
found that challenge with "SIV" propagated in macaque cells had some
additional bands. However, the WBs obtained after the challenge with SIV
propagated in H9 cells were identical with the WBs obtained after
immunisation, but before challenge. In other words, the protein
immunogens in the "virus" were identical with the immunogens in the
"mock virus".
Since both the "mock virus" and "purified" virus contain the same
proteins, then all the particles seen in the banded materials including
what the authors of the 1997 virology papers call "HIV" particles must
be cellular vesicles. Since there is no proof that the banded, "purified
virus", material contains retrovirus particles then there can be no
proof that any of the banded RNA is retroviral RNA. When such RNA (or
its cDNA) is used as probes and primers for hybridisation and PCR
studies, no matter what results are obtained, they cannot be considered
proof for infection with a retrovirus, any retrovirus.
To quote dissident Paul Philpott "I think a very convincing case can
be made against the HIV model. It's just that the points that really do
refute the HIV model have not been taken up as the principal weapons of
our most visible advocates." Any scientist of any persuasion acquainted
with these data must question the evidence for the existence of HIV.
(1) Department of Medical Physics, Royal Perth
Hospital, Wellington Street, Perth 6001; (2) Department of Emergency
Medicine, Royal Perth Hospital; (3) University of Western Australia; (4)
Department of Research, Unversidad Metropolitana Barranquilla, Colombia
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