COMMENTARY ON MONTAGNIER
By Eleni Papadopulos-Eleopulos et al.
Continuum Winter 1997
We would like to thank Djamel Tahi and Huw Christie for asking us to comment
on Professor Luc Montagnier's answers given in his interview
with Djamel Tahi. Before commenting we thought it would be useful to start with a brief
review of the methods used to prove the existence of retroviruses, and Montagnier
et al 1983 evidence for the existence of "HIV".
Methods used to prove existence of retroviruses
It is generally accepted that Peyton Rous discovered retroviruses in
1911 when he induced malignancy in chickens by injections of cell-free
filtrates obtained from a muscle tumour. Similar experiments were repeated
by many researchers and the tumour inducing filtrates became known as filterable
agents, filterable viruses, Rous agents, Rous virus. However, Rous himself
expressed doubts that the agents which caused tumours were infectious in
nature. Indeed, Rous warned, "The first tendency will be to regard
the self-perpetuating agent active in this sarcoma of the fowl as a minute
parasitic organism. Analogy with several infectious diseases of man and
the lower animals, caused by ultramicroscopic organisms, gives support
to this view of the findings, and at present work is being directed to
its experimental verification. But an agency of another sort is not out
of the question. It is conceivable that a chemical stimulant, elaborated
by the neoplastic cells, might cause the tumour in another host and bring
about in consequence a further production of the same stimulant".(1)
In 1928, AE Boycott, the President of the Royal Society of Medicine,
Section of Pathology, in his Presidential Address entitled "The Transition
from Live to Dead: the Nature of Filtrable Viruses", said: "Another
analogous phenomenon takes us, I think, a step further. The products of
autolysis of dead cells in the body, in suitable concentration, stimulate
tissue growth. It is a beautiful self-regulating mechanism in which the
amount of stimulus is proportionate to the amount of cell destruction,
and therefore to the amount of cell growth required, and it is obviously
of the highest importance for survival - a far more potent factor in selection
and evolution than any disease has ever been. As it normally operates in
healing our cut fingers, the final result is simply the restoration of
the cells which were destroyed. But if the normal restraint exercised by
neighbouring tissues is evaded and use made of tissue cultures, the products
of autolysis or metabolism (in the form of extracts of tissues, tumours,
or embryos) stimulate growth indefinitely and a much larger quantity of
tissue may be obtained than we started with. From the autolysis of this
a larger amount of stimulating substance may be obtained, and there seems
no reason why this process of multiplication should have any limit: normal
tissues in the physical isolation of tissue cultures are as immortal as
malignant tissues in their physiological isolation from the rest of the
body...These products of autolysis...have not received nearly as much attention
as they deserve, but they are probably of relatively simple and discoverable
constitutions. Yet applied to cells they cause growth, and in so doing
potentially increase their own quantity; this is very much what the Rous
agent does...As to its origin, all the evidence seems to concur in indicating
that the Rous virus arises de novo in each tumour. There is no epidemiological
evidence that cancer comes into the body from outside; everything we know
supports the classical view that it is a local autochthonous disease. Experimental
sarcomas produced by embryo extract and indol, arsenic or tar have been
transmitted by filtrates. Epitheliomas are easily produced in mice by tar
and in men by chronic irritation; and if we believe that all malignant
tumours contain more or less of a carcinogenic agent akin to the Rous virus,
it follows that we can with a considerable degree of certainty stimulate
normal tissues to produce virus".(2)
Ten years earlier in an article entitled "The Plasmagene Theory
of the Origin of Cancer", Darlington, discussing the induction of
cancer by the Rous agent, the filtrable viruses and the "self-propagating"
particles transmitted by heredity but lying outside the nucleus found in
plants and "known as plasmagenes", wrote: "These infections,
it will be seen, are artificial, or at least unnatural. Now the distinction
between natural and artificial infection has long been known, although
little regarded, in the discussion of plant viruses. A number of aberrant
conditions can be transmitted from stock to scion, and some even have arisen
in a scion after it has been grafted on a healthy stock. These are artificial
diseases; they are not transmitted in nature, but only by grafting. Some
may have arisen by the mutation of self-propagating proteins in the cells
of plants propagated over long periods by vegetative means (as tumours
can be). Others have certainly arisen by the migration or transplantation
of proteins from one organism to another. In either case they have a property
of infection which they can reveal only in artificial circumstances...We
make a great mistake therefore in calling them viruses; they are proviruses...
One more question is worth answering: What form would the mutant protein
be likely to take in the tumour cell? On account of its rapid multiplication
it might well show a higher degree of aggregation than its progenitor.
It would then appear as an alien particle in the mutant cell. This is borne
out by the electron microscope observations on two chicken tumour agents
of provirus type by Claude, Porter and Pickels (1947)".(3)
The electron microscope observation by Claude et al is the first
report of virus-like particles in a tumour, the first electron micrographs
of the "Rous virus". Soon after many other researchers reported
these type of particles in many tumours, and as Boycott predicted in "stimulated
normal tissues". As far as Darlington's prediction that these particles
may be due to "a higher degree of aggregation" of the cytoplasm
it may be interesting to note that: (a) for proteins, nucleic acids or
protein/nucleic acid aggregation (condensation, contraction) to take place,
oxidation is necessary;(4) (b) tumour tissues are oxidised;(4) (c) all the
agents used to "stimulate normal tissues" to induce retroviruses
are oxidising agents.(5-7)
In the 1940s, following the development of the electron microscope (EM)
and the technique of ultracentrifugation in density gradients, the particles
observed in malignant tissues could be isolated and thus purified, that
is, separated from everything else. Because these particles were seen in
malignant tissues "it has been judged that the particles constitute
the aetiological agent of the disease" and by the 1950's Rous's filtrable
agents became known as oncoviruses (onkos = tumour). The principal morphological
characteristic of these particles is a restricted range of diameters and
the main physical characteristic their density.(8) When the ultrastructure
of these particles was determined they were defined as particles with a
diameter of 100-120nM containing "condensed inner bodies (cores)"
and surfaces "studded with projections (spikes, knobs)".(9)
By the 1950's well-known retrovirologists such as JW Beard, recognised
that cells including uninfected cells, under various conditions, were responsible
for the generation of a heterogeneous array of particles, some of which
may look like oncoviruses. This "particle problem" led to the
opinion that to prove the existence of a retrovirus "the scheme of
approach, as well illustrated by that devised and rigorously tested in
investigations of viral agents, is relatively simple. This consists in
(1) isolation of the particles of interest; (2) recovery (purification)
of the particles in a given preparation that are homogeneous with respect
to particle kind; (3) identification of the particles, and (4) analysis
and characterisation of the particles for the physical, chemical, or biological
properties desired". Beard also stressed that "identification,
characterisation, and analysis are subject to well-known disciplines established
by intensive investigations, and the possibilities have by no means been
exhausted. Strangely enough, it is in this field that the most frequent
shortcomings are seen. These are related at times to evasion of disciplines
or to their application to unsuitable materials. As was foreseen, much
of the interest in the more tedious aspects of particle isolation and analysis
has been diverted by the simpler and undoubtedly informative processes
of electron microscopy. While much can be learned quickly with the instrument,
it is nevertheless clear that the results obtained with it can never
replace, and all too often may obscure, the need for the critical fundamental
analyses that are dependent on access to homogenous materials"(10)
Retrovirologists also agreed that "Virions of RTV (retroviruses
) have a characteristic buoyant density, and centrifugation to equilibrium
in density gradients is the preferred technique for purification of RTV".11
At a European meeting on the use of centrifugation in density gradients
held at the Pasteur Institute in 1972 with Jean-Claude Chermann as its
secretary, it was stressed that once the culture fluids (supernatants)
are banded, the density band at which retroviruses are trapped (this varies
slightly with the substance used to manufacture the gradients), must be
thoroughly assayed. The assays consist of the following:
"Assays for RNA Tumor Viruses
Electron Microscopy (neg stain and thin sect.)
60-70S RNA, total RNA
Gel analysis of viral and host proteins and nucleic acids
Infectivity in vivo
Infectivity in vitro
*With specific reagents for enveloped and internal antigens gs and env".(12)
(Reverse transcriptase is an enzyme first discovered in oncoviruses
in 1970 (13) hence their present name retroviruses, and 60-70S RNA, the
"viral" RNA. Retroviruses are sometimes called RNA tumour viruses
because their genome consists of RNA and not DNA).
Thus the method specified at the Pasteur Institute in 1972 is no different
from that discussed by JW Beard two decades earlier. Indeed, the method
is basic logic applied to the definition of a virus. It is impossible to
claim that a protein or an RNA are retroviral unless it is first proven
these are constituents of a particle and that the particle is infectious.
As can be seen, the first step is electron microscopic examination to prove
that the band contains particles with the morphological characteristics
of retroviruses and, as Francoise Barre-Sinoussi and Jean Claude Chermann
pointed out at the Pasteur meeting, that the band is pure, that is, it
contains nothing else but particles with "no apparent differences
in physical appearances".(14)
The second step in assaying the 1.16g/ml material is to prove that the
particles are able to reverse transcribe RNA into DNA. However, as Gallo
himself warned the finding of particles, even those containing reverse
transcriptase, is insufficient evidence to prove a particle is a retrovirus.
The complete proof depends on experiments to: (a) obtain particles from
a culture that are separate from everything else (isolated) and show that
the particles contain proteins and RNA but not DNA and the proteins are
coded by the RNA (the viral genome); (b) show that when the particles are
introduced into a culture of uninfected cells, the particles enter the
cells, the particles' RNA is reversed transcribed into DNA which is incorporated
into the cellular DNA; (c) show that these cells in their turn produce
retroviral-like particles; (d) show that the particles produced by these
cells contain proteins and RNA which are identical with those of the original
particles introduced into the cells; (e) show that cell cultures identical
to those in which the retroviral-like particles were introduced do not
produce such particles when they are cultured in exactly the same conditions
but instead of the retroviral particles one introduces some other culture
material such as cellular microvesicles. This is because, unlike for any
other infectious agent, all cells contain retroviral genomes which under
appropriate conditions may be expressed in culture. That is, may lead to
the appearance of retroviruses known as endogenous retroviruses. It follows
that both the cells in the culture from which the original particles were
obtained as well as the culture into which they were introduced may release
identical retroviral particles even if the particles that were introduced
were not infectious. Therefore it is absolutely imperative to have suitable
Thus, to prove the existence of a retrovirus, one must isolate and analyse
the retroviral-like particles twice. The first time to obtain and analyse
the particle constituents released in the first culture. The second time
to prove that the particles released, if any, by the cell in the second
culture, are identical to the ancestral particles. The crucial caveat in
this procedure is the use of experimental techniques to control for the
effects of cocultivation, chemical agents and the many other factors which
themselves may induce retroviral phenomena independent of exogenous retroviral
In conclusion, by the early 1980's, retrovirologists agreed that to
prove the existence of retroviruses one must first isolate (purify) candidate
particles and the method to achieve this was by banding in a density gradient.
Summary of Montagnier and colleagues 1983 Science paper
In 1983 Luc Montagnier and his colleagues from the Pasteur Institute
and other French researchers published a paper which is considered the
first study in which the existence of "HIV" was proven. The paper
is entitled "Isolation of a T-Lymphotropic Retrovirus from a patient
at risk for Acquired Immune Deficiency Syndrome (AIDS)"(18) with Francoise
Barre-Sinoussi as principle and Jean Claude Chermann as second author.
The authors' claim to have isolated a retrovirus and thus proven its existence
was based on the following experiments:
1. Lymphocytes from the lymph nodes of two patients with lymphadenopathies
as well as peripheral blood mononuclear cells from these patients "were
put in culture medium with phytohemagglutinin (PHA), T-cell growth factor
(TCGF), and antiserum to human a interferon...In the mouse system, we had
previously shown that antiserum to interferon could increase retrovirus
production by a factor of 10 to 50". The supernatants were regularly
assayed for reverse transcriptase activity (RT) using the synthetic template
primer An.dT12-18. "After 15 days of culture, a reverse transcriptase
activity was detected in the culture supernatant of the lymph node culture"
of one of the patients, the first patient. (The level of activity is not
given). "Peripheral blood lymphocytes cultured in the same way were
consistently negative for reverse transcriptase activity even after 6 weeks".
So were both cultures from the second patient. Apparently the detection
of RT activity was considered evidence for infection with a retrovirus.
2. Lymphocytes from an adult healthy blood donor were cultured (culture
conditions not given) and after three days half the culture was cocultured
with lymphocytes from the patient's culture in whose RT was detected. (Conditions
not given). "Reverse transcriptase activity could be detected in the
supernatant on day 15 of the cocultures", (level of activity not given)
but not in the culture of the blood donor. (It is not mentioned if the
conditions in the blood donor culture were the same as the coculture conditions.
However, it is obvious that the blood donor cells were not cocultured with
lymphocytes from lymph nodes of patients who were not at risk of AIDS but
who otherwise had similar clinical and laboratory abnormalities as patient
number one. Given that co-cultivation leads to the appearance of endogenous
retroviruses this is a significant omission from the experimental protocol).
3. Normal umbilical cord lymphocytes were cultured for three days (culture
conditions not given), after which supernatants from the coculture and
polybrene were added. "After a lag period of 7 days, a relatively
high titer of reverse transcriptase activity was detected". (In fact
the activity was relatively low, no more than 8,000 counts/min. Background
activity as high as 4000 counts/min have been reported.(19) "Identical
cultures" to which supernatant has not been added remained negative.
(Since no supernatant was added the cultures could not have been identical.
Since supernatant from non-infected cultures added to normal non-infected
cells leads to the appearance of endogenous retroviruses this is also a
significant difference). Commenting on the findings in the three experiments
the authors wrote: "These two successive infections clearly show that
the virus could be propagated on normal lymphocytes from either newborns
or adults". The data from the three experiments apparently were also
considered proof of "isolation", however, "That this new
isolate was a retrovirus was further indicated by its density in a sucrose
gradient, which was 1.16".
4. The evidence from the sucrose gradients consisted of two parts. (a)
the supernatant from the cord blood lymphocytes in which RT activity was
detected was banded in sucrose density gradients. Maximum RT activity was
reported at the 1.16g/ml band. (b) to the cord blood lymphocyte culture
in which RT activity was detected [35S] methionine was added, that is radioactive
methionine, an amino acid which is incorporated into growing protein chains
and whose radioactivity allows detection of such proteins. Two types of
experiments were performed with this culture, one with the cells and the
other with the supernatant: (i) a cell extract was lysed (broken apart)
and centrifuged. To parts of the cellular supernatant various sera (containing
antibodies) were added and the proteins were electrophoresed (separated
using an electric field) on a polyacrylamide-SDS slab gel. Many proteins
were found to react, not only with the sera from the two patients with
multiple lymphadenopathies but also with sera from a healthy donor and
a normal goat. (ii) the culture supernatant was banded in a sucrose density
gradient. Although no mention is made of EM studies of the 1.16g/ml band,
it was claimed that the band represented "purified, labelled virus
from patient 1". The 1.16g/ml band was reacted with the sera of the
two patients as well as two healthy blood donors and was processed in the
same way as the cellular extract. Although in the published manuscripts
it is virtually impossible to distinguish proteins reacting with any sera,
even with the sera from the two patients, in the text it is stated that
"when purified, labelled virus [the 1.16g/ml band] was analysed
[reacted with the sera] three major proteins could be seen: the p25 protein
and proteins with molecular weights of 80.000 and 45.000. The 45K protein
may be due to contamination of the virus by cellular actin which was present
in imunoprecipitations of all cell extracts." (italics ours) EM studies
of the cord blood lymphocytes culture "showed characteristic immature
particles with dense crescent (C-type) budding at the plasma membrane...The
virus is a typical type-C RNA tumour virus".
Comments on answers Montagnier
A1. 1. If "culture, purification of the material by Ultracentrifugation,
Electron Microscopic (EM) photographs of the material which bands at the
retrovirus density, characterisation of these particles, proof of the infectivity
of the particles" is not isolation, then why did Montagnier and his
colleagues claim in 1983 to have isolated "HIV" by either performing
or claiming to have performed all but one (no EM photographs of the banded
material) of these procedures? Why in the 1984 paper where they claimed
the first isolation of "HIV" from haemophiliacs, as well as in
their other studies that year in which they also claim "HIV"
isolation they have either performed or claimed to have performed all but
one of these steps?(20-21) Why in their study entitled "Characterisation
of the RNA depended DNA Polymerase of a new human T lymphotropic retrovirus
(lymphadenopathy associated virus)"(22) did they state that the virus
was "purified on sucrose gradient using isopycnic centrifugation (8)"?
Reference 8 is the paper presented by Sinoussi and Chermann at the 1972
Pasteur Symposium where they stressed the importance of showing that the
banded material contained nothing else but particles with "no apparent
differences in physical appearances".(14)
2. The finding of some or all of the phenomena Montagnier outlines are
not proof of isolation. These phenomena can be considered only proof for
viral detection and then, if and only if, they are specific to retroviruses.
The word "isolation" is derived from Latin "insulatus"
meaning "made into an island". It refers to the act of separating
an object from all the extraneous matter that is not that object. Here
the object of interest is a retroviral particle. The words 'isolation'
and 'passing' have different and distinct meanings. 'Isolation' means to
obtain an object, a retrovirus particle for example, separate from everything
else. 'Passing' means to transfer an object (which may or may not be isolated)
from one place to another, for example, from one culture to another. Therefore,
even if one assumes that the "something" which Montagnier and
his colleagues passed from one culture to another by means of transferring
cells or culture supernatants was a retrovirus, and that it was passed
to an infinite number of successive cultures, it still is not evidence
for isolation. For example, if one has a series of bottles containing water
in which the first has a dye added, then takes part of the first and puts
it in the second, and from the second passes a sample into the third et
cetera, clearly this procedure has not isolated the dye from the water.
A culture contains a myriad of things and thus by definition is not evidence
for isolation of an object. The only way possible to claim that one has
"made a culture of the virus", is to have had proof for the existence
of the virus before making a culture. The only thing which Montagnier and
his colleagues have proven is the emergence in the coculture with "lymphocytes
from a blood donor" of RT activity. Detection of an enzyme in a culture,
even if specific to retroviruses is not evidence for isolation. For example,
the measurement of cardiac or liver enzymes in cases of myocardial infarction
or hepatitis respectively cannot be construed as "isolation"
of the heart or liver. The finding in the culture of particles with the
morphological characteristics of retrovirus and of reverse transcriptase
activity either in the culture or the 1.16g/ml band, even if "truly
specific of retroviruses" is not evidence for retroviral isolation.
Even if Montagnier and his colleagues knew beforehand that some of the
proteins present in the culture or the 1.16g/ml band were retroviral, and
the patients had retroviral antibodies which reacted with these proteins,
such a reaction is not evidence for isolation. Argument based on analogies,
or even on knowledge of other retroviruses, cannot be construed evidence
for isolation. For example, observing something in the ocean which looks
like a fish (even if it is a fish), is not equivalent to having the fish
in your frypan separate from everything else that occurs in the ocean.
3. We agree with Gallo that Montagnier et al did not present
proof for "true isolation" of a retrovirus, any retrovirus, either
old or new, exogenous or endogenous.
4. The "knowledge of other retroviruses" shows that not all
particles with RT activity and "visual properties of retrovirus"
are viruses. This is a fact acknowledged even by Gallo well before the
AIDS era.(23) It also shows that RT is not "truly specific of retroviruses".
Non-infected cells as well as bacteria or viruses other than retroviruses
have RT. According to some of the best known retrovirologists including
its discoverers, as well as Nobel Laureate and Director of the US National
Institutes of Health, Harold Varmus, reverse transcriptases are present
in all cells including bacteria.(13,24-25) Indeed RT activity has been
reported in many of the cell lines from which "HIV" is "isolated",
including H9 and CEM as well as normal lymphocytes even when they are not
infected with "HIV".(26-27) Montagnier, Barre-Sinoussi and Chermann
themselves have shown that RT activity is not specific to retroviruses.
In their 1972 paper Barre-Sinoussi and Chermann wrote: "There was
significant activity in the sample zone and the fastest sedimenting peak,
consisting mainly of cell debris. This enzymatic activity can be explained
by the presence of some virus particles in these regions, and, since similar
polymerase activity has been found in normal cells, may be mainly ascribed
to the cellular enzyme". In this interview, Luc Montagnier answering
question 14 says: "For example, one day I had a very fine peak of
RT, which F Barre-Sinoussi gave me, with a density a little bit higher,
1.19 and I checked! It was a mycoplasma, not a retrovirus". How is
it then possible for Montagnier to say that RT is specific to retroviruses?
We agree that RT activity is characteristic of retrovirus. However, 'specificity'
does not have the same meaning as 'characteristic'. Hair is characteristic
of human beings but not every animal with hair is human.
5. Isolation means to obtain an object separate from everything else.
Retroviruses are particles and no amount of "analogy" can prove
that one has isolated a retroviral particle. "Knowledge of other retroviruses"
can be of assistance in choosing the best method to obtain isolation. The
"knowledge of other retroviruses" shows that the best, but by
no means perfect method to isolate and prove the existence of retrovirus,
is to perform isopycnic (identical density of particle and portion of the
gradient) banding and to perform all the assays specified at the 1972 Pasteur
symposium. The "knowledge of other retrovirus" also shows that
there is nothing specific about the morphology of retroviral particles,
protein-antibody reactions or even banding at the density of 1.16g/ml in
sucrose density gradients. Retroviral particles band at the density of
1.16g/ml but not everything at that density, including particles with the
morphology of retroviral particles, is a retrovirus.(11-13,28) To remind
ourselves this is the case, one needs go no further than to consider the
"first" human retrovirus, "HL23V".
In the mid 1970's Gallo and his colleagues reported the isolation of
the first human retrovirus. In fact the evidence for the isolation of "HL23V"
surpassed Montagnier's et al and everybody else's evidence for "HIV"
in at least three important aspects. Unlike "HIV", in the case
of "HL23V" Gallo's group: (a) reported the detection of RT activity
in fresh, uncultured leucocytes; (b) did not need to stimulate their cell
cultures with various agents. (Both Montagnier and Gallo concede that none
of the phenomena which they say prove the existence of "HIV"
can be detected unless the cultures are stimulated with several agents);
(c) published an electron micrograph of virus-like particles banding at
a sucrose density of 1.16g/ml.(23-29) However, today nobody, not even Gallo,
considers "HL23V" as being the first human retrovirus or even
a retrovirus. (For a more detailed discussion see Papadopulos-Eleopulos
et al (30-32)). One also must not forget the following additional
knowledge in relation to retroviruses: (a) the lesson of the enzyme adenosine
triphosphatase. Like RT, this enzyme was considered to be specific to retroviruses
and at least in the 1950s was used not only for their detection and characterisation
but also for their quantification.(8-11) Yet at present it is accepted
that this is one of the most widely spread enzymes. (b) a much higher percentage
of sera from AIDS patients and those at risk reacts with proteins of endogenous
retroviruses than the sera of healthy people, 70% versus 3%.(33)
A2. 1. It is true that Montagnier and his colleagues found a
peak of RT activity at the density of 1.16g/ml. However, finding this peak
is not proof that the band was made up of retrovirus particles either pure
or impure. Therefore this evidence cannot be considered that "one
has fulfilled this criterion for purification".
2. In the same issue of Science where Montagnier and his colleagues
published their study Gallo pointed out that "the viral envelope which
is required for infectivity is very fragile, it tends to come off when
the virus buds from infected cells, thus rendering the particles incapable
of infecting new cells". Because of this Gallo claimed that "cell-to-cell
contact may be required for retroviral infection".(34) At present
all "HIV" experts agree that for "HIV" infectivity
gp120 is absolutely necessary. In 1993 Montagnier himself said that for
the "HIV" particles to be infectious they must first bind to
the cellular CD4 receptor and that "The gp120 is responsible for binding
the CD4 receptor".(35-36) However, to date nobody has published EM
of cell-free particles having the dimension of retroviral particles and
also knobs, spikes, that is gp120, not even Hans Gelderblom and his colleagues
from the Koch Institute in Berlin who have conducted the most detailed
electron microscopy studies of the particles present in culture/cocultures
containing tissues derived from AIDS patients. In one of their latest publications
where this matter is discussed they estimate that immediately after being
released, "HIV particles" possess an average of 0.5 knobs per
particle but also pointed out that "it was possible that structures
resembling knobs might be observed even when there was no gp120 present,
i.e., false positives".(37)
This means that neither Montagnier and his colleagues nor anybody else
subsequently could infect the cultures with cells from healthy donors,
umbilical cord lymphocytes or any other cultures with the "purified
HIV" or, even the cell-free fluids (the culture supernatant) even
if the "purified" virus contained nothing else but particles.
In other words, it is impossible for Montagnier and his colleagues to have
had any infectivity even "a little" with either the culture supernatant
or the "purified labelled virus". For the same reason the "second
strain" could not be contaminated by "the first". Furthermore,
since Montagnier et al provided Gallo with cell-free supernatants,
it would have been impossible for the Gallo cultures to be contaminated
with BRU, LAI or a mixture.
3. Montagnier's virus did not come "from an asymptomatic patient"
but a patient with "lymphadenopathy and asthenia". Neither in
their study nor even today, after nearly fifteen years of "HIV",
is there proof for the existence of a human retrovirus which has the ability
to "kill cells". The study which at present is most often quoted
as proving "HIV" kills T4 cells, considered to be the "hallmark"
of AIDS, was published in 1984 by Montagnier and his colleagues. They cultured
CD4+ (T4) cells from a haemophilic patient who was "an asymptomatic
virus carrier", "in the presence of phytohemagglutinin (PHA)
followed by IL-2". In the culture they detected RT activity and "virus
particles characterised by a small eccentric core". The number of
T4 (CD4+) cells in the culture were measured by counting the number of
cells able to bind a monoclonal antibody claimed specific for the CD4 protein.
The number of cells which were able to do so decreased with time. Discussing
their finding they wrote, "This intriguing phenomenon may be due to
virus-induced modulation at the cell membrane, or by steric hindrance of
the antibody binding site", that is, the decrease is not due to cell
Given their data, the conclusion that the decrease in T4 cells is not
due to cell killing is not surprising. However, their conclusion that the
effect may be induced by the "virus", is surprising. Montagnier
and his colleagues were aware of the experimental evidence which showed
that under certain conditions, (including exposure to PHA, IL-2 and other
oxidising agents) decrease in T4 cells appears in the absence of HIV. In
this type of culture, T-cells lose their CD4 marker and acquire other markers,
including CD8, while the total number of T-cells remains constant.(40-43)
Furthermore, they had evidence that in "infected cells, this phenomenon
cannot be detected unless the culture is stimulated by substances such
as PHA or antigens. (Proteins such as the "non-HIV" proteins
present in the "infected" cultures (39)) Given the above facts
it is even more surprising that Montagnier and his colleagues did not have
controls, that is, cultures of T4 cells originating from patients who were
not at risk of AIDS but who nonetheless were sick and to which they added
PHA and IL-2. Such experiments were reported in 1986 by Gallo and his colleagues.
They presented data on three cell cultures which contained 34% CD4 cells
to begin with: One culture was "infected" and stimulated with
PHA, the other was not infected but was stimulated with PHA and the third
was neither infected nor stimulated. After two days of culture, the proportion
of CD4+ cells in the stimulated-uninfected and stimulated-infected culture
was 30% and 28% respectively, while at 6 days the number was 10% and 3%.
The number of CD4+ cells did not change significantly in the non-infected
By 1991 Montagnier and his colleagues had performed experiments with
uninfected, unstimulated cells when they studied "HIV" induced
apoptosis, which was said (and is still said by many), to be the principle
mechanism by which "HIV" kills cells. They showed that in acutely
"HIV infected" CEM cell cultures in the presence of mycoplasma
removal agent, cell death (apoptosis) is maximum at 6-7 days post infection,
"whereas maximal virus production occurred at Days 10-17", that
is, maximum effect preceded the maximum cause. In chronically "infected"
CEM cells and the monocytic cell line U937, no apoptosis was detected although
"these cells produced continuously infectious virus". In CD4
lymphocytes isolated from a normal donor, stimulated with PHA and "infected
with HIV" in the presence of IL-2, apoptosis becomes detectable 3
days post infection and clearly apparent at 4 days. "Intriguingly,
on the 5th day" apoptosis became detectable in "uninfected",
PHA stimulated cells. They concluded: "These results demonstrate that
HIV infection of peripheral blood mononuclear cells leads to apoptosis,
a mechanism which might occur also in the absence of infection due to mitogen
treatment of these cells".(45) In conclusion, all the presently available
data shows that "HIV infection" in the absence of stimulating
agents neither decrease the T4 cell number, nor induce apoptosis, while
stimulating agents (similar to the those patients at risk of developing
AIDS are exposed) do so in the absence of "HIV". That is, neither
the "HIV", which Montagnier and his colleagues "stumbled"
at the beginning, nor any other "HIV" since then has been shown
to "kill cells".
A3. Retrovirus are not esoteric, nuclear or cosmological notions
whose postulated existence can only be inferred by indirect observations.
They are particles which can be seen, albeit not with the naked eye. Since
Montagnier and his colleagues admit to not seeing particles at the 1.16g/ml
band having the morphology of retrovirus, to claim the presence of a retrovirus
much less a "purified virus" is totally unsubstantiated and defies
belief. The 1.16g/ml band can be likened to a fishing net. The difference
is that the band traps objects according to their density, not their size.
Imagine a fisherman who sees in the ocean many different objects some of
which may be fish. He throws the net, waits, and upon retrieval of the
net performs a thorough examination of its contents and shows that it contains
many sea creatures but nothing that looks like a fish. Yet strange as it
may seem, he claims to have caught a fish. In fact, he claims that the
net has nothing else but pure fish.
A4. Although budding from the cell membrane is the manner in
which retroviral particles appear, this process is not virus specific.
In other words, just because a particle buds and has the morphological
characteristics of retroviral particles does not prove it is a retrovirus.
That this is the case can be illustrated by two facts and by quoting two
of the best known retrovirologists: "Budding virus-like particles"
have been found in non-infected "T-cell lines CEM, H9 and C8166; In
2 lines of EBV transformed B-cell lines; and in cultures of primary human
lymphoid cells from cord blood, which were either PHA stimulated or not
and grown with or without serum and in cord lymphocytes directly after
Ficol separation"(46) (italics ours). Following an extensive,
in vivo study conducted by O'Hara and colleagues from Harvard, "HIV
particles" were found in 18/20 (90%) of patients with enlarged lymph
nodes attributed to AIDS. However, identical particles were also found
in 13/15 (87%) of patients with enlarged lymph nodes not attributed to
AIDS and at no risk for developing AIDS. These data led the authors to
conclude, "The presence of such particles does not, by themselves
indicate infection with HIV".(47)
In 1986 Gallo and his colleagues discussing the "First isolation
of HTLV-III" wrote: "At the time we obtained LAV it was the contention
of several experts in virus morphology that the particles shown in the
electron micrograph published in Science by Barre-Sinoussi et al
was an arena virus...Since we considered the mere detection of virus particles
in cultures from AIDS and ARC patients to be insufficient to confirm scientifically
our hypothesis that such particles were implicated in the aetiology of
the disease, we decided first to obtain specific reagents against the new
virus in order to publish definite results concerning AIDS aetiology".(48)
According to Peter Duesberg the "HIV" "particles and proteins
could reflect non-viral material altogether".(49)
A5. In their study Montagnier and his colleagues wrote: "Electron
microscopy of the infected umbilical cord lymphocytes showed characteristic
immature particles with dense crescent (C-type) budding at the plasma membrane...This
virus is a typical type-C RNA tumor virus". In 1984 Montagnier, Barre-Sinoussi
and Chermann reported that their virus was "morphologically similar
to D particles such as those found in Mason-Pfizer virus or the virus recently
isolated from simian AIDS".(38) (By 1984 researchers from the primate
research centres in the United States claimed the existence of AIDS in
monkeys and that the cause of AIDS was a type-D retrovirus similar to the
Mason-Pfizer virus, a typical type-D retrovirus and suggested that the
monkey AIDS and these retroviruses could be helpful in the study of human
AIDS and "HIV").
In the same year, in yet another publication, Montagnier et al claimed
that the "HIV" particles had "morphology similar to that
of equine infectious anaemia virus (EIAV), and D type particles".
The EIAV and the visna virus are neither type C nor type D retroviruses
but lentiviruses, that is, viruses which have totally different morphology
and said to induce diseases long after infection. (By the time this paper
was published it was realised that patients who had a positive "HIV"
antibody test did not develop AIDS immediately, that is, there was a delay
between the positive test and the appearance of AIDS.) It is most astonishing
that the morphology of one and the same virus is able to change genus from
a typical type-C to a typical type-D particle and then to a completely
different subfamily, namely a typical lentivirus, apparently at will. (The
family Retroviridae is divided in three subfamilies, Oncovirinae, Lentivirinae
and Spumavirinae. Oncovirinae are in turn divided into genus type-B,-C
and -D particles. These findings are analogous to describing a new species
of mammal as human, a gorilla and an orang-utan).
A6. 1. Apart from retroviruses other particles may possess "the
assemblage of properties" (the density, RT, budding and the analogy
with the visna virus). It follows that the detection of particles having
this "assemblage of properties" is not proof that the detected
particles are retroviruses. In fact, Montagnier and his colleagues did
not report the detection of "HIV" particles having this "assembly
of properties". Since Montagnier and his colleagues could not find
particles with the morphological characteristics of retrovirus at the "density"
of 1.16 gm/ml, even after "a Roman effort", it follows that the
evidence for the existence of "HIV" from the density gradient
was not only non-specific but was non-existent. (This fact alone is sufficient
to dismiss any claim of proof for the existence of a retrovirus, no matter
what else they found anywhere including budding particles from the cell
surface, retrovirus-like particles in the culture, RT at the "density"
or proteins at the same density which react with patient sera). 2. It is
true that Montagnier et al reported RT activity at the density of
1.16g/ml but since: (a) Barre-Sinoussi and Chermann accept that cells and
cellular fragments also have RT activity; (b) at the 1.16g/ml band no particles
with the morphological characteristics of retrovirus were seen; (c) at
that density Montagnier et al found cellular fragments, it follows
that the evidence for the existence of "HIV" by detecting RT
activity at that density was not only not specific but non-existent. Given
the facts that: (a) there are significant differences in the nature of
the budding processes between type-C, type-D particles and lentiviruses50
and that in 1983 Montagnier et al reported their retrovirus as type-C
and in 1984 as either type-C or type-D, and even later that year as EIAV;
(b) visna virus and EIAV are lentiviruses, it follows that at least up
mid 1984 Montagnier's et al evidence for the existence of "HIV"
(if "HIV" is a lentivirus) from "pictures of budding"
and the analogy with EIAV and visna virus was not only non specific but
A7. We agree there are endogenous retroviruses (but it is of
interest that up until 1994 "there are no known human endogenous retroviruses"(51)).
These endogenous retroviruses cannot be distinguished from exogenous retroviruses
either morphologically or chemically. Furthermore, evidence exists which
shows that 70% of AIDS patients and those at risk compared with 3% of people
not at risk have antibodies to endogenous retroviruses.(33) Given these
facts and the culture conditions which Montagnier and his colleagues and
all other "HIV" researchers use to detect "HIV" together
with the presently available data on "HIV" and AIDS, it is more
probable that "HIV" (if proven to exist) is an endogenous retrovirus
rather than an exogenous retrovirus.
Part of the data related to the culture conditions can be summarised
as follows: In culture, cells sooner or later start to release endogenous
retrovirus. The appearance of endogenous retrovirus can be accelerated
and the yield increased up to a million fold by stimulating the culture
with mitogens, co-cultivation or by adding to the culture supernatant from
normal, unstimulated cell cultures. Indeed, as far back as 1976 retrovirologists
recognised that "the failure to isolate endogenous viruses from certain
species may reflect the limitation of in vitro cocultivation techniques".(52)
To detect the "assemblage" of the "four characteristics"
of "HIV", Montagnier et al (as well as everybody else) employed
at least two of the above techniques. In fact, both Montagnier and Gallo
admit that not one of the four "characteristics" can be detected
unless the cultures are stimulated. Similarly, part of the data related
to "HIV" and AIDS can be summarised as follows: (a) It is true
that endogenous retroviruses may have no pathological role in AIDS, but
it is also true that to date neither is there such proof for "HIV".(53)
According to Montagnier and Gallo the "hallmark" of immunodeficiency
in AIDS is the decrease in T4 cells, said to be the result of killing of
T4 by "HIV". However Montagnier and his colleagues admit as far
back as 1984 that at least in vitro the observed decrease in T4 cells after
"HIV" infection is not due to cell killing but decreased binding
of the T4 (CD4) antibody to the cells. Two years later the Gallo team's
experiments proved beyond doubt that the decrease in T4 cells (of the CD4
antibody binding) was not due to "HIV" infection but to the PHA
which was present in the "HIV" preparation. As mentioned, at
the beginning of the AIDS era there was ample evidence that treatment of
cell cultures with PHA and other oxidising agents leads to decreased binding
of the CD4 antibody and to increase binding of the CD8 antibody, that is,
a decrease in T4 cells was accompanied by increase in T8 cells, while the
total cell number remained constant. AIDS patients and individuals belonging
to the AIDS risk groups are continuously exposed to strong oxidising agents.
At present it is accepted that in both AIDS patients and those at risk,
the decrease in T4 cells is accompanied by an increase in T8, while the
T4 + T8 cell number remains constant.(53) Also, it is of interest to note
that as far back as 1985 Montagnier wrote: "This syndrome [AIDS] occurs
in a minority of infected persons, who generally have in common a past
of antigenic stimulation and of immune depression before LAV infection"(54),
that is, Montagnier recognised that in the AIDS risk group, immune deficiency
precedes "HIV" infection. In 1984 Montagnier and his colleagues
including Barre-Sinoussi and Chermann stated that "Definite evidence
will require an animal model in which such viruses [LAV, HTLV-III=HIV]
could induce a disease similar to AIDS." Up to today, no such model
exists. Nonetheless, when pursued by the Nobel Laureate Kary Mullis for
even one scientific paper proving the HIV theory of AIDS, Montagnier advised
him "Why don't you quote the work on SIV" (Simian immunodeficiency
(b) Unlike endogenous retroviruses which are transmitted vertically,
"HIV" is said to be transmitted horizontally especially by sexual
intercourse. Indeed at present it is generally accepted that the vast majority
of individuals have been infected via heterosexual contact. According to
Montagnier and Gallo the first study to have proven beyond doubt that "HIV"
is a bidirectionally heterosexually transmitted virus was published in
1985 by Redfield et al. However, in a book published in 1990 entitled
AIDS and Sex, its editors, Bruce Voeller, June Machover Reinisch
and Michael Gottlieb, discussing this cross-sectional study, as well as
other similar studies, wrote: "government researchers published data
indicating that United States armed forces personnel infected with HIV-1
had caught the virus from prostitutes, triggering calls for increasing
campaigns against prostitution. When infected soldiers were interviewed
by nonmilitary researchers whom they trusted, it became clear that nearly
all had been infected through intravenous drug use or homosexual contact,
acts for which they could be expelled from the armed services, which prevented
them from being candid with the original military researchers. In each
of these flawed published studies, researchers, journal editors, and peer
reviewers failed to correct mistakes that should have been recognised".
Nancy Padian from the Department of Epidemiology and Biostatistics,
University of California, and her colleagues, who to date have conducted
the most thorough studies on heterosexual transmission discussing Redfield's
et al study as well as other studies who claimed proof of such transmissions,
wrote in 1991: These "studies may not have adequately controlled for
other confounding nonsexual routes of transmission such as risks associated
with intravenous drug use. At first blush, cases that appear attributed
to heterosexual transmission may, after in-depth interviewing, actually
be linked to other sources of risk...because partner studies are by definition
not random samples, and most reported results are based on retrospective
or cross-sectional analyses, some studies may overselect couples in which
both partners in a couple are infected because such couples may be more
easily identified, thus biasing transmission rates. Furthermore, it is
often difficult to establish the source of infection in such couples. When
few prospective data are available, enrolling monogamous couples in which
the serostatus of the partner is unknown, as was the case for most couples
in this study, is one of the only ways to control for this bias".(56)
Indeed, there is no proof from the prospective studies, few as they are,
that "HIV" is sexually transmitted.(57-58)
In her ten year study, unquestionably the longest and the best study
of its kind, Padian (59) and her colleagues have spared no effort in an
attempt to prove that "HIV" is heterosexually transmitted. There
were two parts in her study, one cross-sectional, the other prospective.
In the former, of 360 female partners of infected male index cases, "The
constant per-contact infectivity for male-to-female transmission was estimated
to be 0.0009". The risk factors for seroconversion were: (i) anal
intercourse. (Montagnier himself showed that a positive antibody test reverts
to negative and a low T4 cell count to normal by stopping anal intercourse,
which means that the positive outcome is not due to a retrovirus;(60) (ii)
having partners who acquired this infection through drug use (Padian herself
says that this means that the women may also be IV users); (iii) the presence
in the female of STDs. (antibodies to their causative agents may cross-react
with the "HIV" proteins;(31) Of 82 negative male partners of
positive female index cases only two seroconverted. They estimated that
the likelihood of female-to-male transmission was 8 times lower than for
male-to-female. Padian herself questioned the validity of these two cases.
For the first one she gave several reasons in 1991, when this case was
reported for the first time. In the second case they mentioned the fact
that "chlamydia was transmitted simultaneously or close to transmission
of HIV is striking", that is, the positive "HIV" antibody
test appeared at the time when he became infected with chalmydia.
In the prospective study, starting in 1990, "We followed 175 HIV-discordant
couples over time, for a total of approximately 282 couple-years of follow-up...The
longest duration of follow-up was 12 visits (6 years). We observed no seroconversions
after entry into the study...At last follow-up, couples were much more
likely to be abstinent or to use condoms constantly ...Nevertheless only
75% reported consistent condom use in the 6 months prior to their final
follow-up visit". Note: Not only seroconversion were reported only
in the cross-sectional study but all the cases were diagnosed before 1990.
However: (i) All the "HIV" experts agree that the specificity
of the test kits used then was inferior to those used at present; (ii)
The WB criteria used to define "infection" then are not sufficient
at present. Even if one accepts Padian et al data from the crossectional
study, they have estimated the risk to a non-infected male of acquiring
"HIV" infection from his infected female partner per contact
is 0.00011 (1/9000). This means that on average, males having sexual intercourse
daily with an infected female partner for sixteen years (that is, 6000
contacts at 365 per year), would score a 50% probability of becoming infected.
If sexual intercourse takes place on average weekly then it would take
one hundred and fifteen years to reach the same probability. Under such
circumstances one must question how "HIV" could become epidemic
as the result of bi-directional heterosexual transmission.
A8. 1. In the Montagnier et al 1983 study, the detection
of nothing else but RT activity in the stimulated cultures of lymphocytes
originating from a gay man was considered proof that he was infected with
a retrovirus. The finding of the same activity in the supernatant of a
co-culture of the same cells with lymphocytes from a healthy blood donor
was considered proof of passing the retrovirus from the gay man's lymphocytes
to the donor's lymphocytes and also for virus isolation. However, passing
an activity (RT) is not the same as passing an object (retrovirus).
Furthermore, since non "HIV" infected lymphocytes as well
as many bacteria and viruses other than retrovirus possess RT activity
(RT activity has been reported in many non-"HIV" infected cell
lines used to isolate HIV such as H9 and CEM and as far back as 1972 in
normal, PHA stimulated lymphocytes), finding RT activity in successive
lymphocyte cultures each of which contains material which originated from
the preceding one, is not proof even for passing RT activity. To illustrate
what Montagnier and his colleagues have done, let us return to the analogy
of the fisherman and his net: Assume the fisherman casts his net and catches
some sea creatures. He leaves a few in the net as bait and then throws
it out again. This time, in addition to sea creatures he catches some fish
as well. He removes the fish, leaves some sea creatures in the net, throws
the net again and this time he catches even more fish. He repeats the procedure
several times and every time he catches more fish. Like Montagnier et
al who remove the cells and re-use the supernatants, the fisherman
removes the fish and re-uses the sea creatures ("the bait").
Clearly the fish caught in the net are not offspring of the "bait".
The purpose of the "bait" is to create the right conditions for
fish to appear in the net. (Indeed, real fisherman spend a lifetime determining
the right conditions). All the fisherman is "passing" is the
means for catching the fish, not the fish themselves. Similarly, Montagnier
et al appear to be "passing" the conditions to generate
RT activity thus generating the illusion of "passing" RT activity.
2. Having a peak of RT activity is not proof for having "replication"
of a retrovirus. Keeping track of RT is not the same thing as keeping "track
of the virus".
3. Let us assume that one has isolated and proven the existence of a
retrovirus in cultures with tissues originating from humans. "The
first question put" by Nature is: 'Is it an endogenous retrovirus?'
Only when one has evidence that it is neither an exogenous nor an endogenous
human retrovirus does the question of "laboratory contamination"
with animal retroviruses arise.
4. What the patient had was antibodies which reacted with a protein
which in sucrose density gradients banded at 1.16g/ml. Since at that density
Montagnier and his colleagues could not find particles with the morphological
characteristics of a retrovirus, the evidence that this protein was retroviral
was non-existent. In fact they had no evidence that the protein was embodied
even in non-retroviral particles, any particles whatsoever present at that
5. If Montagnier and his colleagues somehow knew beforehand that the
protein which banded at 1.16g/ml and reacted with the gay man's serum was
the protein of a retrovirus which was present in his lymphocytes (and not
the lymphocytes of the healthy donor or the umbilical cord), and at the
same time that the antibodies were directed against "his own virus",
why was it necessary to have all these experiments to prove its existence?
A9. Even though they had RT activity, at the density of 1.16g/ml
they had no evidence for the existence of retroviral particles and thus
the activity could not be considered proof for the existence of such particles.
A10. In 1983, Montagnier, Barre-Sinoussi and Chermann and their
colleagues proved the existence of the enzyme reverse transcriptase "using
the ionic conditions described for HTLV-I", that is, "5mM Mg2+"
and "poly(A).oligo-(dT)12-18 as template primer". These conditions
and this template primer may be characteristics for retroviruses but they
are not specific for retroviral RT nor indeed any RT. Even before the AIDS
era it was known that this template-primer, under the conditions used by
Barre-Sinoussi, Montagnier and their colleagues, can be transcribed not
only by RT but by cellular DNA polymerases as well. Suffice to mention
the study entitled: "Characteristics of the RNA dependent DNA polymerase
[RT] of a new human T lymphotropic retrovirus (lymphadenopathy associated
virus)" ("HIV") in which Montagnier, Barre-Sinoussi, Chermann
and their colleagues "characterised" the "HIV" RT.
There they used the same ionic conditions as in 1983 and three template
primers "Activated DNA", poly (A).oligo-(dT)12-18 and poly Cm
.oligo-dG 12-18. They reported that while poly Cm .oligo-dG 12-18, "a
reverse transcriptase specific template primer" was transcribed only
by the "HIV infected" cells, "Activated DNA" and poly
(A).oligo-(dT)12-18 were transcribed by both infected and non-infected
cells.22 In other words, finding RT activity by using the template primer
An.dT12-18 is not even proof for the existence of RT and even less for
the existence of a retroviral RT.
A11. No comment.
A12. No comment.
A13. We agree with Montagnier that when using lymphocyte cultures
infected with exogenous retroviruses such as MT2, MT4 and H9 (HUT-78),
all of which originated from patients with "adult T4-cell leukemia",
said to be caused by HTLV-I, it "is a real soup". However, given
the existence of endogenous retroviruses, when one uses lymphocytes from
normal individuals and umbilical cord lymphocytes, the result is still
"a real soup". Maybe a different soup, but nonetheless still
"a real soup".
A14. We agree that patients with AIDS and those at risk are infected
with a "stack of things". Furthermore, the cultures with tissues
from these patients in addition to these agents may also be infected in
vitro with other agents, such as mycoplasma.
A15. It may be true that sometimes it is easier to detect a particle
with the morphological characteristics of retrovirus in the culture than
in the plasma. However, since the viral "concentrate" is obtained
from the culture supernatant and since by definition a "concentrate"
would have more particles per unit volume than the culture supernatant,
it follows that it should be much easier to see a particle in the concentrate
than in the culture. Since Montagnier and his colleagues "saw nothing
major" in the "concentrate", that is, in the 1.16g/ml band,
then why in their 1983 paper did they state the "concentrate"
not only contained viral particles but "purified" virus? In the
electron microscope picture which Montagnier and his associates including
Charles Dauget published there are buds on the cell surface, some of which
are more pronounced than others. But what is the evidence that they are
virus or they are in the process of becoming a virus?
A16. We agree it could be anything.
A17. We agree that familiarity may sometimes enable one to distinguish
between retroviral-like particles and other viral-like particles using
morphological features. However, there are particles which are NOT viruses
(including retroviruses) that exhibit identical morphological features
as retroviruses. Therefore from morphological considerations both the buds
and cell-free particles cannot be considered to be retroviruses. Furthermore,
cultures of tissues derived from AIDS patients contain a plethora viral-like
particles with diameters ranging from 65-250nM, shapes which are spherical,
angular and tear drop, surfaces with and without spikes, and which contain
cone shaped, bar shaped, centrosymmetric and tubular cores, as well as
double cores and a mixture of cores. Like the several particles of varying
taxonomy deemed the HIV particle, none of these particles have been purified
and characterised and, like HIV, their origin and role must remain conjecture.(9,61-64)
A18. 1. If they did not purify the particles why did they claim
to have done so and continue with the same claim up to this interview?
2. It is true that they reported the peak of RT activity at the density
of 1.16g/ml, that is, at the density in which they claimed to have "purified,
labeled virus". However, how is it possible to claim that the RT activity
"was soundly that of a retrovirus", when they "didn't take
the peak...or it didn't work", that is when at that peak they did
not even find retrovirus-like particles, not to mention retroviruses? To
pass a retrovirus from one culture to another, one must first have proof
for the existence of a retrovirus in the first culture. "Passing"
non-specific phenomena is no proof for passing a retrovirus. Furthermore,
since all the phenomena which Montagnier and his colleagues considered
as proof for the existence of a retrovirus, including RT activity and virus-like
particles, could arise de novo in the cultures, especially under
the culture conditions they used, they cannot claim proof for passing anything.
How did Montagnier and his colleagues know that if they had suitable controls,
the same phenomena would not have occurred in the blood donor's culture
as well as the umbilical lymphocytes even if they were not "infected"
A19. 1. If the stage of purification (isolation) is not necessary,
then why did Montagnier and his colleagues claim to have proven the existence
of "HIV" because they "isolated" it, "purified"
2. Since any piece of DNA can be cloned and amplified, cloning and amplifying
a piece of DNA provides no information whatsoever in regard to its origin,
that is, if it is retroviral or not. Neither is it possible by sequencing
a piece of DNA to say that it is "truly a retrovirus" unless
prior proof exists that these sequences are present in a retroviral particle
and nowhere else. There is nothing specific about the "structure of
retroviruses". If indeed there is a unique "sequence of DNA"
indicating "it is truly a retrovirus" and "all the retroviruses
have a familiar genomic structure with such and such a gene", then
no such proof exists for the "HIV genome".(32). Suffice to mention
that to date no two identical sequences for the "HIV genome"
have been published. One and the same patient may have different "HIV
DNA" sequences. According to researchers from the Pasteur Institute,
"an asymptomatic patient can harbour at least 106 genetically
distinct variants of HIV, and for an AIDS patient the figure is more than
108.(65-66) The genetic differences may reach 40%.(67) (Compare this to
the 1-2% differences between hominid DNAs, some of which code for identical
proteins such as haemoglobin a and b chains of chimpanzees and humans).
The length of the "HIV DNA" has been reported to be between 9-15Kb.
In 1985 the Pasteur researchers reported that "The deduced genetic
structure is unique; it shows, in addition to the retroviral gag,
pol, and env genes, two novel open reading frames we call
Q and F".(68) In 1990 the "HIV" genome was said to consist
of ten genes,(69) in 1996 Montagnier reported that "HIV" possesses
eight genes (70) and, according to Barre-Sinoussi, (71) "HIV"
has nine genes.
A20. 1. For isolation of retroviruses the stage of purification
IS obligatory. One CANNOT ISOLATE retroviruses WITHOUT PURIFYING. By definition,
isolation means "to place apart or alone" (Concise Oxford
Dictionary) and purify means "to clear of foreign elements"
(Concise Oxford Dictionary). Thus, unless the contaminants are removed
from around the "HIV" particles (that is, to purify the "HIV"),
the "HIV" particles are NOT ISOLATED.
2. We agree that to transmit a retrovirus one does not need pure material.
However, to transmit something, one first must know what one is transmitting,
that is, one must have proof for its existence. For retroviruses such evidence
can only be obtained by isolating (purifying) the particles, determining
their physical and chemical properties and proving they are infectious.
A21. Yes, it is impossible to determine the identity of the proteins
including that of RT without isolation. 1. Montagnier and his colleagues,
even after a Roman effort could not find even retrovirus-like particles
at this density thus, from his experience (experimental evidence), there
are zero chances and NOT 999 out of 1000 that RT activity at the density
of 1.15, 1.16 represents a retrovirus in their case.
2. We agree that it could be a retrovirus of different origin. The existence
of endogenous retroviruses, together with the presence in AIDS patients
and those at risk of antibodies which react with their antigens, means
that even if Montagnier et al had proven the existence of a retrovirus,
it would have been impossible to say that the retrovirus originated in
the gay man and not in the donors or umbilical cord lymphocytes.
3. The "molecular biology", the "cloning and sequencing"
of the "HIV" genome has been discussed in detail elsewhere.(32-49)
Suffice to mention here that:
(a) proof for the existence of "HIV" and indeed for its causative
role in AIDS was claimed before any "molecular biology", "cloning
(b) since any piece of nucleic acid can be cloned and sequenced, cloning
and sequencing of a piece of nucleic acid cannot be used to prove the existence
of a retrovirus or of its genome. To the contrary, proof for the existence
of viral nucleic acids (viral RNA and cDNA) can be accepted if and only
if it is shown that the RNA is a unique molecular entity belonging to particles
with morphological, physical and replicative characteristics of retroviral
particles. This can only be done by separating the particles from everything
else, by purifying them. Instead, Montagnier and Gallo used "a real
soup" of cultures and co-cultures (Montagnier's group even purposely
infected the cultures with Epstein-Barr virus). The supernatant from these
cultures was banded in sucrose density gradients. From all the RNA (and
DNA) which banded at 1.16g/ml they arbitrarily chose some RNA using totally
non-retroviral specific criteria and called it "HIV RNA", without
any proof that the band contained even retroviral like particles;(32)
(c) the first, absolutely necessary step in proving that the "HIV
RNA", retroviral or not, originated from the lymphocytes of "HIV"
infected individuals, is to perform hybridisation experiments using fresh,
uncultured lymphocytes and the "HIV DNA" (obtained by reverse
transcription of the "HIV RNA"), as a probe. It is hard to understand
why Montagnier and his colleagues did not report such experiments. Gallo's
group did and the results were negative. In 1994 Gallo was quoted in this
magazine as saying: "We have never found HIV DNA in the tumour cells
of KS...In fact we have never found HIV DNA in T-cells".(72) At present
there is no study proving the existence of even one single copy of the
"full-length HIV genome" in the fresh T-cells even of a single
AIDS patient or a patient at risk of AIDS; (d) Currently the number of
"HIV" particles in the plasma is quantified by measuring "HIV
RNA", the viral load which is reported to be "15 x 103
to 554 x 103 virions per ml".(73) Many studies claim proof
that the "viral load", the "HIV RNA", can be decreased
to undetectable levels by the use of both RT and protease inhibitors. However,
since: (i) it is accepted that the "HIV RNA" is a transcript
of the "HIV DNA"; (ii) by their nature neither the RT nor the
protease inhibitors have any effect on DNA transcription, they only inhibit
infection of new cells, that is, the decrease in "HIV RNA" is
a consequence of the decrease in "HIV DNA"; one would expect
that the effect of these drugs would be determined by measuring the level
of "HIV DNA". Yet hardly any such studies have been published.
The very few which exist show that neither RT nor protease inhibitors have
any effect on "HIV DNA",(74-76) which means that no relationship
exists between "HIV RNA" and "HIV DNA".
4. In 1984 Montagnier and his colleagues reported that "preincubation
of T4+ lymphocytes with three different monoclonal antibodies directed
at the T4 glycoprotein blocked cell infection by LAV", that is, blocked
the detection of RT activity in T4 cells "infected" with "HIV".
They concluded their "findings strongly suggest that the T4 glycoprotein
is at least associated with all or part of the receptor for LAV".(38).
However, blocking a non-specific "HIV" phenomena, namely RT activity,
cannot be considered proof of blocking "HIV" infection or association
of "HIV" with T4 cells.
A22. We agree that "analysis of the proteins of the virus
demands mass production and purification. It is necessary to do that".
In this respect they have not just partially failed, but TOTALLY FAILED.
If the "analysis of the proteins of the virus demands mass production
and purification", so does the analysis of "nucleic acids, cloning
etc". If one fails to purify the virus then it fails:
(a) to characterise the viral antigens and to obtain a gold standard
for the antigen-antibody reaction, that is, one cannot use antibody tests
to define infection with the retrovirus;
(b) to obtain and characterise the retroviral nucleic acids, RNA (cDNA)
and thus probes and primers for hybridisation and PCR studies, that is,
one cannot use molecular tests to define retroviral infection. That this
is the case is accepted by Donald Francis, a researcher who with Gallo,
played a significant role in developing the theory that AIDS is caused
by a retrovirus. In 1983, Francis, then the chief collaborator of the AIDS
Laboratory Activities, US Centers for Disease Control and former chief
of the WHO smallpox program, speculated on a viral cause for AIDS: "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"(77) (italics
A23. It is impossible to characterise two viral unknowns, namely
its proteins and the antibodies directed against them, by the formation
of an antibody/antigen complex let alone characterise the "virus".
By what means did Montagnier know that somebody had antibodies against
the proteins of the virus and that the proteins with which the antibodies
react were viral? It is a scientific impossibility to know that somebody
has antibodies to a virus and at the same time, the 1.16g/ml band contains
proteins of the same virus before one has proven its existence.
A24. 1. It is true that Montagnier had controls but the controls
were not suitable. Montagnier and his colleagues reacted the proteins which
banded at 1.16g/ml with the sera from two gay patients with lymphadenopathy.
The patients with AIDS and those at risk were already known to have a plethora
of antibodies, all with potential for cross-reactivity. Therefore, one
would have expected that Montagnier et al to have used as controls
sick individuals who did not have AIDS or pre-AIDS and who were not at
risk for AIDS but who also had a plethora of antibodies, all with potential
for cross-reactivity. Instead their controls consisted of two blood donors
whose state of good health is characterised by lower levels of antibodies.
2. Montagnier et al did not obtain proof for "a specific
reaction". The sera from the patients and the donors were reacted
with both the "purified virus", that is the 1.16g/ml band, and
extracts from the "infected" cells. In their published strips,
with "purified virus", it is not possible to distinguish any
reacting proteins with any of the sera. In the text they state: "When
purified, labelled virus [the 1.16g/ml band] from patient 1 was analysed...three
major proteins could be seen; the p25 protein and proteins with molecular
weight of 80.000 and 45.000". No such reactions were reported with
the donors' sera. In the published strips with extracts from the "infected
cells", it is obvious that many proteins reacted with both the patients'
and the healthy blood donors' sera. One year later Montagnier and his colleagues
confirmed that "sera from some AIDS patients bound a lot of cellular
proteins...This banding was apparent in the RIPA and only sera which specifically
precipitated the p25 were regarded as positive". In other words, for
some unknown reason, they concluded that from all the reacting proteins
only p24 (their p25) was retroviral and from all the antibodies only the
one which reacted with p24 was directed against the retrovirus. Even if
one considers the reaction between the p24 which bands at 1.16g/ml and
the antibody present in the sera specific, that is, not due to cross-reactivity,
from such a reaction it is impossible to draw the conclusion that p24 is
retroviral protein and the antibody is elicited as a result of infection
with this retrovirus. Indeed given the fact that Montagnier et al could
not even detect retrovirus-like particles at 1.16g/ml, their conclusions
regarding p24 and the antibody reacting with it completely defies scientific
A25. 1. No antibodies, not even monoclonal antibodies are "very
specific" or even specific.(78-84) Indeed, there are instances where
"cross-reactive antigen binds with higher affinity than the homologous
antigen itself...The most obvious fact about cross-reactions of monoclonal
antibodies is that they are characteristic of all molecules and cannot
be removed by absorption without removing all reactivity...Even antigens
that differ for most of their structure can share one determinant, and
a monoclonal antibody recognising this site would then give a 100% cross-reaction.
An example is the reaction of autoantibodies in lupus with both DNA and
However, "It should be emphasised that sharing a "determinant"
does not mean that the antigens contain identical chemical structures,
but rather that they bear a chemical resemblance that may not be well understood,
for example, a distribution of surface charges".(80) It is of importance
to note that "HIV" experts concede "cross-reactivity"
as the reason for "indeterminate" antibody reactivity seen in
the "HIV" Western blot, as well as, for example, reactivity between
monoclonal antibodies to the "HIV" p18 protein and dendritic
cells in the lymphatic tissues of a variety of patients with a number of
non-AIDS related diseases (85) and normal tissues taken from "non-HIV"
infected individuals.(86) For one to be convinced that all "antibodies
[including monoclonal] are polyspecific, that is, they are able to react
with various dissimilar antigens such as: proteins, nucleic acids and haptens",
"they are able to react with more than to self or non-self antigens,
often without any apparent antigenic similarities", all one has to
do is to read the scientific publications of the researchers from the Pasteur
Institute such as Stratis Avrameas.(83-87)
2. It cannot be concluded that a protein which bands at 1.16g/ml is
viral merely because it reacts with an antibody present in the patient's
sera even if somehow one knows that the antibodies present in the sera
are monoclonal. Let us assume an ideal situation where: (a) all the antibodies
present in the patients' sera are monoclonal and "very specific";
(b) the 1.16g/ml band contains in addition to the many unembodied and microvesicles,
embodied proteins of cellular origin and maybe of bacterial, fungal and
viral origin (constituents of the many infectious agents, other than retroviruses,
present in the culture and the patients) and, as shown in a 1997 France/German
study, a number of retrovirus-like particles. Even in this ideal situation,
it is NOT POSSIBLE TO CLAIM that just because a protein such as p24, p41,
or others is found in this band and reacts with the sera, the protein is
a constituent of the retrovirus-like particles.
3. The reality is that: (a) all AIDS patients and those at risk have
a plethora of antibodies including auto-antibodies. The auto-antibodies
include anti-lymphocyte, and as Montagnier and his colleagues have shown88
anti-actin and anti-myosin antibodies, that is antibodies to the two ubiquitous
cellular proteins actin and myosin. (b) all the antibodies present in the
sera have the potential of cross-reactivity. (c) the proteins from the
supernatant of non-infected lymphocytes which in sucrose density gradients
band at 1.16g/ml, the mock virus, include proteins having the same molecular
weights as the "HIV" proteins;89 (d) animals inoculated with
the mock virus develop antibodies which react with the "SIV"
proteins, a "retrovirus" whose proteins share the same molecular
weights as the "HIV" proteins and is said to be the closest relative
of "HIV";90 (e) AIDS patients and those at risk are repeatedly
subjected to allogenic stimuli including allogenic lymphocytes; (f) up
till 1997 no evidence existed showing that the 1.16g/ml band contained
even retrovirus-like particles. Given this reality, to claim that just
because a protein bands at 1.16g/ml and reacts with antibodies present
in the patients' sera is at best no different than the following: (i) A
researcher has two bowls, one of them contains a mixture of raw eggs, some
known and maybe some unknown, and maybe some milk originating from several
animals. The other contains several acids. Again some known and maybe some
unknown. Once the contents of the two bowls are mixed he gets a precipitate.
He claims that the precipitation proves the existence in the bowl of milk
from a previously unknown animal and an unknown acid and that the reaction
is between the unknown acid and a protein of the previously unknown milk.
(ii) This claim is scientifically impossible since any protein in the eggs
could have reacted with any acid to produce the observed precipitate.
Thus, given the reality as outlined in (a) to (f) above, it is completely
unscientific to claim that the reaction between proteins which band at
1.16g/ml and react with antibodies present in the patients' sera is proof
of the existence of "HIV". To claim that the reaction between
proteins which band at 1.16g/ml (in the absence of evidence that the band
contains even retrovirus-like particles) with antibodies present in the
sera indicates not only the band contains retroviral proteins, but proteins
of a new retrovirus, is no different than the following: A fisherman who
has sea creatures but no fish in a net. He throws some animals into the
net. The fisherman observes that the animals eat some proteins present
in the net and claims that the proteins were not just fish proteins but
the proteins of a completely new fish, a fish which nobody has seen before,
a golden fish.
A26. 1. It is not possible for both Montagnier and Gallo to be
"reasonably right". Both Gallo and Montagnier reacted the 1.16g/ml
band with patient sera. Irrespective of the method used to detect the reaction
(RIPA or WB), or the number of reactions performed, they should have found
the same reacting proteins.
2. In their 1983 study, Montagnier and his colleagues found three proteins,
p25, p45 and p80. Regarding p45 they wrote: "The 45K protein may be
due to contamination of the virus by cellular actin which was present in
immunoprecipitates of all the cell extracts". In a study published
in 1984 they had "a prominent p25, a p18, a low molecular weight protein
at the bottom of the gel (p12), and three proteins of high molecular weight
(43.000, 53.000, 68.000). The band at 43.000 may include a component of
cellular origin, since it was also found in a similar preparation made
from the control uninfected cells".
3. Since both patients' and healthy blood donors' sera repeatedly reacted
with the p45/p43 protein from both infected and in-infected cells one would
have expected Gallo to also detect this protein. However neither Gallo
nor anybody else since then reported such a band irrespective of the method
used to detect the antigen/antibody reaction. The discrepancy can be resolved
if one takes into consideration the fact that the migration of proteins
in an electrophoretic strip, in addition to the molecular weight, may be
also influenced by other factors, for example the charge carried by the
protein. Thus one and the same protein may appear to have slightly different
molecular weight when detected by either RIPA or the WB. For example, both
p25 detected by Montagnier and the p24 detected by Gallo at present are
considered to be both one and the same "HIV" protein p24.
4. The molecular weight of actin is neither 45,000 nor 43,000 but 41,000.
At present there is ample evidence that the 1.16g/ml band the "Pure
HIV" contains cellular actin (91-94) and as has been already mentioned
Montagnier himself showed that the sera of AIDS patients and those at risk
contain antibodies which react with actin. In other words when the 1.16g/ml
band is reacted with patients' sera, irrespective of the presence of "HIV",
a p41 (p45/43) band must be present, and represent cellular actin. (If
Montagnier now believes that p41 is an "HIV" protein, why does
he persist in excluding this band from his criteria for a positive Western
A27. The p24 protein is not sufficient for diagnosing "HIV"
infection because it is not specific. Indeed, no other "HIV"
protein not even p41 (p45/43) has been reported to react more often with
sera from healthy (at no risk of AIDS) individuals. Neither has a monoclonal
antibody to any of the other "HIV" proteins been found to react
more often with proteins present in non "infected" cultures or
sera from individuals at no risk of AIDS. According to Montagnier because:
(a) "these are cellular proteins that one meets everywhere - there
is a non-specific background noise"; (b) one such protein, having
a molecular weight of 45/43, is actin; (c) this protein reacted with sera
from individuals at no risk of AIDS; the p45/43 represents a cellular and
not a viral protein. However, since: (i) myosin is as ubiqitous as actin.
(ii) myosin has a light chain with a molecular weight of 24,000. (iii)
the cytoskeletal proteins (of which actin and myosin are the most abundant)
have been reported in "pure HIV".(91-94) Indeed, myosin and actin
are said to play a crucial in budding and release of the "HIV"
particles.(91) (iv) Montagnier has shown that patients with AIDS and at
risk of AIDS have anti-myosin antibodies. Why should not one consider the
p24 band as representing myosin?
A28. We agree that no protein is sufficient to diagnose "HIV"
infection. The problem then, as it is today, was not "to know whether
it was an HTLV or not", but whether it was retroviral or not. Not
everything which is not HTLV is retroviral.
A29. 1. To date there is no proof that any of the proteins which
band at 1.16g/ml are "HIV" proteins. The only reason that 20%
of the proteins which band at 1.16g/ml are said to be "HIV" is
that this fraction of proteins is found to react with different AIDS patient's
sera at some time or another.
2. We agree that with the technique used by Montagnier's group, one
cannot prove which proteins (or nucleic acids) are cellular and which are
3. We agree. The only way one can prove the existence of the viral protein
(nucleic acids) is "to purify the virus to the maximum", that
is, to obtain density gradients which contain only particles with the morphological
characteristics of retrovirus and nothing else. This has never been done
to prove the existence of the "HIV" proteins and nucleic acids.
4. If one always "stumbles on the same proteins" in successive
gradients, this is no proof that these proteins are viral and the ones
which disappear are cellular.
A30. 1. No matter how many times the banding is repeated, if
one starts with no retrovirus-like particles one will end with no such
particles. Some times, by successive bandings, one may be able to eliminate
non-retroviral components and obtain a band which contains nothing else
but particles with morphological characteristics of retroviruses. However,
to be able to do so, even after the first banding, one must begin with
a relatively high proportion of retrovirus-like particles.
2. Once again, the origin of the proteins cannot be determined by molecular
analysis, that is, by sequencing the proteins.
3. We agree that if the proteins of a retrovirus are coded by its genome,
as is generally accepted, then it may be possible to characterise the retroviral
proteins by its genome. However, to do this one must first prove that the
RNA (cDNA) is a constituent of a retroviral particle. This has not been
done for the "HIV" genome. In fact even today there is no proof
that the "HIV" RNA is a constituent of a particle, any particle
viral or non viral.
4. To date there is no proof of a relationship between the sequences
in the "HIV" RNA (DNA) and the sequences in the proteins "observed
with immunoprecipitation or with gel electrophorosis". In fact there
is no relationship even between the size of the proteins coded by the "HIV"
genes and the size of the proteins "observed with immunoprecipitation
or with gel electrophorosis". For example, in 1987 Gallo and his associates
performed a "computer-assisted analysis" of the "amino acid
sequences of the envelope protein complexes derived from the nucleic acid
sequences of seven AIDS virus isolates", and concluded that "gp41
should be about 52 to 54 daltons by calculation".(96)
5. One of the many puzzling aspects of "HIV" is the following:
(a) "HIV" experts agree that no two "HIVs" have the
same genomic sequences and the difference may be as high as 40%;(67) (b)
They also admit that the vast majority (99.9%) of the "HIV" genomes
are defective, that is, either part of a gene(s) or whole gene(s) are missing;
How then is it possible: (i) to measure the viral burden ("HIV DNA")
and the viral load ("HIV RNA") by using one and the same hybridisation
probes and PCR primers? (ii) to perform antibody tests by using kits containing
the same antigens for all the different "HIVs"?
6. Indeed, the history as to how "HIV" researchers have tried
to prove the existence of p120 and how they ultimately agreed on its existence
is very interesting and informative.32 However, given the fact that the
p120 protein is said to be present only in the knobs, no cell-free "HIV"
particles possessing knobs have been reported so far. It follows neither
the particles in the culture supernatant nor the "pure" virus
will have gp120. In other words, it is impossible for either the RIPA or
the WB strips to have a "HIV" protein of molecular weight 120,000.
A31. No such proof can be found in the published literature.
A32. 1. Prior to March 1997 no group of "HIV" researchers
had published even a single electron micrograph of material banding at
the density of 1.16gm/ml in a sucrose density gradient. The first EMs of
material banded in sucrose density gradients appeared in 1997 in two publications,
one Franco/German and the other from the US National Cancer Institute (NCI).(89)
The Franco/German EMs are from the 1.16 gm/ml sucrose density gradient
whereas it is not possible to tell from which density the NCI data originate.
The data from both studies reveal that the vast majority of the material
is "non-viral", "mock" virus, cellular "microvesicles",
that is, the banded material is virtually all cellular. These particles,
like the retroviral particles, contain nucleic acids in addition to proteins
but they are not as condensed.
2. The EM micrographs in both studies also contain a small minority
of particles which have morphologies more closely resembling retroviral
particles than the "mock" particles. Both groups claim the fewer
particles are "HIV".
3. In the NCI study no reasons are given for the claim that these particles
are "HIV". The authors of the Franco/German study claim that
the particles are "HIV" because they have: (a) "diameters
of about 110nm;" (b) a "dense cone-shaped core"; (c) "lateral
bodies"; and because no such particles were seen in the banded material
from the non-"infected" control cells. However, according to
well known retroviral researchers such as Bader and Frank, one type of
"oncoviral particle" can change to another, and immature cores
to "mature", merely by changing the extracellular conditions.(11-97)
However the culture conditions in the "infected" and non-infected
cells were not the same. A diameter of 100-120nm and surface knobs are
two morphological characteristics shared by all retroviruses. None of the
particles appear to have knobs and none has a diameter of less than 120nm.
Averaging the major and minor diameters of the particles indicated and
said to represent "HIV" and, assuming all particles are spherical,
shows that in the Franco/German study the particles are 1.14 times larger
than bona fide retroviral particles and the NCI particles are 1.96 times
larger. These data translate into volumes 50% and 750% greater respectively.
Since density is the ratio of mass to volume these particles must therefore
have correspondingly higher masses. Given the maximum diameter of retroviral
particles and the fact that such particles contain a fixed mass of RNA
and protein, it appears untenable that the particles which both groups
regard as "HIV" are the same particle or are retroviral particles.
The only other explanation for these data is that the electron micrographs
are not from the 1.16gm/ml band or the banding has not been to equilibrium
in which case one must redefine the buoyant density of retroviruses.
The "HIV" particles are said to have a cone shaped viral core,
with dense lateral bodies at either side of the core. No such feature can
be seen in the EM published in these two studies. Thus, by definition,
the particles cannot even be said to be retrovirus-like.
Taking into consideration that in both studies the control "non-infected"
cultures were of H9 cells and the fact that Gallo as far back as 1983 claimed
that these cells are infected with HTLV-I, the non-reporting of virus-like
particles in the banded material from these cultures is an enigma.
A33. Pictures of the 1.16g/ml are of profoundly significant interest.
How else can it be known that there are retrovirus-like particles there,
especially since even Montagnier admits that other things may band there.
For any scientist who claims proof for isolation, purification of a retrovirus
using sucrose density gradient banding, it is vital and absolutely necessary
to obtain electron micrographs of the 1.16g/ml band showing nothing else
but retrovirus-like particles.
A34. If this is the case why is such data not available in the
A35. In one of their 1984 papers (22) Montagnier and his colleagues
wrote, "Several characteristics indicate that LAV or LAV related viruses
belong to the retroviruses family. Budding particles at the plasma membrane
have been observed in electron microscopy. The density of the virus in
sucrose gradient is 1.16 and a Mg2+ dependent reverse transcriptase activity
has been found to be associated with RNA containing virions". However,
in this interview Montagnier admits: (a) "We published images of budding
which are characteristic of retroviruses. Having said that, on the morphology
alone one could not say it was truly a retrovirus... With the first budding
pictures it could be a type C virus. One cannot distinguish... No... well,
after all, yes... it could be another budding virus". (b) at the sucrose
density of 1.16 gm/ml not only did Montagnier and his colleagues not see
a retrovirus particle, they repeatedly said they did not see retroviral-like
particles; (c) although at the sucrose density of 1.16 gm/ml they detected
reverse transcription of the template primer An.dT12-18 in the presence
of Mg2+, they had no particles and thus no evidence for "reverse transcriptase
activity found to be associated with RNA containing virions".
Furthermore, in this study (22), they showed that DNA polymerases beta
and gamma and of non-infected cells reverse transcribe An.dT (12-18) in
the presence of Mg2+. Thus, Montagnier's own conditions and data do not
prove his claim that what he has "seen" and "encountered"
is a retrovirus. If "HIV" "exists", and it is "clear"
to Montagnier that he has "seen it" and "encountered it",
where is his proof? *
Eleni Papadopulos-Eleopulos (1) Valendar F.Turner (2) John M. Papadimitriou (3)
Barry Page (1) & David Causer (1)
(1) Department of Medical Physics, (2) Department of Emergency
Medicine, Royal Perth Hospital, Perth, Western Australia; (3) Department
of Pathology, University of Western Australia.
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