Evidence-based scientific responses to Jeanne
Bergman re House of Numbers
Eleni Papadopulos-Eleopulos
Valendar F. Turner
John M Papadimitriou
David
Causer
December
2009
INTRODUCTION
We agree with
Bergman that scientific answers must be based on “evidence-based science”. In science there are no fake questions – only
fake answers. Bergman’s “answers” to the
questions raised in House of Numbers
consist of proclamations without one iota of “evidence-based science” to back
her up. Hence, by her own definition,
her answers are fake.
We remind Bergman:
1. Scientists are obliged to deny nothing and question everything.
The “legitimate scientist” and Nobel laureate Jacques Monod: “In science, self-satisfaction is death. Personal self-satisfaction is the death of the scientist. Collective self-satisfaction is the death of the research. It is restlessness, anxiety, dissatisfaction, agony of mind that nourish science”.
Perter Abelard: The first key to wisdom is assiduous and
frequent questioning…For by doubting we come to inquiry, and by inquiry we
arrive at truth”.
Neither is there “incontrovertible
evidence” for anything in science.
Richard Feynmann: “Scientific knowledge is a body of statements of
varying degrees of certainty – some most unsure, some nearly sure, none absolutely certain”.
2.
Scientists respond when challenged.
Howard Temin, the
father of modern retrovirology: “when
an experiment is challenged no matter who it is challenged by, it’s your
responsibility to check. That is an
ironclad rule of science, that when you publish something you are responsible
for it…even the most senior professor, if challenged by the lowliest technician
or graduate student, is required to treat them seriously and consider their
criticisms. It is one of the most fundamental
aspects of science” (emphasis in original).1
HIV scientists do not respond
to challenges. In fact, according to the
rules at AIDSTruth, “We will not engage
in any public or private debate with AIDS denialists or respond to requests
from journalists who overtly support AIDS denialist causes”. Apparently these “legitimate scientists”
cannot stick to their own rules.
For over a quarter
of a century the Perth Group has denied nothing but questioned every aspect of
the HIV theory of AIDS. In our scientific publications, including
peer-reviewed publications, we have raised many questions but virtually no HIV
expert has responded. In order to draw
attention to the problematic nature of the HIV theory of AIDS we published many
papers with questions included in the text or titles. These include the following:
1. Papadopulos-Eleopulos E. Reappraisal of AIDS: Is
the oxidation caused by the risk factors the primary cause? Med Hypotheses 1988;25:151-162. http://www.theperthgroup.com/SCIPAPERS/reappraisalofaids.html
2.
Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Is a positive Western blot proof of HIV infection? Biotechnology
1993;11:696-707. http://www.theperthgroup.com/SCIPAPERS/biotek8.html
3. Papadopulos-Eleopulos E, Turner VF, Papadimitriou
JM, Causer D. The Isolation of HIV: Has it really been achieved? Continuum 1996;4:1s-24s. http://www.theperthgroup.com/CONTINUUM/pgvsduesbergreward.html
4.
Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Page BA. HIV antibody tests and viral load – more unanswered
questions and a further plea for clarification. Curr Med Res Opinion
1998;14:185-6. http://www.theperthgroup.com/SCIPAPERS/furtherplea.html
5. Papadopulos-Eleopulos E, Turner VF, Papadimitriou
JM, Stewart G, Causer D. HIV antibodies: further questions and a plea for
clarification. Curr Med Res Opinion 1997;13:627-34. http://www.theperthgroup.com/SCIPAPERS/epcurmedres97.html
6. Papadopulos-Eleopulos E, Page BA, Causer D, Turner
VF, Papadimitriou JM, Alfonso H. Would Montagnier please clarify whether HIV or
oxidation by the risk factors is the primary cause of AIDS? Med Hypotheses 2006;67:666-8. http://theperthgroup.com/SCIPAPERS/PGMontOSMH2006.pdf
7.
Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Page BA, Causer D,
Alfonso H et al. A critique of the Montagnier
evidence for the HIV/AIDS hypothesis. Med Hypotheses 2004;63:597-601. http://www.theperthgroup.com/SCIPAPERS/MHMONT.pdf
8. Turner VF. Reducing agents and AIDS – Why are we
waiting? Med J Aust 1990;153:502. http://www.theperthgroup.com/SCIPAPERS/RedAgent.pdf
9. Turner VF. The HIV Western blot. Med J Aust
1994;160:807-808. http://www.theperthgroup.com/SCIPAPERS/VFTDax.pdf
Still no response.
Apart from publications we also put questions
directly to many HIV/AIDS experts, including John Moore. Almost without exception none have
responded. In 2006 we emailed John Moore
with several questions and a request for a dialogue. He wrote back:
Turner,
You have gone through 21 drafts and a considerable amount of effort to say
absolutely nothing that is of any conceivable interest to me. I’m glad you
wasted your time though, as communicating with me (or
trying to) is harmless, compared to the damage you AIDS denialists do to
innocent people you attempt to confuse and thereby cause to be harmed. So,
continue to knock yourself out, so to speak. All you will
receive from me is my continued contempt, and derision.
John Moore.
(It was not 21 drafts. It was 2 drafts. John Moore was not familiar with the way MS
Word saves files attached to emails that are returned with the same file name. Furthermore, we are not AIDS denialists).
You are confusing me for
someone who is interested in what you have to say, and you are confusing
yourself for someone who merits a more detailed response. Kindly correct
yourself of those delusional tendencies. I despise you and your fellow AIDS
denialists, and I regard your level of “scientific analysis” as pitiful and
laughable.
One expert, Luc Montagnier, did not respond although
he promised to do so on more than one occasion.
At the beginning of the AIDS era one of us (EPE)
wrote a paper entitled Reappraisal of
AIDS: Is the oxidation caused by the risk factors the primary cause? After two rejections by Nature in 1986 it was published in 1988 in Medical Hypotheses. 2 In 1991 a few
of our papers including our Medical
Hypotheses paper was sent to Montagnier who promised he would study it and
come back to us with his comments. http://theperthgroup.com/VARIOUS/MontagniertoEPE1Oct1991.jpg
He did not come back to us.
In 1990 the journal Research in
Immunology, a Pasteur Institute publication, opened its “columns to
Dr P Duesberg and Dr L Montagnier, who have agreed to discuss the matter of
whether HIV is the causative agent of AIDS” and “invited other contributions on
this topic”. In our contribution
entitled “Oxidative Stress, HIV and AIDS” we wrote “As long ago as 1983, one of
us (E.P.-E.) proposed that oxidative mechanisms are of critical significance in
the genesis of AIDS (acquired immune deficiency syndrome). A prediction of this hypothesis was that the
mechanisms responsible for AIDS could be reversed by the administration of
reducing agents, especially those containing sulphydryl groups (SH
groups). The discovery of HIV resulted
in a broadening of this hypothesis in that it considered oxidative stress as a
principal mechanism in both the development of AIDS and expression of HIV”.3
In the same contribution as well as earlier4 we
presented evidence that cellular activation is an oxidative phenomenon”. Montagnier may have agreed to discuss matter
but failed to do so, either with us or Peter Duesberg.
However, to our surprise, nine years after the
publication of the oxidative theory, six years after he received our papers and
five after our Research in Immunology publication, Montagnier and his
colleagues published a paper in which they wrote “In AIDS pathogenesis,
oxidative stress is proposed as a metabolic alteration that favours
disease progression by inducing both viral replication and apoptotic
death...Indeed, the evidence that oxidative stress induces, while antioxidants
inhibit, HIV replication and apoptosis suggests the use of these molecules as
an antiretroviral therapy to reduce cell death in AIDS patients”5 (italics ours).
When we read Montagnier’s book “Virus”,
published in 2000,6 and his presentation to the European Parliament in
2003,7 we published a letter in Medical Hypotheses
entitled “Would Montagnier please clarify whether HIV or oxidation by the risk
factors is the primary cause of AIDS?”.8 Montagnier
never responded.
SPECIFIC
RESPONSES
Bergman: But Leung is an HIV denialist—he has said he is “neutral” on the issue of
HIV/AIDS, which means he rejects the evidence-based science that has
conclusively proved the existence of HIV and its causative role in AIDS, a
fatal disease syndrome.
Neutral does not mean non-acceptance. A journalist, making a film, presenting points of view, is not there to proselytise. He makes no judgment either way because his personal views are neither the subject nor the issue. His job is to present all sides, ask questions and make the viewer think.
All HIV experts including Robert Gallo and the Nobel committee accept that
the “evidence-based science” for the existence of HIV was published by
Montagnier et al in an historical
paper published in 1983 entitled Isolation
of a T-lymphotropic retrovirus from a patient at risk for acquired immune
deficiency syndrome (AIDS).
In keeping with the title of
Montagnier’s seminal paper, all “HIV” experts, including Montagnier, claim the
existence of “HIV” has been proven by a procedure known as “virus isolation”. Yet few “scientists, doctors and advocates”,
much less laypersons, are aware that in virology the word “isolation” is devoid
of its everyday meaning. The Perth Group
has polled clinicians, non-scientist professionals and laypersons asking each what
he or she understands by the title of Montagnier’s paper. As one would expect all give a description of
an object obtained on its own separate from all other objects. Furthermore, it is a given that only objects
that exist can be isolated. In other
words, “isolation” = existence. Fait accompli.
“Isolation”, which is
derived from the Latin “insulatis”, means
“made into an island”. Either wittingly
or unwittingly, but at great convenience, this word has been misappropriated by
virologists to the point where it almost qualifies as spin. Ex cathedra
pronouncements, announcements or statements that “HIV” has been “isolated” are
accepted by virtually everyone as proof of the existence of a unique retrovirus
without raising a single question of veracity.
However, when the rare individual does probe the oratory, the “HIV”
experts are loath to elucidate. This is well
exemplified in the House of Numbers by
Leung’s interviews with David Baltimore and Robin Weiss:
“I [Leung] asked Nobel
Laureate Dr. David Baltimore and Dr. Robin Weiss how they would isolate and
photograph this elusive virus”.
According to Bergman, at the
time of this interview
Nonetheless, whatever it is virologists claim is “isolation” in terms of proving the existence of a virus, they, like everyone else, including Montagnier and Gallo (see below), accept that, in order to determine the biochemical constituents of a virus, the virus particles must first be isolated=separated=purified from the cells in which it is cultured. Why? Because viruses and cells are made of the same stuff. Distinguishing between viral proteins and nucleic acids and cellular proteins and nucleic acids is an absolute requirement in order to establish what is viral and what is cellular. Especially given the use of viral proteins and nucleic acids as reagents for diagnostic tests. If a scientist does not know which proteins and nucleic acids are viral and which are cellular he will never know what he is testing for. In the 26 years since the “discovery” of “HIV” no scientist has presented evidence for this elementary step—the purification of “HIV”. To the contrary, all the evidence proves none of the taxonomically distinct particles all said to be one and the same retrovirus, “HIV”, have been purified.12 13 Hence there is no “evidence-based science” whatsoever for the existence of “HIV” proteins or nucleic acids and thus “HIV” and “HIV” tests.
What follows is a summary of Montagnier’s experiments as described in
his “Isolation” paper from 1983. Bergman
can judge for herself whether Montagnier’s evidence for the “isolation” and
hence the existence of “HIV” has any substance.14-17
1. Lymphocytes from a patient at risk of AIDS (BRU) were
cultured with many chemical agents and then transferred to another culture
which contained lymphocytes from a healthy blood donor mixed with the same
chemicals. In both cultures Montagnier and
his colleagues detected reverse transcriptase activity. They claimed detection of RT in the BRU
culture proved BRU was infected with a retrovirus and the finding of RT in the
co-culture proof the BRU retrovirus was transmitted to the healthy blood donor
cells. However, as far back as 1973, the
first and second authors of the Montagnier paper knew that RT is not specific
to retroviruses and can be found in normal, uninfected cells.18 “This enzymatic activity [RT] can be
explained by the presence of some virus particles in these regions [sucrose
density bands other than 1.16 g/ml], and since similar polymerase activity has
been found in normal cells, may be mainly ascribed to the cellular enzyme”.18 In other words, 10 years before they made
their claim, they knew it had nothing to do with “evidence-based science”. At present, knowledge of the non-specificity
of RT is so widespread it has even appeared in the popular press, in material
read by people contemplating investment in biotechnology stocks.19
2. The supernatant fluid from
the co-culture was added to a culture of umbilical cord blood lymphocytes. In this culture they found RT and particles
bearing some of the morphological characteristics of retroviruses, “typical
type-C” particles. They claimed this
proved the retrovirus from BRU was transmitted to the umbilical cord
lymphocytes. However, in 1983 every
retrovirologist (Montagnier and the first and second authors of the 1983 paper
are retrovirologists), must have known that type-C particles are found in
nearly all normal human placentas20 and budding retroviral-like particles are a feature
of cultured, umbilical cord lymphocytes.21 In other
words, Montagnier et al’s claims had
nothing to do with “evidence-based science”.
3. Montagnier claimed the
particles visualised in the umbilical cord culture were retrovirus particles
because, in a sucrose density gradient, they banded at the density of 1.16
g/ml. “That this new isolate was a
retrovirus was further indicated by its density in sucrose gradient, which was
1.16 [g/ml]”. In fact they claimed the
1.16 g/ml band was “purified, labeled virus”.
That is, it contained nothing else but retroviral-like particles. This claim was made despite the absence of any
electron microscopic data and hence proof that the banded material Montagnier
called “purified” virus contained particles of any kind, retroviral, non-retroviral,
pure or impure. Montagnier later justified
this particular claim on the basis that “we published in Science (May 1983) a [sucrose density] gradient which showed that
the RT had exactly the density of 1.16.
So one had a peak which was RT.
So one has fulfilled this criterion for purification”.22 In other
words, not only did Montagnier regard RT as proof for isolation and transmission
of “HIV”, he also regarded detection of this enzyme activity in a density
gradient as proof for purification of “HIV”.
This bizarre conclusion is the basis of the “incontrovertible evidence” for the “overwhelming scientific
consensus” that HIV exists and is the cause of AIDS”.
When BRU’s serum
(antibodies) was added to the proteins in the 1.16g/ml band three proteins were
found to react - p25, p45 and p80. They
did not provide any additional information on p80 but it was not designated an “HIV”
protein. p45 was said to be cellular and
p25, now known as p24, and the antibodies which reacted with it, to be “HIV”. Because the p25 (p24) protein did not react
with antibodies directed against the retrovirus HTLV-I p24 protein, Montagnier
claimed he had discovered a new human retrovirus. One should note that since Montagnier discovered
only one “HIV” protein, p24, not only had he discovered a new retrovirus, he
had also discovered the world’s first (and only) “one protein” retrovirus.
One does not have to be a scientist to realise that
if two out of the three proteins present in “purified” virus are not “HIV” then
the 1.16 g/ml band cannot be “purified” virus.
If two proteins are not “HIV” then why is the third? And on what basis are the antibodies which
reacted with p24 “HIV”, while those that reacted with p45 and p80 not “HIV”? The scientific truth came to light in 1997
during an en camera interview
Montagnier gave to the French investigative journalist Djamel Tahi. In response to the question “But there comes a point when one must do the
characterisation of the virus. This means: what are the proteins of which it’s composed?”,
Montagnier replied: “analysis of the proteins of the
virus demands mass production and purification.
It is necessary to do that”. Yet
in response to further questioning he admitted he and his colleagues did not
purify HIV. “I repeat we did not purify”.22
The minimum absolutely necessary but definitely not
sufficient condition for Montagnier to claim his solo p24 protein is an “HIV”
protein is to have proof for the existence of at least some particles with the
morphology typical of retroviruses in the 1.16 g/ml banded material. Montagnier did not publish electron
micrographic images of the “purified” virus hence, during the same interview, he
was asked why not. His answer was
stunning. He said that in the “purified”
virus, even after a “Roman effort”, Charles Dauget, the Pasteur Institute
electron microscopist, was unable to find any particles with “the morphology
typical of retroviruses”. Much less
purified particles of any morphology. In
a subsequent interview with the same journalist Charles Dauget himself
confirmed that the “purified labeled virus” consisted of cellular debris. There were no retroviral particles at all in
the “purified” virus (DT personal communication).
This is as good “evidence-based science” as one can
get that Montagnier and his colleagues never had proof for a retrovirus in any
of their cultures or the patient BRU.
And the most specific “HIV” protein, p24, is nothing more than a
cellular protein.
In 1986 Robert Gallo claimed he had presented “clear
cut”23 evidence that HIV is the cause of AIDS in four
papers published in Science in May
1984. This claim has been accepted by
HIV experts including Montagnier (sometimes) and Bergman. The HIV theory of AIDS states: HIV infection à T4 cell destruction à clinical syndrome à death. To assert
such a claim Gallo must have evidence which proves:
To prove the existence of “HIV” Gallo relied on the
same phenomena as Montagnier. That is,
RT, particles visualised in the cell culture and reactions between the proteins
in the 1.16 g/ml band, which he also called “purified” virus, and antibodies in
patient sera. However, as far back as
1976 Gallo knew that particles with the morphology of retroviruses are not
necessarily retroviruses, even if they contain RT. “Release of virus-like particles
morphologically and biochemically [with RT] resembling type-C virus but apparently
lacking the ability to replicate have been frequently observed from leukaemic
tissue”.24 There were
two main differences between Gallo’s and Montagnier’s experiments: (a) Gallo used an immortal cell line, HUT78
(H9) in place of umbilical cord lymphocytes.
The HUT78/H9 cell line originated in a patient with leukaemia. According to Montagnier this type of cell
line contains “a real soup” of retroviruses.22 (b) Gallo tested
more patients.
In a 2007 court case Gallo acknowledged that, to
identify the proteins and the RNA of a new retrovirus, one must purify the
retroviral particles. “You have to
purify”.25 During the
same court case Gallo was asked: “In his
[Montagnier’s] 1983 Science paper he referred to the 1.16 band as the purified
virus. Is this right?” Gallo answered “He did a 1.16 cross [sucrose]
– gradient in that paper, yes. I don’t
know if he said it was purified. If you
do that you don’t have much virus” [page 1300].
Like Montagnier, Gallo claimed the 1.16 g/ml band was “purified”
retroviral particles but also like Montagnier published no electron microscopic
data—neither in 1984 nor at any other time.
In court he stated: “A sucrose
gradient barely purifies”.25 If banding in
density gradients “barely purifies”, and in the 1.16 g/ml band “you don’t have
much virus” why (a) did Gallo use the density gradient banding to purify “HIV”; (b) did he call the 1.16 g/ml “purified virus”?; (c) were the two proteins, p24 and p41, which
reacted with antibodies in patient sera, said to be “HIV” proteins and the antibodies
“HIV” antibodies? Since both Gallo and
Montagnier agree purification is necessary to prove the existence of a new
retrovirus and Gallo did not know “if he [Montagnier] said it was purified”, why
did Gallo (a) recommend the publication of Montagnier’s paper; (b) submit his own papers for publication?
Notwithstanding, Gallo reported the “isolation” of “HIV”
from 37% of AIDS patients and that 88% had antibodies that reacted with
proteins in the 1.16 g/ml band, the “purified” virus, using either the ELISA or
Western blot. However, at that time even
the HIV experts accepted the specificity of the ELISA was very low. The criteria used for a positive WB was a
reaction with p41, a protein which, according to Montagnier and other
researchers12 from the AIDS
Vaccine Program, SAIC, National Cancer Institute-Frederick Cancer Research and
Development Center, Frederick, Maryland, is the ubiquitous cellular
protein actin.16 Most
importantly, in none of the four Gallo papers is there any attempt to prove HIV
kills the T4 cells, much less that a decrease in T4 cells (immune deficiency,
AID) is the cause of the diseases from which AIDS patients die. Obviously, if one bases one’s opinion on “evidence-based
science” one has no choice but to conclude in 1984 Gallo did not prove HIV
causes AIDS.
In January 1986 Montagnier wrote the “…cytopathic
effect of LAV [“HIV”] can ONLY be observed in activated T4 cells” (emphasis
added). In the same year Gallo and his
associates reported experiments where they prepared T-cell cultures (which
contained 34% T4 cells), from normal donors.
Cultures were stimulated with
Hence by 1986 Montagnier and Gallo were in agreement that:
1. “HIV” by itself → no T4 destruction.
2. “HIV” plus
stimulation → T4 cell destruction;
3. Stimulation by itself → T4 cell destruction.
In other words, in the 1980s
Montagnier and Gallo showed that “HIV” is not sufficient for a decrease in T4
cells. And Gallo’s evidence shows that
in the presence of antigenic stimulation (activation), which is typical and
intense in AIDS patients, it is not even necessary. Yet, for more than 20 years all of Bergman’s “legitimate
scientists, doctors and advocates” led the world to believe that “HIV” is the
cause of the immune deficiency and the clinical AIDS syndrome.
Bergman: “House of Numbers” asks if there is really a
scientific consensus about HIV/AIDS. The real answer is: YES. There is
an overwhelming scientific consensus, based on incontrovertible evidence, that
HIV exists and is the cause of AIDS.
“Overwhelming scientific
consensus” is the mantra of every “HIV” protagonist. Daniel Kuritzke’s recent posting at www.houseofnumbers.org/Kuritzkes__Statement.html
is no exception. The origin of
the “HIV” theory lies with a handful of scientists who claim to have proven the
existence of a new retrovirus in 1983/84.
This claim, without which there cannot be a retroviral theory of AIDS,
has been accepted by virtually all scientists and doctors despite the fact few
know the details or could defend the theory.
The only thing “overwhelming” about the “overwhelming consensus” is the “overwhelming”
numbers of “scientists, doctors and advocates” who accept and support it.
It appears as
if Bergmann and the Perth Group read different scientific journals. In 2008 Montagnier was awarded the Nobel
Prize in Physiology or Medicine for his historical paper published in Science,
May 1983 for proving the existence of HIV.
In 2003, in the
In 1997 Goudsmit29 wrote: “The BRU lymph node was
first cultured in early January 1983 and, on January 15, it shed an enzyme
absolutely unique [sic] to the
lentivirus group…The BRU virus grew slowly and with difficulty, but its
identity and activity were reported in the May 20, 1983 issue of Science…The Pasteur Group was widely
acclaimed but very worried. In the world
of virology, finding a new virus is not enough:
You must propagate and isolate the organism for analysis by other
virologists. The French had not yet
isolated their new lentivirus”.29
In 2009
Vahlne,30 published a paper in Retrovirology
in which he stated “Regarding whom
should get the credit for the discovery of HIV, this review should enable the
reader to come to his or her own conclusion.
Mine, however, is different from that of those of my fellow faculty
members that presently make up the Nobel Committee for the Nobel Prize in
Physiology or Medicine…In reality, in my view there is no evidence whatsoever
in this paper [Montagnier’s 1983 Science
paper] that a new human retrovirus has been isolated!” Since Vahlne’s paper was promptly posted at AIDSTruth.org, we
assume the “legitimate scientists, doctors and advocates” at AIDSTruth agree
with his analysis. Needless to say, when
the Perth Group submitted a response to Vahlne’s paper, it was rejected by Retrovirology.
Is this the overwhelming consensus for the discovery
of the virus that has killed 25 million people?
In 1988 Gallo and Montagnier wrote: “after two weeks of culture,
reverse-transcriptase activity was detected in the culture medium. A retrovirus was present”.31 In 2002 Montagnier wrote: “Fifteen days
later, Françoise Sinoussi (by then Barré-Sinoussi) found the first traces of RT
in the supernatant of the lymphocyte culture, indicating the presence of a
retrovirus”. However, as mentioned
above, according to Barré-Sinoussi and Chermann, the first and second authors
of the 1983 Science paper, the “evidence
based science” as far back as 1973 showed that RT activity does not indicate a
retrovirus. “This enzymatic
activity [RT] can be explained by the presence of some virus particles in these
regions [sucrose density bands other than 1.16 g/ml], and since similar
polymerase activity has been found in normal cells, may be mainly ascribed to
the cellular enzyme”.18
This was confirmed by Gallo in 1976: “Many laboratories
subsequently reported the detection of reverse transcriptase in extracts from
normal cells”.32 Gallo and his colleagues themselves
reported: “An endogenous and completely
RNA-dependent…
Harold Varmus
agrees. “…reverse transcription is hardly unique to
retroviruses; it is now recognized as a widespread phenomenon in eukaryotic
cells”.34; “evidence has made it clear that reverse
transcription takes place…in the uninfected cells of yeast, insects and mammals”.35 Is this more scientific consensus?
In his 1983 paper Montagnier
said that his retroviral particle were “typical type-C”. In 2007, in a court case Gallo stated, “…although
I am a co-author, I contributed really nothing to that paper. It was Gonda that recognised the
lenti/retrovirus nature, not me. He
corrected a mistake from lack of the structural familiarity by almost all
retrovirologists with this family known by veterinarians. That is the answer. Montagnier, of course, did not know”. He also pointed out that HIV is a lentivirus “it
is clear even by its genomic analysis”.
Gallo’s testimony, page 1307.25 Commenting
on the paper by Gonda and Gallo36 Montagnier, in his 2000 book Virus, wrote: “Science published an article by his
[Gallo’s] group that showed similarities of sequences between HTLV-I, -II, and
–
Elsewhere in the same book
Montagnier referred to his experimental evidence that Visna and LAV were also biologically
different: “But then the horse virus [a lentivirus]
refused to grow in human lymphocytes, and our virus [“HIV”] would not grow in
horse lymphocytes. Moreover, neither the
horse virus not the Visna sheep virus would attack T4 lymphocytes or cause
immunosuppression”.
The one electron micrograph
Montagnier showed of “HIV” during his Nobel lecture has barely any of the
principal morphological features of retroviruses, much less, a lentivirus.37 The question
then is: what is the “evidence-based
science” which led the “legitimate scientists, doctors and advocates”,
including Montagnier and Gallo, to conclude “HIV” is a lentivirus? What exactly is the “evidence-based science”
upon which the consensus on the lentiviral nature of “HIV” is based?
The “HIV” experts cannot
agree even how many knobs are present on the surface of the “HIV” virus
particle. These are the knobs which,
according to the “legitimate scientists, doctors and advocates”, are a MUST for
infectivity. No knobs=no infection.
In Virus, Montagnier wrote: “Particles
of HIV are shaped like little spheres, each with roughly 80 rounded projections
shaped like pegs”.
In the 2005 textbook38 co-authored by Niel Constantine (who appears in the House of Numbers) and Professor
Elizabeth Dax, Head of the Australian National Serology Laboratory and
International Expert on HIV testing, there are “72 knobs or spikes of the
external envelope of HIV”.
According to Hans Gelderblom
and John Moore, immediately after being released from the cell membrane “HIV particles”
possess an average of 0.5 knob per particle which are rapidly lost, but also
pointed out that “it was possible that structures resembling knobs might be
observed even when there was no gp120 [knobs] present, i.e. false positives”.39 That is, there may not be any knobs.
In 2003 Kuznetsov and his
colleagues40 reported a study utilising atomic force microscopy
that contradicted what all “HIV” experts claim.
They reported that “The clusters of gp120 do not form spikes on the
surface of the HIV as is commonly described in the literature. The clusters are hardly protrusions at
all. We suggest that spikes, knobs,
observed by negative-staining electron microscopy may be an artifact of the
penetration of heavy metal stain between envelope proteins. Indeed, the term “spike” appears to have
assumed a rather imprecise, possibly misleading definition, and might best be
used with caution”. In other words, this
posits zero knobs on the so-called “HIV” particle.
Hence the “evidence-based”
scientific consensus has knob counts for the “HIV” particle of 80, 72, 0.5 (on
average), possibly zero and actually zero.
Of
interest is the picture at the very top of the AIDSTruth homepage. Presumably the custodians of the AIDSTruth website
believe this image lends weight to the existence of “HIV” on the basis of the particles
illustrated in the image. This is a scanning
electron microscope (
AIDSTruth is not alone. At its website “Focus on the
HIV/AIDS Connection” the National Institutes of Allergy and Infectious Diseases
present their evidence “Why is there overwhelming scientific consensus that HIV causes AIDS?”.
The answer to this “consensus” includes an invitation to visit http://www.virology.net/Big_Virology/BVretro.html in order to see “Electron micrographs and other
images of HIV”. Of these 25 images the majority are diagrams, artists’
renditions or computer graphics. Only eight images are electron
microscopic pictures and none identify the source or nature of the material portrayed.
Significantly, none has a size bar, that is, in no EM is it possible to determine
the dimensions of the particles or other morphological features.
Publishing
electron-micrographs of “the retrovirus HIV” devoid of the requisite
morphologies features of a lentivirus is not confined to AIDSTruth or the
NIAID. On
The front page
of the International AIDS Society Newsletter, March 2007, is entitled “AIDS
Denialists. This edition’s feature
article examines the global impact of AIDS denialism”. About 75% of this page is occupied by a dazzlingly
multi-coloured picture more appropriate for a discotheque than a scientific
publication. Apparently it is meant to
represent an electron micrograph of part of a cell with budding and cell free “HIV”
particles. However, anybody who is
familiar with electron micrographs will realise that the picture is a computer graphic. The picture has a caption which reads: “Image: HIV daughter cells bud on the surface
of a T-cell”.41
Anyone with even rudimentary
knowledge of medicine or biology knows that viruses are not cells and are
gender free. The term “daughter cells”
is absurd.
On what “evidence-based
science” is Bergman’s “overwhelming scientific consensus” based?
In House of
Numbers there is the following dialogue:
Luc Montagnier: “I am a promoter of the role of co-factors in
AIDS.”
Harry Haverkos: “Well, co-factors just says that the cause of
a disease is by more than one factor.”
Joe Sonnabend: “Just simply being infected by HIV is not
going to do it. You need certain co-factors.”
Anthony Fauci MD, Director, National Institute of
Allergy and Infectious Diseases:
“Co-factors are not
necessary.”
Joe Sonnabend: “Dr. Fauci would say: HIV causes AIDS without the
need of anything else. That is kind of ridiculous.”
Anthony Fauci: “The data that indicate that any different
type of infection like mycoplasma or something like that is a necessary
co-factor, I believe those theories have been debunked.”
Francoise Barre-Sinoussi PhD, Director, RRI,
Jay A. Levy MD, Director, Laboratory for Tumor and AIDS Virus
Research, UCSF: “How HIV depletes the T-cells so an individual
advances to AIDS is probably due to multi-factorial elements. One is it
will kill the cell eventually that it affects.”
Joe Sonnabend: “What the fuck does he mean? I’m sorry, what
does he mean that there are no co-factors. Where is he coming from?
There’s co-factors for everything.”
Robert Gallo: “Co-factor implies something specific.
It really gets us off into tracks that are wandering.”
Harry Haverkos: “Gallo isn’t going to change his mind when he’s
probably 70 years plus now. He is going to remember things, we all
remember things that are good for us and we forget the bad things…The
co-factors are important to really understand how people get ill, why
they get ill.”
As far
back as 1986 Gallo wrote: “the results
revealed a cytopathogenic [cell killing] mechanism that may account for T4 cell
depletion in AIDS patients and suggest how repeated antigenic stimulation by
infectious agents such as malaria in Africa or by allogenic blood or semen, may
be important determinants of the latency period in AIDS”.26 Is it possible that without such antigenic
stimulation the latency period may well be infinite in “HIV” “infected”
individuals? If antigenic stimulation is
the absolutely necessary co-factor then “HIV” may be a co-factor which is
absolutely unnecessary.
Ten years ago researchers
from the
According to the dictionary
consensus means “agreement in the judgment or opinion reached by a group as a
whole”. Unless she has her own
definition of “consensus”, even Bergman would have to agree that the “evidence-based
science” proves there is barely any consensus amongst “HIV”/AIDS experts on
anything. Bergman claims the “HIV”
experts were deceived by Leung, he “cut up their words and edited them to make
it appear as if there is no consensus among experts about the nature of HIV and
the disease syndrome it causes, known as AIDS”. The fact is Leung did no
such thing. The “HIV” experts gave an
honest account of their various opinions and their words, which were not “cut
up”, reveal what they apparently would rather deny - there is no consensus.
Bergman: “HIV…is the
cause of AIDS”
The HIV theory of AIDS was put forward to
account for two diseases in gay men, Kaposi’s sarcoma (KS) and Pneumocystis carinii pneumonia (
In 1990 Friedman-Kein published “evidence-based
science” confirming the fact that in some homosexual men KS can occur in the
absence of both immune deficiency and “HIV”.44 Since then, “HIV”
experts have accepted that “HIV” is neither the direct nor the indirect cause
of KS. Yet KS, not caused by “HIV”,
remains an indicator disease of a syndrome caused by “HIV”. Another example of AIDS “evidence-based
science”?
For Bergman’s interest, in 1988 the Perth
Group paper45 arguing that HIV does not cause Kaposi’s sarcoma was
thrice rejected by the Medical Journal of
Australia on the advice of an “established expert”. The reviewer stated, “The author tries to
argue that Kaposi’s sarcoma cannot be caused by HIV infection, and that
therefore AIDS is not due to HIV infection. The arguments put forward by the author are
quite unsatisfactory, and are not supported by even a desultory reading of the
literature quoted. In addition, the author fails to examine the body of
epidemiological, immunological and cellular literature concerning the pathology,
pathogenesis and clinical associations of this fascinating manifestation of HIV
infection”. Yet this is the very “epidemiological, immunological and cellular
literature” which eventually led all the “established experts” to accept that “this
fascinating manifestation of HIV infection”, is not caused by HIV infection. This as good an example as any that “AIDSTruth”
is not truth until AIDS experts say it is.
In 1995 Gallo stated: “The first thing I can tell you is that we’ve
been able to regularly culture from Kaposi’s tumors what pathologists say is a
tumor cell. We asked: What is the role
of HIV in all this? And we found that inflammatory cytokines ... were the very
likely initiatory events in creating this cell. We said, “Oh, the role of HIV
is likely to be in increasing these inflammatory cytokines.” But we have
learned – this should be of interest to everybody that isn’t completely married
to HIV – that the inflammatory cytokines are reportedly increased in gay men
even without HIV infection. Inflammatory
cytokines are usually promoted by immune activation, not by immune
suppression. So here was a paradox....So
the inflammatory cytokines may be increased by HIV, but I wish I knew what else
was increasing them before a gay man was ever infected with HIV. Maybe it’s nitric oxide, maybe it’s a
sexually transmitted virus, maybe it’s all of them, maybe it has to do with
rimming because it’s immune stimulation with non-specific infections”46 (emphasis added).
(As mentioned, contrary to Bergman’s “evidence-based science”, KS, a
disease not caused directly or indirectly by “HIV”, still remains an AIDS indicator
disease).
In 2006 three prominent HIV/AIDS experts from the US,
including Clifford Lane from the Division of Clinical Research and Laboratory
of Immunoregulation, National Institute of Allergy and Infectious Diseases,
Bethesda, commented on the Rodriguez 2006 JAMA
paper.47 “The findings
presented by Rodríguez et al provide support to those who favor nonvirological
mechanisms as the predominant cause of CD4 cell loss; however, these data should be interpreted
with caution, and the issue of a single viral load as a prognostic marker
should be separated from the role of viral replication in HIV pathogenesis”. In other words, the AIDS “evidence-based
science” appears to be sliding in the dissident direction.
In
1985 Montagnier stated “This [clinical AID] syndrome occurs in a minority of
infected persons, who generally have in common a past of antigenic stimulation
and of immune depression before LAV [HIV] infection”.49 That is, at the beginning of the “HIV” era
Montagnier recognised that in the AIDS risk groups AID appears before HIV
infection. He is still saying it.
In a talk he gave to the European Parliament,
Bergman: “…people knowledgeable
about HIV are clear that HIV is a hard virus to get”
If this is “a hard virus to get” how did
millions of people get it in such a short interval? Why was it increasing exponentially in gay
men in the
Bergman: HIV…is
transmitted by the…sexual fluids of infected people
There has never been any
proof that “HIV” is transmitted by the “sexual fluids of infected people”. All the “proof” of sexual transmission is
based on epidemiological studies which document the relationship between a
positive antibody test (“infection”) and various sexual behaviours, in both gay
men and heterosexuals. (Apparently,
despite much “evidence-based science” to the contrary,50 “HIV” experts regard “HIV” antibodies in the blood as
synonymous with infectious “HIV” particles in “sexual fluids of infected people”).
We remind Bergman that
sexually transmitted infections or diseases are transmitted bidirectionally. That is, from the active (semen donating)
partner (heterosexual or gay male) to his passive (semen accepting) partner
(male or female) and vice versa. Hence epidemiological “evidence-based” proof
that HIV/AIDS an infectious disease must demonstrate beyond all reasonable
doubt that both the passive and the active partner are at risk of developing a
positive antibody test or AIDS. We
further remind Bergman that the interpretation of epidemiological evidence in
gay men is complicated by the fact that gay men commonly practise both active
and passive sex. Thus, in order to determine
the relationship between sexual contact and a positive antibody test in the
active partner, epidemiologists must provide data on gay men who exclusively
practise active sex. While there is
ample evidence the passive partner is at risk of acquiring a positive antibody
test or AIDS, there is no evidence the active partner is similarly
afflicted. In fact, not only do the data
show there is no increased risk for the active partner, there are no data that any
active partner acquires a positive antibody test or AIDS from his or her
passive sexual partner. Let Bergman cite
one study to the contrary. Here we list
the relevant evidence. Note: we, like
epidemiologists, discount findings from cross-sectional studies. That is, studies where both partners are
simultaneously found to be “HIV” positive.
This type of study cannot prove sexual transmission and it is for this reason
that epidemiologists resort to the much more difficult, time consuming and
expensive prospective studies. It also
must be stressed that in these studies epidemiologists rely on self-reported
data on sexual activity and behaviours which, as epidemiologists themselves accept,
are inherently problematic. This is an
especially significant factor when interpreting the low numbers of “transmissions”
universally reported in such studies.
In regard to such
fallibility, as far back as 1988 Padian and Donald Francis wrote: “Over the
years, a constant theme in the AIDS field has emerged from groups working in
settings as different as blood bank donor deferral and AIDS-case categorization. Every group has found that extracting
sensitive risk-behaviour information is often difficult for even the most
experienced interviewer”.51
In 2006 Maria Gallo from the CDC
reported a study on self-reported sexual behaviour in 332 female sex
workers. She tested the women for
intravaginal, prostate specific antigen (
Robert Gallo and his
associates were among the first to study the relationship between sexual activity
and the acquisition of a positive antibody test. In 1984 Gallo reported: “of eight different sex acts, seropositivity
correlated only with receptive anal intercourse…and
with manual stimulation of the subject’s rectum…and was inversely correlated
with insertive anal intercourse”.52 It goes
without saying that an inverse relationship is totally at odds with the
existence of a sexually transmitted, infectious agent.
In an updated study
published in 1986 they wrote: “Data from
this and previous studies have shown that receptive rectal intercourse…is an
important risk factor for HTLV-
By 1994 many
epidemiological studies, including prospective studies, were conducted in gay
men. Reviewing more than 20 such studies
Caceres and van Griensven concluded: “the cited reports yield convincing evidence
that unprotected anogenital receptive intercourse poses the highest risk for
the sexual acquisition of HIV-1 infection…there is mounting epidemiological
evidence for a small risk attached to orogenital receptive sex, biologic
plausibility, credible case reports and some studies show a modest risk,
detectable only with powerful designs;…no or no consistent risk of the
acquisition of HIV-1 infection has been reported regarding insertive
intercourse and oro-anal sex”.54
Unquestionably,
the largest, longest, best designed and executed prospective study in gay men
is the Multicenter AIDS Cohort study (MACS).
The authors of this study showed that “receptive anal intercourse was
the ONLY sexual practice shown to be independently associated with an increased
risk of seroconversion to HIV in this study”.55 The same authors also reported: “…greater sexual activity [receptive anal
intercourse] following establishment of HIV-1 infection leads to exposure to
promoters or co-factors that augment (or DETERMINE) the rate of progression to
AIDS” 56 (emphasis added). This finding is at odds with the general
accepted view for sexually transmitted diseases, namely, a person needs to be
infected only once with a microorganism in order to develop and die from that
illness. However, there is evidence that
semen itself (or another, non-infectious factor associated with passive anal
sex) is the cause of both a positive test and AIDS.
There have been only two
longitudinal studies in heterosexuals: the European Study Group published
by de Vincenzi and her colleagues57 and Nancy Padian’s58 in the
In her cross-sectional studies de Vincenzi reported that sexual practices “other
than anal intercourse...were not associated with infection of the partner”.
In
their four year prospective study the authors of the European Group claimed 4
men and 8 women became infected following sex with the seropositive
partner. This study was criticised by
other researchers including Stuart Brody.
He questioned their conclusion by pointing out that “The
problem of subjects’ lying (often euphemistically termed “social
desirability responding”) about engaging in anal intercourse and
intravenous drug use plagues most studies of behavioral risk factors
for the transmission of HIV, and the study by de Vincenzi and
colleagues is no exception. How was
the absence of homosexual contact verified? How was the absence of
anal intercourse among the women verified? If only 4 men and 6 women
among the 121 couples inconsistently using condoms lied when they
denied engaging in anal intercourse (or misreported the facts for
other reasons), there would be no cases attributable to vaginal
intercourse without a condom. At least this much lying should be
expected. Before vaginal and anal
intercourse are assigned comparable degrees of risk and condoms
given the credit for saving lives, the alternative explanation that
the disease is spread almost exclusively by anal and intravenous
transmission must be more rigorously examined. Other
investigators found that HIV infection in women was related to anal intercourse
(especially among partners of bisexual men) and the number of exposures to the
index patient, but not to condom use or the total number of sexual partners”.59
Responding,
de Vincenzi wrote: “We agree with Dr
Brody that our prospective analysis lacks statistical power to show an
increased risk associated with anal intercourse. [That is, they could not exclude the
possibility that the positive antibody tests were the result of anal and not
vaginal intercourse.] Indeed, we found
such an association in the cross-sectional analysis. However, from a public health point of view,
no one should state that there is no risk of HIV transmission through vaginal
sex, since the vast majority of cases of AIDS throughout the world are acquired
in this manner”. It is significant that de Vincenzi
admitted her evidence did not prove HIV is transmitted by penile-vaginal
intercourse. Neither did she cite
evidence to prove her claim “the vast
majority of cases of AIDS throughout the world are acquired” by penile-vaginal
transmission.
Unquestionably, Padian’s
study, which began in 1985, is the longest, largest, best designed and executed
study ever conducted in heterosexuals.
At the 1988 Amsterdam International AIDS Conference, Padian described
her study as follows: “Objective.
To examine the efficiency of
heterosexual transmission of HIV [emphasis ours] and associated risk
factors. Methods: We enrolled the opposite sex partners of
individuals infected with HIV or diagnosed with AIDS or ARC throughout
As was the case in the European study, the Padian study
was divided into two parts: cross-sectional
and prospective. The first findings from
the cross-sectional study were published in 1987, in a paper entitled: “Male-to-Female Transmission of Human
Immunodeficiency Virus”: “Ninety-seven
female sexual partners of 93 men infected with human immunodeficiency virus
were studied…23% of the women were infected…Anal intercourse significantly
discriminated between seronegative and seropositive women…The number of sexual
contacts (whether vaginal, anal or oral, was significantly associated with
infection…whereas general sexual activity (as measured by number of sexual
partners [median 2,5 for seropositive; 4
for seronegative women] and number of sexually transmitted diseases) was not
associated with HIV infection”.61
In 1991 Padian et al published yet another paper
describing their findings from the cross-sectional part of their study, this
time entitled “Female-to-Male Transmission of Human Immunodeficiency Virus”.62 They pointed
out that “since 1985, we have been conducting a study of the heterosexual
transmission of AIDS”, but by 1991 of 72 infected women, only the partner of
one of them was found positive. However,
for a number of reasons they could not say with certainty that the man was
infected by his female partner…We cannot be absolutely certain that we
correctly classified this case as female-to-male transmission…Of course,
because we are relying on risk histories, the same caveats apply to
classification of male-to-female cases of transmission as well”. By 1997 Padian and her colleagues described
one more case of female-to-male transmission about which they were equally
uncertain. Trying to explain the
differences between their findings and that of others, who claimed high rates
of female-to-male transmissions, they wrote:
“studies may not have been adequately controlled for other confounding
non-sexual 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”.58
In 1997 in a paper
entitled “Heterosexual Transmission of Human Immunodeficiency Virus (HIV) in
“TABLE 3. Risk behavior at baseline and most recent
(final) follow-up
visit
among 175 human immunodeficiency virus (HIV)-discordant couples
recruited
in
a
total of 3,384 couple-months of follow-up)
Baseline Final
Visit (%)
follow-up visit (%)
Abstention 0
14.5*
Consistent condom use
32.2 74*
Any anal intercourse 37.9 8.1*
* p < 0.0005 (by McNemar’s test for matched pairs).”
Despite an extraordinary
effort educating her study subjects in safe sexual practices, Padian and her
colleagues were not entirely successful, as can be seen from their Table
3. Furthermore, “approximately 97% of
behaviour changes was reported between baseline and the first follow-up visit”. Yet, they “observed no seroconversion”, that
is, no uninfected individual developing positive antibody test. Discussing the lack of sexual transmission,
Padian and her associates wrote: “Nevertheless,
the absence of seroincident infection over the course of the study cannot be
entirely attributed to significant behaviour change. No transmission occurred among the 25% of
couples who did not use condoms consistently at their last follow-up nor among
the 47 couples who intermittently practiced unsafe sex during the entire
duration of follow-up”.58 Hence Padian’s data prove “HIV” is not
transmitted to the active partner.
Padian
consistently refuses to accept the “evidence-based science” conclusion of her
own studies. She has even felt (or was)
compelled to defend her “proof” of heterosexual transmission at AIDSTruth. Padian wants everyone to accept that, because
she later decided to label her study as “behavioral interventions” to prevent
HIV transmission, it is iniquitous to use her data to question proof of HIV
transmission. Hence the title of her
paper, Heterosexual transmission of human
immunodeficiency virus (HIV) in
From
the very beginning of the AIDS era, with few exceptions, there has been an
unhealthy bias towards an infectious cause of a positive antibody test and
AIDS. Scientists have not conducted
research that might elucidate whether non-infectious factors, semen for
example, may play the direct role in the development of a positive antibody
test or AIDS. This is despite published
data that, in the case of semen, it is both toxic and immunosuppressive. Virtually all epidemiological studies on
sexual transmission illustrate this bias although it would have been a
relatively simple matter to collect data to test whether the risk from passive
anal sex is an infectious agent in semen or semen itself. For infectious agents the risk increases as the
number of sexual partners. For semen itself
or other non-infectious agents the risk increases as the number of episodes of
sex. In case this
distinction is not clear consider the following: The volume of the male ejaculate is reported
to be 0.1-11 ml. Let us choose 5 ml as a
typical quantity. Over a period of three
months for example, a passive gay man could have a hundred partners, each once,
which would expose him to 500 ml of semen.
Or he could have 50 partners, four times, which would expose him to a
litre of semen. That is, half as many
partners could expose him to twice the dose of semen. If an infectious agent is the cause of a
positive antibody
test or AIDS then the hundred partners should pose more of a risk than the
fifty partners. And vice versa. By performing
such a study one could obtain data to distinguish between these possibilities. However,
virtually no epidemiological study reports such data. What is reported is the number of (different)
sexual partners, not the frequency of sex.
There are two exceptions.
One of the two studies is
the 1987 Padian et al study61 where she found that “The number of sexual contacts
(whether vaginal, anal or oral was significantly associated with infection…whereas
general sexual activity (as measured by number of sexual partners…was not
associated with HIV infection.
The other exception is a
study by Janet Nicholson published in the Annals of Internal Medicine. “In the year before testing,
homosexual men who were seropositive tended to have a greater number of sexual
partners (p = 0.009), more episodes of receptive anal intercourse (p <
0.001), and more frequent active (p < 0.001) and receptive (p = 0.023)
insertion of hands into the rectum…The number of episodes of receptive anal
intercourse per year was the variable most highly associated with HTLV-
Hence epidemiologists dismissed the early
notion that semen may have been a cause of immunosuppression and AIDS to the
point where evidence that could have added weight to this theory was not even
collected. Yet these data should have
been part of each and every study. Even
when studies such as these are published, their “evidence-based science”, which
does not support the existence of an AIDS causing, sexually transmitted agent,
is ignored.
In summary the only
possible interpretation of the epidemiological data is that, unlike all the other
sexually transmitted agents and diseases, “HIV” (a positive antibody test) or
AIDS, is not bidirectionally transmitted.
The passive partner acquires “HIV”/AIDS through sexual activity but
cannot transmit either to the active partner.
To use an analogy, AIDS is like pregnancy. It can be acquired by the passive partner but
not transmitted to the active partner.
The difference is that pregnancy can be acquired by a single act of vaginal
intercourse while for the acquisition of a positive antibody test and AIDS, a
high frequency of anal intercourse is necessary.
In the case of “HIV”/AIDS
either:
(i) The active
partner acquires “HIV” by means other than sex, and then transmits it to the
passive partner; or
(ii) The cause of
AIDS and of the positive antibody test in the passive partner is not a
retrovirus “HIV”.
The most parsimonious
explanation for the epidemiological data in both gay men and heterosexuals is
that “HIV”/AIDS is not sexually transmitted because there is no infectious
agent to transmit. Appreciation of this
should have led “legitimate scientists, doctors and advocates” to question the “isolation”
of “HIV” and a retroviral theory of AIDS.
Bergman: HIV tests are extremely reliable, sensitive and specific…The
ELISA or EIA test screens for the presence of HIV antibodies in blood or oral
fluids… Because there is a small risk of a false positive, every HIV test is
then confirmed with a Western Blot test. The two-test protocol is over
99.9% accurate (original emphasis)
For a long time immunologists thought
and taught that antibodies react only with the inducing antigen. Now they accept (but mostly ignore the obvious
scientific consequences) that antibodies react with a plethora of other antigens.64-66
Hence it does not follow that an antigen/antibody reaction proves the
antibody arose as a result of exposure to or infection with a particular antigen. The “accuracy” of a test encompasses several
parameters including its specificity.
Probably unknowingly, specificity is the test parameter of most interest
to the patient because it raises the possibility that a positive result has a
cause other than what Bergman would have us all believe.
As Bergman states, specificity means “recognizing everyone who is a true negative, who doesn’t
have the virus or whatever is tested for”.
If a test is truly capable of “recognizing everyone who is a true
negative [not infected]” then the test specificity is 100%. This is most often not the case – most tests
are not 100% specific. The definition of
specificity may be difficult to grasp because it involves two negatives, that
is, the proportion of non-infected individuals who have negative tests. It is much easier to understand specificity
in terms of the test being positive if and only if infection is present. In other words, a 100% specific test is never
positive unless infection is present. All
non-infected persons have a negative test.
Every non-infected person who does have a positive test reduces the test
specificity from its theoretical maximum.
As usual, Bergman provides no evidence
for her assertion but she does know specificity can only be determined by
experiment. This experiment consists of
testing a statistically significant (=large) number of individuals which must
include (a) healthy individuals at no risk of AIDS; (b) people at risk of AIDS; (c) those suspected of being “infected” (AIDS
patients); (d) sick individuals with
clinical and laboratory abnormalities which closely resemble AIDS but are not
AIDS. For example, since AIDS patients
are oxidised and have hypergammaglobulinaemia, both highly typical of AIDS
patients, so must the controls. Since
the antibody test is claimed to diagnose HIV infection, for each individual the
experiment must determine (a) the antibody test status; (b) the presence of absence of “HIV”. The method of determining (b) cannot be (a)
because this would amount to a test evaluating itself and hence be
scientifically invalid. Therefore method
(b) must be a method which is independent of (a) and is usually known as the gold standard for the test. The
gold standard is a crucial sine qua non and
represents the tenet upon which rests the scientific proof of validity.67 No gold standard no validity.
Hence, when the blood samples are
obtained they are divided into two portions:
one to test for antibodies, the other to isolate “HIV”. From these data the following table is then
constructed where a, b, c and d are the numbers of individual categorised as
per the table:
Antibody test result |
HIV present |
HIV absent |
Positive |
a |
b |
Negative |
c |
d |
Specificity is defined as d/(b+d)
For example, if there are 500 individuals from whom “HIV” cannot
be isolated and one such individual has a positive antibody test the
specificity is 499/(1+499) = 99.8%.
Nowhere in the 150,000 papers published to date on “HIV”/AIDS is
there such a table. We challenge Bergman
to produce even one instance of this table and post it at AIDSTruth. If she cannot she can only conclude there is
no “evidence-based science” for her assertions.
In the absence of these data the specificity of the “HIV” antibody
tests is unknown. It may be 100% or it
may be zero or any number in between. Since
the “HIV” theory is solely based on a correlation between a positive antibody
test and the clinical syndrome, in the absence of such data, there is no proof
for this theory. If Bergman wants to
seriously undermine the view of some of the “AIDS denialists” she could do no better
than produce this table. Furthermore, if
Bergman takes the time to examine the fundamental failure of “evidence-based
science” to provide a gold standard for the antibody tests she will discover this
is a direct consequence of the failure of HIV experts to purify “HIV”.12 13
Manufacturers of the “HIV” antibody test kits are fully aware of
the need for a gold standard but, at the same time, accept it does not exist. Statements to this effect are regularly included
as disclaimers in test kit packet inserts.
For example, the Abbott Western
blot antibody test kit insert: “At
present there is no recognized standard for establishing the presence or
absence of HIV-1 antibody in human blood”. Obviously biotechnology companies understand
consequences that “HIV” experts deny.
Some “HIV” experts themselves agree there
is no gold standard:
William Blattner: “One difficulty in assaying the
specificity and sensitivity of human retroviruses [including HIV] is the
absence of a final “gold standard”“. In
the absence of gold standards for both HTLV-I and HIV-1, the true sensitivity
and specificity for the detection of viral antibodies remains imprecise”.68
Philip Mortimer: “Diagnosis of HIV infection is based almost
entirely on detection of antibodies to HIV, but there can be misleading
cross-reactions between HIV proteins and antibodies formed against other
proteins, and these may lead to false-positive reactions. Thus,
it may be impossible to relate an antibody response specifically to HIV
infection”69 (emphasis
added).
Elizabeth Dax (co-author with Niel
Constantine) does not appear to understand the concept of a gold standard, much
less the absolute need for a gold standard in establishing the specificity of
an antibody test.25
There being no gold standard, “final” or
otherwise, for the “HIV” antibody tests, Blattner, Gallo and their colleagues
used AIDS as the gold standard. It is
greatly ironic that Bergman herself knows this is wrong. She correctly defined specificity as “recognizing
everyone who is a true negative, who doesn’t have the virus or whatever
is tested for” (emphasis added). The “HIV” antibody tests are tests for “the
virus” “HIV”, not AIDS. If a
scientist uses AIDS as a gold standard he obtains the sensitivity and
specificity of a test for AIDS, not “HIV”.
Yet, the title of the Blattner and Gallo paper is “Screening Test for
HTLV-
In 1984 Gallo used the antibody test to obtain “clear-cut
evidence” that “HIV” is the cause of AIDS while in the above paper he used the
presence of AIDS as a gold standard to prove that the antibodies are specific
to “HIV”. This is a circular argument in
which “HIV” is bypassed. Furthermore, as
already mentioned and as Bergman fully understands, if AIDS is used as a gold
standard, since the vast majority of people who test positive do not have AIDS,
the vast majority of positive tests are false positives.
Niel Constantine, who appears in the House of Numbers, wrote a text book38 entitled “Retroviral testing and quality assurance.
Essentials for laboratory diagnosis”.
Addressing the determination of test parameters he wrote: “All serological confirmatory tests have
guidelines or criteria that must be met to determine whether result fulfils the
requirements to classify the sample as HIV positive, negative, or
indeterminate. These criteria have been determined in two ways.
First, manufacturers of test kits have predetermined the requirements for
results based on studies of individuals who have been classified as positive or
negative by other means (clinical status, culture etc.) (emphasis added)”.
Since to date nobody has proven the
specificity of the antibody tests for “HIV” infection by the use of an “HIV”
isolation gold standard, it is unreservedly valid to ask whether the antibodies
that react with the test kit antigens are induced by factors or antigens that
are not in any manner related to a putative retrovirus “HIV”.
According to Constantine et al:
“The best antigen preparations to
detect established HIV infection are viral lysates because these contain native antigens from virtually all structural
components of the virus”. “Viral lysates”
is the material from the culture supernatant which in sucrose density gradients
bands at the density of 1.1 6g/ml. The
most important “viral proteins” used in the “HIV” antibody tests are p24, p32,
p41, p120 and p160. However, as stated
earlier, in the “viral lysates”, where Montagnier identified the “HIV” p24,
there was only cellular debris, no retroviral particles. That is, according to the “evidence-based
science”, p24 is a cellular protein.
Also according to Constantine: “The gp160 molecule is a precursor, being
subsequently cleaved to form gp120 and gp41…It has been demonstrated that the
gp160 antigen on Western blots may actually be tetramers [X4] of the gp 41
antigen (and not the precursor env protein);
this may occur during the disruption and electrophoresis
procedures. Therefore, antibody
reactivity to the gp160 antigen (and gp41) may actually represent reactivity to
gp41 only. Also, the env specific
antigen in the position of gp120 is in fact a mixture of the trimer [X3] of
gp41 and true outer membrane protein gp120”.
Hence there is no evidence that the p120 or p160 band on the Western
blot contain any protein other than p41.
According to Montagnier, p41 is the cellular protein actin and Bess et al have published data that all the “HIV”
proteins with molecular weights higher than 30,000 (including p41) are all
cellular proteins. In other words, none
of the protein antigens from the “viral lysates” used in the “HIV” antibody
test kits are viral. Rather they are all
cellular proteins.
Bergman admits that individuals who have autoimmune diseases but not AIDS may
react in the “HIV” antibody tests. At
present there is ample evidence that oxidised globulins behave as autoantibodies.71 Given that:
it is very likely
that a positive antibody test is a non-specific marker, similar to, for
example, the erythrocyte sedimentation rate, that indicates a propensity for the development of
particular diseases (AIDS) but devoid of any connection to a putative retrovirus
“HIV”.
Bergman’s claim that the “HIV” antibody tests are
99.9% specific is not shared by some of the best known “HIV” experts, including
some who appeared in House of Numbers:
Robin
Weiss: “I don’t think the Western Blot is a useful
diagnostic test; I don’t think it’s worth doing…You don’t need a Western Blot! And it’s become a dogma in HIV research that
you need one ELISA followed by a western; you don’t. You need two different kinds of ELISAs made in
two different formats”.
Weiss’ recently expounded on these statements at the
bogus House of Numbers website set up
by Bergman. He claims he was discussing
screening tests, not diagnostic tests. In
“What interviewees say” Weiss states “In my recollection (I don't have a tape
of the interview) Leung was pressing me about HIV antibody tests in reference
to screening blood donations. When I said ‘I don't think the Western Blot
is a useful diagnostic test; I don't think it's worth doing’, I was referring
to relatively high throughput screening for blood banks, and in the mid 1980s”. In the House
of Numbers it is quite clear Weiss is discussing diagnostic assays. The “dogma” “you need one ELISA followed by a
western [blot] is not relevant to “relatively high throughput screening for
blood banks”. Weiss also affirmed his
opinion “You don’t need a Western blot!” as “ELISA tests made by two different
manufacturers can also provide a confirmed result”.
As far back as 1991 Philip Mortimer, Director,
Sexually Transmitted and Blood Borne Virus Laboratory, United Kingdom, published
a paper in Lancet entitled “The
fallibility of the Western blot”: “Interpretation of these reactions is often difficult, even
for experienced personnel….Interpretation of western blot patterns differs
according to the observer and laboratory, and attempts to standardise western
blotting by establishing interlaboratory guidelines for reading the strips have
been met with only limited success. Manufacturers
list their own criteria for interpreting western blots, as do the Centers for
Disease Control (CDC) and at least five other
In “What interviewees say” Weiss concedes there are “doubts about the
precision or reliability of tests that were devised as research tools in 1984”,
which include the Western blot. Yet
Weiss appears to forget that thousands of individuals were diagnosed with HIV
using tests of such doubtful “precision and reliability”, including one test,
the “confirmatory” Western blot, that “should have remained, a research tool”. Now, Weiss assures us, there are “mass
produced commercial tests, which had to go through extensive quality control
before they were marketed or used in clinics and blood banks”. Western
blot tests may be mass produced but the problems enumerated by Mortimer still
remain. More importantly, no antibody
test, whether mass produced or produced in a research laboratory, should be
introduced into clinical practice without proof of its specificity. Weiss compares “HIV” serology 1984 and now with
“Roentgen's original fuzzy X-ray pictures” and today’s “radiological imaging
systems for hospital diagnosis”. The
reality is there has never been “a picture” of the Western blot, “fuzzy” much
less “non-fuzzy”.
Robert Redfield MD, Director, Clinical Care and Research
Institute of Human Virology: “We
have a group now, about 40 patients that have no detectable virus in their body
but they’re not being treated. So the first question is, ‘are they really being
infected?’”
*Leung: “So the
Western Blot could have false positives?”
Robert Redfield: “No, the
Western Blot was negative too. But they were told they were positive by a lab,
yes, which misread the Western Blot.
*Leung: “Heavyweight
champion Tommy Morrison tested positive in 1996. Eleven years later, in 2007,
he tested negative multiple times, allowing him to return to the ring.”
Harold Jaffe: “There’s
constant discussion in the community of people who do diagnostic testing and
the blood bankers about how to read these tests.”
*Leung: “When you’re
looking at this, this western blot, how do you determine whether it’s a
positive?”
Claudia Kucherer: “You need a certain number of bands
being present. It depends a little bit on the producer of the test.”
*Leung: “It depends
on the manufacturer.”
Claudia Kucherer:
“Yeah.”
*Leung: “Is there a
different criteria for what might be a positive?”
Claudia Kucherer: “Yeah. Yes. There are
different criteria from the manufacturer, thank you for the word, and also
there are guidelines from the WHO and UNAIDS.”
James Curran: “HIV
infection is diagnosed with rather, now, routine laboratory tests for which
there are criteria for diagnosis established by the manufacturer, FDA.”
*Leung: “Claudia
showed me the package insert that comes with the western blot. It contains
eight different sets of criteria for diagnosis HIV infection.”
*Leung: “Since a
false positive looks like a true positive how can you ever distinguish whether
it’s truly a positive or negative?”
Max Essex: “ELISA and WB results should be interpreted with caution when screening
individuals infected with M. tuberculosis or other mycobacterial
species…ELISA and WB may not be sufficient for HIV diagnosis in AIDS-endemic
areas of Central Africa where the prevalence of mycobacterial diseases is quite
high”.72
(Tuberculosis is a highly prevalent AIDS defining disease).
Constantine
et al: “The purpose of
serologic confirmatory tests is to rule out false-positive results by screening
tests, not to confirm that a person is unequivocally infected with HIV”.38
Since the antibody tests are the “proof” that “HIV”/AIDS has afflicted
and killed millions of people around the world but their specificity for “HIV”
infection has never been determined, how it is possible to measure the harm
done by all the “legitimate scientists, doctors and advocates”?
Bergman: “…the
current generation of antiretroviral drugs for HIV are effective”
There are NO randomised, double blind, placebo controlled
trials of ARVs. So after 28 years of
AIDS there is still no Level 1 evidence on the effects of ARVs on health or
survival. So much for “evidence-based”
AIDS medicine. Even if patients do improve
while taking ARVs, as witnessed for example by Joe Sonnabend, this does not
prove these drugs are “antiviral” or that HIV exists and causes AIDS.
A decade ago Giorgi wrote: “Of interest, if antiretroviral drug use did
affect survival in our study, the drugs did not seem to operate by effect on
CD4 cell count or virus load, since these values were not different in the 2
groups…Our finding that virus burden did not associate with survival time is
unlikely to be due to technical factors”.42 The “two
groups” were the long and short term survivors.
According to Mary Ann Chiasson, assistant
commissioner of the New York City Department of Health, improvements in AIDS
therapies may be “linked more closely to an increase in federal funding in 1994
for AIDS patients, which led to better prevention and treatment of opportunistic
infections”.76
Indeed, in the same year, Zaunders et al presented unequivocal scientific
evidence that any benefits of HAART cannot be the result of an “anti-HIV”
effect.77
Bergman: The makers of “House of
Numbers” deceived legitimate HIV researchers, infectious disease doctors, and
AIDS activists and philanthropists to get interviews with them..
Bergman paints a sorry picture of gullible yet highly
intelligent people. These scientists
typically work in large institutions, run large departments as well as face the
annual gauntlet of funding applications, with all the attendant politics. Bergman leads us to think they were so naïve they
did not know journalists seek all views on a subject. Perhaps the truth is they saw Leung as a
young man keen to find out as much as he could and most were more than willing
to share their knowledge. In their
eagerness they simply did not conceive Leung would seek anyone else’s point of view. In spite of the fact such views have been
published in peer-reviewed scientific journals and are on the internet. The deception is not Leung’s. Leung was just doing his job.
Bergman: These facts have been
established in laboratories, clinically, and by epidemiology, and published in
tens of thousands of peer-reviewed publications.
More catechism without evidence. Name a scientific paper that proves HIV
exists. Name a paper that proves “HIV”
Bergman: We have much still to learn about HIV and AIDS, and some
scientists don’t like each other, but no legitimate, qualified scientist or
doctor questions the existence or consequences of the virus.
The vast majority of scientists
and “qualified” doctors (are there unqualified doctors?) could not defend the
HIV theory of AIDS. Most doctors cannot
explain a Western blot test. Bergman seems to think adjectives such as “legitimate”
and “qualified”, applied to scientists, are all you need to prove HIV exists
and causes AIDS.
Bergman: Differences in diagnostic
criteria by region reflect lack of access to HIV testing technologies and
different clinical approaches: specifically, most African countries’ health
systems cannot afford HIV testing. That doesn’t mean that HIV doesn’t exist or
that poverty causes AIDS. Where HIV tests are not available, an AIDS diagnosis
obviously cannot include HIV status as an element of an AIDS diagnosis, so the
diagnosis is based on the presence of opportunistic infections that would only
afflict a person with a compromised immune system.
It is ridiculous to defend a diagnosis of AIDS, caused by
HIV, without evidence of HIV infection.
Would Bergman accept a diagnosis of syphilis without a test for Treponema pallidum? Would she accept a diagnosis of AIDS or HIV
infection in herself or a relative without an “HIV” test? The fact that testing is not available does
not alter this fact. Doesn’t Bergman
know that “immune deficiency” has been present in
Bergman: *Val
Turner MD
This is an artifact of test design and does mean HIV
infection differs from one country to another.
This statement loses Bergman or whoever is advising her all
credibility. Bergman appears quite
comfortable with the fact that diagnostic criteria for the virus that “gradually destroys the human immune system, resulting in
AIDS, a syndrome manifesting in various diseases…and ultimately death in people
with advanced HIV disease” varies by laboratory, institution and
country. This variation refers to the
designated and number of bands required for a positive Western blot “confirmatory”
antibody test. For example, a p24 and
p41 band is positive in parts of the
For Bergman’s interest, in 199481 we asked the Head of the Australian National
Serology Reference Laboratory for proof of the Australian criteria for a “confirmatory”
Western blot. Her response avoided answering
the question but nowhere did she even suggest it was “an artifact of test
design”. Perhaps Bergman could enlighten
her. http://www.theperthgroup.com/SCIPAPERS/VFTDax.pdf
Padian Endnote
Bergman and everyone else knows Padian’s study
required proof of the infection status of her cohort members. Without such proof her studies would be
meaningless. Like most epidemiologists,
Padian accepts on trust the antibody tests have proven specificity and rarely provides
details as to how the tests are interpreted.
The one exception was in her 1987 paper61 where she states: “The HIV serologic status was determined by a
commercially available enzyme linked immunosorbent assay test, and seropositive
results were confirmed by Western blot analyses.9” Reference 9 states a positive result was “the
presence of antibodies to p24 (core polypeptide) and/or gp41 (envelope
glycoprotein)”82. A single p24
or p41 Western blot band is not considered proof of infection anywhere in the
world. Hence the “evidence-based science”
is that unknown numbers of Padian’s cohort, which could be every person, are
not infected with “HIV”.
BACK
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