Following this I surmise Professor Weiss read the Montagnier
interview. In the meantime, believing that Weiss would not reply
(mistakenly and I must give Professor Weiss full credit for being the
only HIV protagonist who has taken the time to debate us), I emailed Rex
Ranieri, a documentarian from TV Channel Nine in Australia. He emailed
Weiss on 29th March:
Dear Professor,
I have been observing the HIV/AIDS debate with some interest and I
have recently been contacted by Val Turner. He have sent me some
questions which he has put to you recently together with the subsequent
email discussion .
It appears to me that the argument for the existence of HIV is not
sufficiently rigorous.
Is there a bigger story developing here?
I look forward to your reply
Kind regards,
Rex
Rex Ranieri
Channel 9
Perth, Western
Australia
rranieri@perthtv9.net.au
+61 8 9449 9999
Fax +61 8
9449 9905
Mobile 0411 258344
Professor Weiss replied immediately:
If HIV does not exist, then neither did smallpox virus (variola), nor
does polio virus, tobacco mosaic virus in plants, etc. etc. If you wish
to deny the existence of viruses, and virus diseases, go ahead, but
leave scientists like me out of the picture.
Robin A Weiss
To which Rex Ranieri replied:
Professor,
My understanding is that Dr. Turner and his colleagues have
questioned not whether a number of other viruses exist. Only HIV. As far
as I am aware, a scientist does not prove that a particular virus exists
by pointing to the existence of others.
I am well versed with some of the argument so far (for a lay person)
so naturally your response contributes little to my questions.
I appreciate your desire to be left "out of picture" however as you
are a world renowned researcher who has spent some time on the question,
it is difficult for me to accept that you can bow out of the
discussion.
Naturally, It is your perogative not to respond, however I think that
this would ultimately be damaging to both sides of the argument. We have
seen many examples of media debacle which can result from lack of
discussion.
I realise that your time is valuable and I urge you to respond to my
questions. Please accept that my intentions are to arrive at the truth,
whatever that may turn out to be.
Kind regards,
Rex
Weiss responded to this email approximately two months later (see
Addendum III).
Meantime I sent reminder emails to Weiss. Eventually he replied:
March 26th
I am very tied up with work at present and will give you a considered
reply in due course.
Robin A. Weiss
I responded:
Dear Professor Weiss,
Thank you for your reply. I fully understand that you have been busy
moving from Fulham Road to Clevland Street and setting up your new
department. I am also sure that you understand how anxious both my
clinical and non clinical colleagues and I are to examine your
considered reply.
Yours sincerely,
VF Turner
After more reminders Weiss emailed me:
April 15th
Dear Dr Turner
You have breached my correspondence with you as an academic colleague
by forwarding it to a journalist, Rex Ranieri. In your message to him,
you write that that you do not hold any great hope that I shall answer a
second time, and yet to me you express your understanding that I'm busy
with other things. So here is my second response. I hope it is my last
response, because I find the issue of 'purification' quite sterile, and
unconnected with matters of medical importance. We are simply talking at
cross-purposes.
There appears to be a consortium of medical people and biophysicists
in Perth who have a fixation of HIV purification. Perhaps you are
influenced by this. It is also a 'cause' championed by the British based
magazine 'Continuum' founded by Jodi Wells whom I knew and who sadly
died of an AIDS-like disease a few years ago. He initially supported
Peter Duesberg's view that HIV indeed exists and can be purified, but
that it is harmless. Then he shifted into a denial that there is any
such thing as HIV. With Harold Jaffe I argued against Duesberg's view in
Nature nearly 9 years ago (Nature 345: 659-660, 1990). I've nothing more
to say on this issue, save that with the efficacy of combination
anti-retroviral drugs, Duesberg seems to have lost his constituency of
support among 'lay' gay men.
Now, to turn to your points sent on March 10 regarding my first
reply:-
1. and 2. You confuse isolation and purification. I see no
contradiction between what I wrote - in 1986 or in 1999 - and what
Barre-Sinoussi and colleagues had reported previously. One can isolate
some viruses by propagating them in cells in culture. For example, HIV,
smallpox virus, measles virus, polio virus. There are other viruses
which no-one has yet succeeded in serially propagating in culture
following isolation because they require specialized, differentiated
cells; for example, hepatitis B virus, human papilloma virus types 16
and 18 (associated with cervical cancer), and so on.
In both cases, viral genomes can be isolated, indeed highly
'purified' by molecular cloning using recombinant DNA methodology. Thus
it is almost routine now in our lab and may other research labs to clone
the HIV genome as DNA in bacterial vectors, and then recover them again
in infectious form by transferring that DNA back into human lymphocytes.
It is difficult to conceive anything 'purer' than the complete cloned
virus without any proteins, particles, etc.
3. I do not think Barre-Sinoussi et al misled the scientifically
community by calling the 1.16 g/ml band purified virus. But if you and
your colleagues prefer to call it enriched but not yet completely pure,
I would happily concur with that opinion. This illustrates what I mean
by a sterile argument: how pure is pure? Is distilled water 'pure'? Yes,
but it will still have a few parts per million or per billion of other
soluble molecules.
Are your surgical instruments sterile? Yes regarding bacteria and
viruses, if they have been heat-treated or autoclaved. No, regarding the
agent of Creuzfeld-Jakob disease which partially resists such treatment.
Yet, every surgeon knows what others mean by sterile. Let's not get
bogged down in how pure is pure.
The important thing is serial propagation of the microbe. Koch and
Petri over 700 [70] years ago 'purified' bacteria by propagating them as
colonies (clones) on gelatin in Petri's dishes - nowadays we use
agar-agar with nutrients in place of gelatin. Did Koch purify the
microbes. Yes in his and my terms, maybe not in yours. Certainly he did
purify [?not] them by biophysical methods such as sucrose gradients, but
nothing else kept reproducing itself on the 'impure' nutrients. So it is
the same for viruses. As intercellular [intracellular] parasites, of
course, they can only be propagated in living cultured cells (or in
plants, animals or humans) but one can 'plague-purify' them - a term
dating from early bacteriophage studies in the 1920s. Animal viruses
were similarly plague-purified: polio in 1952; vaccinia around 1955. We
used a plaque 'purification' or biological cloning technique for HIV in
1989. No, these were not physically pure, but they were biologically
pure, ie they were cloned. Molecular cloning, however, as I mentioned
already is one step better. Both methods to my mind, are sufficiently
purified to draw scientific conclusions, although one must be cautious
not to draw conclusions beyond the validity of the data, including the
kind of purity, biological, molecular, chemical or physical.
4. My definition of isolation of HIV by Barre-Sinoussi et al. Gallo
and Levy and others in the early days of AIDS research is propagation in
culture. Today, however, we more often use molecular cloning, then
recover the cloned genome or partial genome and characterise its
phenotype.
5. Yes, I do claim that visualization of HIV by electron microscopy
was, in 1983/84, an important component of the collective data on virus
isolation. Taken together with virus propagation, reverse transcriptase
activity and enrichment of particles by isopycnio [density] gradients,
it convinced me that HIV is a retrovirus. Even more so, it was
Montagnier's electron micrographs published in April 1984 and previously
shown at Cold Spring Harbor Laboratory in September 1983 that convinced
me that HIV was probably a lentivrius among retroviruses, as they
resembled particles of equine infections anaemia virus - a lentivirus
first propagated by inoculating a filtrate too small for bacteria to
pass through into horses and donkeys and causing disease. So yes, I am
definitely arguing that, disregarding your meaning of 'purification',
but with my meaning of 'isolation', you can make quite large amounts of
HIV proteins and smaller amounts of RNA.
6. Barre-Sinoussi et al published electron micrographs of early
budding forms of virus only, that were not immediately identifiable as
retrovirus particles. By September 1983, Montagnier's electron
micrographs looked more typical.
7. There are many different tests for HIV-specific antibodies.
Today's commercial test kits are based on oligopeptides and on proteins
manufactured from cloned HIV DNA. No biological test for anything is
100% specific and 100% sensitive, but today's HIV tests are as good as
tests for any other human viral pathogen. Likewise, today's PCR primers
are highly specific and sensitive for the major strains of HIV in
developed countries. Some 'outlier' strains, especially in Gabon and
Cameroon are not picked up quite as sensitively and therefore estimates
of viral load with these 'outlier' infections should be interpreted
cautiously.
There will always be a few people who cannot be convinced by the data
before our eyes - or who emotionally wish to deny what the rest of us
regard as facts. Of course, interpretation will change over time.
Newetonian physios still serves pretty well for the dynamics of road
accidents, but Einstein's relativity superseded it on a cosmic scale. In
my view, to deny the existence of HIV is a bit like denying the Nazi
holocaust.
If we are to doubt HIV as a cause of AIDS, we must cast even more
doubt on variola as a cause of smallpox, and the existence of measles,
mumps, influenza and respiratory syncytial virus. None of these would
pass your definition of purification. None of these has been 'purified'
even by culture propagation (my sense) to the extent that has been
achieved for poliovirus and for HIV.
This terminates our debate.
Robin A Weiss
Although Professor Weiss terminated the debate, my colleagues and I
were far from satisfied. Eleni Papadopulos and I spent many weeks
preparing a response (see below). This was sent in late July with the
following note:
22/7/99
Dear Professor Weiss,
I apologise for the length of the attached file [35 pages] but it is
impossible to debate this topic without data and citations. I trust you
appreciate this necessity.
I greatly appreciate your reply to the questions in my last email.
Let me say that eighteen years ago neither I nor my colleagues in the
Perth Group set out to frustrate the efforts of scientists such as
yourself. Rather, we began as you and many others did in the early
1980s, to make a contribution to solving the problem of AIDS. Certainly
we are poles apart from the mainstream but, as Philebus says in the
Dialogues of Plato, I hope "we are not simply contending in order that
my view or that of yours may prevail, but I presume we ought both of us
to be fighting for the truth"..
I am disappointed that you do not intend to continue the exchange but
I respect your decision. Sometime in the near future I intend to put our
debate on the Perth group website. Thus, if you would like to add or
alter your replies in any way I will encompass these in the posting. If
you would like to contribute anything else at all, scientific or perhaps
philosophical including your views on dissent and dissenters, I would be
very pleased to post these as well.
I look forward to hearing from you once again.
Yours sincerely,
VF Turner
31/8/99
Dear Dr Turner
I have been in your country during August without opening my e-mails.
We shall have to agree to differ on the nature and existence of HIV. I
have no additional comments to make for your website.
Robin A Weiss
My response to this was:
1/9/99
Dear Professor Weiss,
Thank you for your email. I am truly sorry you are unwilling to
continue the debate. Eleni Papapdopulos and I spent several weeks
preparing what I consider a worthy reponse and believe it your
responsibility to answer the points I have raised. This especially
applies to the arguments related to the extant HL23V. As far as I can
tell evidence for the the "isolation" and thus the existence of HL23V is
better than that for HIV. Yet HL23V has disappeared from the scientific
literature and no longer exists.
I am disappointed you did not look us up while you were in Australia.
My colleagues and I would have been delighted to take you out for a meal
in Perth's Kings Park overlooking the Swan River. We have some excellent
wines which I am sure you would have appreciated. We would have enjoyed
your company and the invitation is open should you ever return.
I would like to thank you once again for your time and effort on
behalf of this debate. This is not a polemic about any particular person
winning. Any fighting is about "fighting for the truth".
Yours sincerely,
Val Turner
REPLY TO PROFESSOR R WEISS BY DR. VF TURNER OF THE PERTH GROUP
JULY 21ST 1999
Dear Professor Weiss,
Scientists should be particularly hard on hypotheses. An hypothesis
must explain and predict everything. For example, the HIV theory has to
explain why, in Western countries, HIV/AIDS has remained in the original
risk groups. It is claimed that HIV/AIDS is spread predominantly by
sexual contact of one kind or another and "everyone is at risk" from "a
virus that does not discriminate". But prostitutes who do not use drugs
are not infected with HIV. In Australia for example, a decade after the
beginning of the AIDS era, the number of prostitutes infected by sexual
intercourse, despite their being "seriously at risk of HIV infection",
was zero. In 1994, Manaloto reported on the "Natural history of HIV
infection in Filipino females commercial sex workers". Over seven years
72/53,903 (0.01%) were found to be HIV positive and "Intravenous drug
use was denied in all cases". We can take a step further and examine an
instance where we can be sure of unprotected sexual intercourse in
heterosexuals, that is, new born babies. Again in Australia, in 1989 a
study testing 10, 217 blood samples of newborn babies found no babies
and thus presumably none of their mothers or fathers HIV positive. These
data are supported by Nancy Padian and colleagues’ ten year study of
heterosexual couples (1986-1996). There were two parts to this study,
one cross-sectional, the other prospective. Of the HIV negative male
partners of 82 positive female cases only 2 were found HIV positive but
under circumstances considered ambiguous by Padian. In the prospective
study, starting in 1990, 175 HIV-discordant couples were followed for
approximately 282 couple-years. At entry, one third used condoms
consistently and in the six months prior their last follow up visit, 26%
of couples consistently failed to use condoms. There were no
seroconversions after entry including the 47 couples not using condoms
consistently. Based on the 2/86 men who became HIV positive in the early
study, the risk to a non-infected male from his HIV positive female
partner was reported to be in the order of 1/9000 per contact. From this
statistic one can calculate that on average, a male would need to have
6000 sexual contacts with an infected female to achieve a 50% chance of
becoming HIV positive. If sexual intercourse were to commence at age 20
and average three times weekly, this would occupy a lifetime; If
heterosexual men so rarely become infected how do heterosexual women
become infected?
Despite the fact that HIV/AIDS experts continuously assert that
epidemiology proves HIV causes AIDS, in my view epidemiological data are
incapable of proving anything . But such data may prove scientifically
useful when inconsistent with the predictions of a particular theory. As
the above data amply illustrate. Thus, in my view and our Group, unless
we entertain extraordinary properties for a putative infectious agent,
it is obligatory for scientists to question the HIV theory of AIDS. Or,
as Simon Wain-Hobson expeditiously put it, "a virus's job" is to spread.
"If you don't spread, you're dead". I could not agree more. Inevitably,
an exercise of this sort leads Homo sapiens to question what the
antibody and genomic tests are measuring. How have their specificities
for a unique, infectious agent been determined and what are they? Since
these tests purport to use "HIV" proteins and RNA (cDNA) as diagnostic
reagents, and since viruses are obligatorily cultured in cells where one
would expect to find hundreds if not thousands of cellular proteins,
RNAs and DNAs, we would expect there to be proof that HIV had been
purified. Otherwise it would be impossible to claim that certain
proteins, RNA or DNA are unique constituents of a retrovirus HIV.
However, the data of Montagnier, Bess and Gluschankof, all HIV
protagonist experts, prove there is no such thing as purified HIV and,
according to you, "purification is not particularly important" and
Montagnier was right "to say it was not purified virus". These being the
case we are left wondering on what basis scientists such as yourself
accept that there is such a retrovirus as HIV. This, of course, is what
you and I are presently debating. I am sure we can at least agree that
without HIV there can be no HIV theory.
Since your definition and understanding especially, but not only of
purification, isolation, virus, viral cloning are different from mine, I
concur we are "talking at cross-purposes". Where we do seem to agree is
on the importance of medical issues, although we seem to disagree
exactly what constitutes these medical issues. You state, "I find the
issue of purification quite sterile, and unconnected with matters of
medical purposes". However:
(a) for more than 15 years
(i) the world has been made to believe that Barré-Sinoussi,
Montagnier and their colleagues claim to have proven the existence of a
unique retrovirus, HIV, by purifying it using "isopycnic gradients";
(ii) in 1997 Montagnier admitted that the 1.16g/ml band in their
isopycnic gradients which they claimed to have proven was "purified
labelled virus" did not contain even retrovirus-like particles. Yet,
this "purified" virus is accepted as being the cause of the black plague
of the century;
(iii) in the name of this virus hundreds of thousands of individuals
have died and the lives of millions of people have been adversely
affected either directly or indirectly.
Surely these are "matters of medical importance"?
(b) According to Montagnier, "analysis of the proteins of the virus
demands mass production and purification. It is necessary to do that.
And there I should say that we partially failed". In fact I venture that
Montagnier totally failed since the proteins and the RNA which he and
his colleagues named HIV proteins and RNA were taken from an isopycnic
gradient (the 1.16g/ml band) which they called "purified labelled
virus", but where, even after a "Roman effort", they could not find even
particles with the "morphology typical of retroviruses", much less
retrovirus particles, not to mention a specific retrovirus, HIV. The
claim that some of the proteins in this "purified labelled virus" were
HIV proteins defies not only scientific reasoning but commonsense. This
is no different from a fisherman claiming to have processed a catch of a
totally new species of fish into unique fish proteins when his net
contained anything but "fish-like" objects, or me as a surgeon going
into an operating room where there are many types of animals, but none
which look human, removing a few hearts and kidneys, transplanting them
into humans in an adjacent operating room and claiming the transplanted
organs were of human origin. Yet:
(i) In the name of one of these "HIV proteins", reverse
transcriptase, (based solely on the detection of which many researchers
publish papers claiming "HIV isolation"), hundreds of thousands of
individuals have been treated for more than 10 years with toxic
drugs;
(ii) In the name of another of these "HIV proteins", protease, in the
last few years even more toxic "cocktails" of drugs have been used;
(iii) Since 1984, in the name of yet another "HIV protein", gp120,
hundreds of millions of dollars have been spent to develop a vaccine
which it is said will be especially useful in the developing countries
where the majority of AIDS cases are tuberculosis. It is the first time
in medical history that a vaccine based on a protein said to be a
retroviral protein, but which never has been shown to be a constituent
of even a retrovirus-like particle, is going to be used to prevent a
disease caused by a bacterium.
(iv) In the name of an antibody test employing these "HIV" proteins
as antigens, millions of people have been told that they are infected
with a lethal retrovirus;
(v) A stretch of RNA (or its cDNA) which never has been shown to be a
constituent even of a retrovirus-like particle much less of a retrovirus
is used as a hybridization probe and PCR primer to prove infection with
a retrovirus claimed to be deadly, and in fact to quantify it.
Surely these also constitute "matters of medical importance"?
For physicians like me, stranded between laboratory scientists and
patients, the meaning of the antibody test and the "viral load" are of
extreme "medical importance". And whether they are aware or not, for
"lay" gay men, drug users, haemophiliacs, blood transfusion recipients,
pregnant women and their offspring, and all their relatives, these are
also matters of extreme "medical importance".
As far as I am aware there are two groups of "anti-retroviral drugs".
The reverse transcriptase inhibitors which are said to prevent the
reverse transcription of "HIV RNA" into "HIV DNA", and the protease
inhibitors which are said to render particles non-infectious. In other
words, the effect of both groups of drugs is to decrease the synthesis
of new "HIV DNA", that is, to decrease the amount of provirus. Since
none of the "anti-retroviral drugs" used to date has any effect on the
transcription of "HIV DNA" into "HIV RNA", a decrease in the latter, the
"viral load", must always be preceded by a decrease in the former (the
"viral burden"). This is not the case. While many studies report
"anti-retroviral" treatment decreases the viral load from millions to
undetectable levels, the "HIV DNA" remains constant. In a study
published this year "of 34 patients on combination therapy who had
plasma HIV-1 RNA levels of less than 200 copies/ml,
replication-competent virus was isolated" from 32 (94%). In longitudinal
studies it was shown that the frequency of isolation did not depend on
the length of combination therapy or the time it was started. Compare
this with the 37% frequency of isolation by the best HIV laboratories of
non-treated patients in a 1994 WHO study. This can be explained by one
or more of the following:
(a) The proviral theory is wrong, that is, there is no relationship
between "HIV DNA" and "HIV RNA"
(b) Either "HIV DNA" or "HIV RNA" or both have nothing to do with a
retrovirus;
(c) The drugs have no anti-retroviral effect, they only mask the
measurement of "HIV RNA".
I venture to say that your present enthusiasm for "combination
anti-retroviral drugs" is matched only by your former enthusiasm for
AZT. However, there are at least two reasons why this drug should never
have been introduced into clinical practice and while its continued use
should be abandoned. First and foremost, the pharmacology of AZT proves
beyond all reasonable doubt that AZT cannot act as a reverse
transcriptase inhibitor, DNA chain terminator. Secondly, even before the
AIDS era it was known that AZT is very toxic.
The Concorde study, the only truly clinical blind study, has
vindicated both John Lauritsen's and Peter Duesberg's claims that AZT
instead of saving lives may endanger them.
In another study published this year by Italian researchers, the
authors followed up, for the first three years of life, HIV seropositive
children born to mothers who either did or did not receive AZT
treatment. The two groups of children were similar with respect to all
variables (year of birth, maternal clinical condition, birth weight and
treatments) apart from age at the beginning of PCP chemopropylaxis,
which was undertaken earlier in these children who were born to mothers
who took AZT. They found that the children born to these mothers "had a
higher probability of developing severe disease" (57.3% versus 37.2%) or
severe immune suppression (53.9% versus 37.5%) and a lower survival
(72.2% versus 81%)".
Given these findings any disinterested scientist, clinician, layman,
even politician would advise against the administration of AZT to
pregnant women. But not HIV/AIDS experts. The authors of this study
concluded: "Findings may suggest a need to hasten HIV-1 diagnosis in
infants of ZDV-treated mothers and undertake an aggressive
anti-retroviral therapy in those found to be infected", and "should not
be misinterpreted as a reason not to use ZDV prophylaxis, which is
effective in preventing perinatal HIV-1 infection". However, since as
the authors of this study claim, "A strong association exists between
high maternal viral load and an increased risk of transmission" and
since none of the many studies conducted to date has shown a decrease in
viral load by AZT, it follows that AZT cannot inhibit maternal
transmission. In the face of such data the authors' conclusions and
recommendations amply illustrate to what lengths some scientists will
strive not to question the HIV theory. If you can offer any other
rational explanation I would be most grateful to hear it.
According to Professor Brian Gazzard, President of the British HIV
Association, treatment with AZT monotherapy is "ludicrous". Yet not only
is AZT monotherapy prescribed to mothers and mothers who object to this
treatment for their children are threatened with having their children
taken from them. Your enthusiasms for combination therapy is shared
neither by the physicians who prescribe it nor by the "lay" gay men who
take it. "As physicians venture into even wilder frontiers of HIV
treatment, the grand experiment with combination therapies, called
Highly Active Anti-Retroviral Therapy, or HAART, is rushing forward
without any data. No-one is keeping track". Apparently one of the few
physicians, if not the only one who tries to make any sense of HAART is
Michael Saag who supervises research and the care of more than one
thousand AIDS patients in Birmingham, Alabama. "In one year, 157 of
Saag's patients collectively took 189 different drug formulas, with only
three patients taking the same mix of HAART drugs…despite such rigorous,
individualized medical attention, Saag says, the HAART 'dam' is already
leaking and there's high danger of it collapsing altogether...Failures
are occurring right and left".
According to Dr Wafaa El-Sadr from Harlem Hospital "it takes a heap
of denial to reach anything but sobering, even grim conclusions"
regarding HAART. Let me also quote a few gay men, who, unlike the
courageous Jodi Wells and the equally courageous and well informed
present editors of Continuum, are not in "denial" regarding the
existence of HIV. "Anything they give me, I suspect would simply create
more side effects and then fail after only a few months, leaving me in
even worse shape than I'm now. As my doctors see it, being of therapy is
doing nothing, and doing nothing is what scares them most...So when they
tell you all is well, they may be doing it less for you than for
themselves" (Stephen Gendin POZ Magazine, January 1999). "None of us
would say that having access to the best available scientific
information every step of the way has helped us
particularly...professional judgement has consistently been way out in
front of evidence. We're going to have to rethink everybody". Saag
agrees: "We don't know what we are doing. Hubris! Hubris! We need to be
scientists every step of the way and do our darndest to seek what
reality is". If the claims for actual reality of HIV are also based on
professional judgement rather than evidence we are indeed guilty of
arrogant presumption and must expect nemesis.
Thus, in your position, I would not uphold "anti-retroviral drugs"
either in support of the HIV theory of AIDS or the existence of HIV. The
only rational conclusion one can draw from the "anti-retroviral"
treatment data is either there are no such drugs or there is no such
thing as a retrovirus, HIV. (Additional data on PIs is at the end of the
reference section*)
Bearing all this in mind, I would like to comment point by point on
your answers regarding claims for the existence of HIV.
ANSWER 1 AND 2
My questions were:
1 Why, in 1986, did you and your colleagues write: "A so-called AIDS
virus isolate was first reported in 1983 by Montagnier and his
colleagues in France who named the material "Lymphadenopathy Associated
Virus One". Did or did not Montagnier isolate, purify a retrovirus?
2. If he did not why did you say that he had? If you were aware that
he did not do this, and this was the reason for you using the word
"material" to describe his finding, why did you not, as a well known and
respected retrovirologist, draw the attention of the rest of the
scientific community to it, especially if one considers the extremely
important consequences?
Your answer was:
You confuse isolation and purification. I see no contradiction
between what I wrote - in 1986 or in 1999 - and what Barre-Sinoussi and
colleagues had reported previously. One can isolate some viruses by
propagating them in cells in culture. For example, HIV, smallpox virus,
measles virus, polio virus. There are other viruses which no-one has yet
succeeded in serially propagating in culture following isolation because
they require specialized, differentiated cells; for example, hepatitis B
virus, human papilloma virus types 16 and 18 (associated with cervical
cancer), and so on. In both cases, viral genomes can be isolated, indeed
highly 'purified' by molecular cloning using recombinant DNA
methodology. Thus it is almost routine now in our lab and many other
research labs to clone the HIV genome as DNA in bacterial vectors, and
then recover them again in infectious form by transferring that DNA back
into human lymphocytes. It is difficult to conceive anything 'purer'
than the complete cloned virus without any proteins, particles, etc.
My response:
I do not accept isolation and purification as being different. The
word "isolation" means to place apart or alone. (From Latin "insulatus",
made into an island). "Purification" means to obtain something free from
impurities. For a particle such as a virus, isolation and purification
are the same thing. The act of placing an object apart or alone,
isolation, is totally different from multiplying, transmitting, that is
propagating that object. The fact that something can be multiplied or
propagated through many generations of cultures neither means that it is
any more or less isolated nor that you are any more aware of its
identity. No object including a virus can be isolated by propagation.
You, more than anybody else, know that there are some very significant
differences between retroviruses and other viruses. The subject of
interest for you and me is HIV. It is of no interest what methods have
been used to prove the existence of other viruses and whether they are
good or bad. What is sufficient for one group of viruses may not be
sufficient for another. What we all want to know is whether the methods
and the evidence which are claimed to prove the existence of HIV and
thus of its proteins and its genome, do so. To claim propagation of a
unique retrovirus, HIV, one must first prove its existence which can be
done only by isolating, purifying it. To date, nobody, not even you, has
achieved this.
By molecular cloning it is meant the production of identical copies
of, for example, a DNA molecule, any DNA molecule, from an ancestral
molecule by splicing it into a suitable cloning vehicle, for example a
bacteriophage. The DNA molecules can be either of viral or cellular
origin. Or they could be artificial. The molecules within the
bacteriophages can, in their turn, be introduced in any cells. If you
want to call these molecules an "infectious form" (I will not) then you
must accept that any piece of DNA, no matter what its origin, is an
"infectious form".
Unquestionably, by molecular cloning one can obtain large amounts of
"purified" DNA, but equally unquestionable is the fact that molecular
cloning tells you nothing about the origin of a particular DNA molecule.
To clone "the HIV genome" one must know beforehand that a particular DNA
is the HIV genome. In other words, one must start with "HIV RNA"
which can be obtained only by prior purification of particles proven to
be retroviral particles. Since this has not been achieved, then what is
the origin of the DNA fragment which is known as the "HIV genome" which
you routinely clone in your lab? If you are using "material" similar to
that used by Montagnier in 1983, in which there is no proof there were
even retrovirus-like particles, then surely nobody, not even you, can
claim this RNA (cDNA) is the genome of a retrovirus, not to mention a
unique retrovirus, HIV.
As an undergraduate medical student I was taught that viruses are
infectious particles of particular morphologies containing nucleic
acids, proteins and lipids. According to all other retrovirologists
including Montagnier, Gallo and Gelderblom, retroviruses are particles
with a diameter of 100-120nM containing "condensed inner bodies (cores)"
and surfaces "studded with projections (spikes, knobs)". If, unlike
other viruses, HIV consists of nothing else but an "infectious form" of
DNA molecules (as you claim: "It is difficult to conceive anything
‘purer’ than the complete cloned virus without any proteins, particles,
etc"), then why do all other retrovirologists, without exception, claim
that the gp120 protein is absolutely necessary for HIV infection? If HIV
is nothing else but a pure nucleic acid molecule (RNA) "without any
proteins", then why is there so much effort, not to mention expense, to
develop a vaccine based on the "HIV" proteins?
ANSWER 3
My question was:
In 1983, when B-S et al published their paper entitled, "Isolation of
a T-lymphotrophic retrovirus from a patient at risk for acquired immune
deficiency syndrome (AIDS)", and called the 1.16g/ml band "pure labelled
virus", did they mislead the scientific community?
Your answer was:
I do not think Barre-Sinoussi et al misled the scientific community
by calling the 1.16 g/ml band purified virus. But if you and your
colleagues prefer to call it enriched but not yet completely pure, I
would happily concur with that opinion. This illustrates what I mean by
a sterile argument: how pure is pure? Is distilled water 'pure'? Yes,
but it will still have a few parts per million or per billion of other
soluble molecules. Are your surgical instruments sterile? Yes regarding
bacteria and viruses, if they have been heat-treated or autoclaved. No,
regarding the agent of Creuzfeld-Jakob disease which partially resists
such treatment. Yet, every surgeon knows what others mean by sterile.
Let's not get bogged down in how pure is pure. The important thing is
serial propagation of the microbe. Koch and Petri over 70 years ago
'purified' bacteria by propagating them as colonies (clones) on gelatin
in Petri's dishes - nowadays we use agar-agar with nutrients in place of
gelatin. Did Koch purify the microbes. Yes in his and my terms, maybe
not in yours. Certainly he did purify them by biophysical methods such
as sucrose gradients, but nothing else kept reproducing itself on the
'impure' nutrients. So it is the same for viruses. As intracellular
parasites, of course, they can only be propagated in living cultured
cells (or in plants, animals or humans) but one can 'plaque-purify' them
- a term dating from early bacteriophage studies in the 1920s. Animal
viruses were similarly plaque-purified: polio in 1952; vaccinia around
1955. We used a plaque 'purification' or biological cloning technique
for HIV in 1989. No, these were not physically pure, but they were
biologically pure, ie they were cloned. Molecular cloning, however, as I
mentioned already is one step better. Both methods to my mind, are
sufficiently purified to draw scientific conclusions, although one must
be cautious not to draw conclusions beyond the validity of the data,
including the kind of purity, biological, molecular, chemical or
physical.
My response:
We cannot call Barré-Sinoussi's 1.16g/ml band pure or even "enriched"
since the scientists who prepared the material conceded it contained no
retrovirus-like particles, much less the particles of a unique
retrovirus. Perhaps it is inconceivable to you that Montagnier made this
admission. In that case let me present you with the actual transcript
from the videotape given to me by Djamel Tahi, the French investigative
journalist who conducted the interview at the Pasteur Institute in July
1997. Montagnier was asked, "Pourquois les photographies du EM publiées
par vous, proviennent de la culture et non de la purifcation?"
Montagnier's reply was: "Il y avait tellement peu de production que
c’était impossible de voir soit dans un culot de virus à partir d'un
gradient. Il n'y avait pas assez de virus pour faire ça. Bien sûr on l'a
cherché, on l'a cherché aussi dans les tissus de départ, de la biopsie
également. On a vu des particules, mais elles n'avaient pas la
morphologie typique des retrovirus. C’était trés différent...
relativement différent. Donc avec la culture il a fallu beaucoup
d'heures pour trouver les première images. C’tait un travail de
romain".
Consider your analogy of pure water. Suppose you are doing a vital
experiment which requires pure water. Your colleagues on the floor above
provide a bottle labelled "pure water" which forms a critical part of
your experiment and ultimately the results of this experiment are used
in a way which affects the lives of millions of people. Fifteen years
later you are informed that the bottle your colleagues gave you, far
from being pure water, contained not even one molecule of water. Would
you not think that your colleagues were wrong to label it "pure water"
and that they had misled you? Would you then be happy to call it water
enriched?
It is not valid to argue that the technique of Koch and Petri
justifies the method used to prove the existence of HIV. They did not
define purification or, if you like, isolation as "propagation in
culture", as you do. They did not "purify them" by biophysical methods
such as sucrose gradients because this method is a much later invention
and is not even necessary. In their cultures Koch and Petri had gelatin
plus particles which could be unambiguously identified as bacteria using
the light microscope. Any proteins (other than gelatin) RNA or DNA found
in the culture could only be of bacterial origin. Any biological effect,
including a plaque produced by an aliquot from this culture which is not
produced by gelatin alone must be induced by the bacteria. But it is not
the "same for virus", especially retroviruses. Unlike the bacteria,
dishes which in addition to bacteria contain only one known protein,
gelatin, the "HIV" dishes contain cells, cellular fragments and perhaps
bacterial fragments as well as mycoplasmas and viruses. As far as the
presence of HIV is concerned, it is sufficient to mention that some
electron micrographs of culture supernatants have shown some particles
with some of the morphological characteristics, but no particles with
all of the morphological characteristics of mature retroviruses.
Even assuming that the particles were those of a unique retrovirus,
the proteins and RNA present in the culture or even the culture
supernatant cannot be assumed to belong to the virus. Induction of a
biological effect by the culture supernatant including "plaque" need not
be due to the virus, but to any of the many other factors present. I am
not aware of any publications describing "plaque 'purification' or
biological cloning technique of HIV in 1989". I would be interested to
know how one can know that a "plaque" or any other biological effect is
induced by a specific object without prior proof for its existence.
"Plaque" and other biological effects are induced by addition and
interaction while isolation (purification) is a process of subtraction
and separation. Biological effects including plaque can be used only to
detect a retrovirus, and then, if and only if, there is a prior
knowledge they are specific to the retrovirus, which can be done only by
first isolating the virus.
I agree with you that one must be cautious not to draw conclusions
"beyond the validity of the data". However, unlike you, I believe that
the claim for the existence of HIV is based on interpretations which go
far "beyond the validity of the data".
ANSWER 4
My question was:
Since it is generally accepted, and makes common sense, that the
existence of a new retrovirus can be proven only by isolating it (both
B-S and Gallo claimed to have proven the existence of HIV by isolating
it) what is the scientific basis for your claims that B-S et al
discovered a new retrovirus?
Your answer was:
My definition of isolation of HIV by Barre-Sinoussi et al. Gallo and
Levy and others in the early days of AIDS research is propagation in
culture. Today, however, we more often use molecular cloning, then
recover the cloned genome or partial genome and characterise its
phenotype.
My response:
In 1983 Barré-Sinoussi et al, in the T cell culture derived from the
lymph nodes from a patient at risk of AIDS, detected reverse
transcriptase activity. The cells from this culture were cultured with T
cells from a healthy donor whereupon the detection of reverse
transcriptase activity in this second culture was considered proof for
isolation of a retrovirus which originated from the patient. Detection
of reverse transcription, even if detected in thousands of consecutive
cultures is not proof for the isolation of the enzyme reverse
transcriptase, much less the isolation of a unique retrovirus, HIV. 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. In fact, detection of reverse transcription is
not even proof of reverse transcriptase as other enzymes ably perform
the same task.
Reverse transcription is non-specific. Indeed, in 1996 you wrote:
"Now we know that a broader group of genetic elements than retrovirus
utilise reverse transcription at some stage of replication; these
include hepadnoviruses (including hepatitis B virus), cauliflower mosaic
virus and retrotransposons of eukaryotes and prokaryotes". If this is
the case, given the right conditions, one would expect to detect reverse
transcription in all cultures, irrespective of the presence or absence
of a retrovirus. Then, surely you would agree that the finding of
reverse transcription is not even proof for the detection of a
retrovirus, much less its isolation, even if one uses your definition.
In 1984, Levy et al cultured cells from patients with Kaposi's sarcoma a
disease which everybody agrees is not caused by HIV. The supernatants
were tested for RT activity, the cells for reactions with serum from
Barré-Sinoussi's patient BRU. Some cultures were examined by electron
microscopy. The finding of a positive result with "any of those tests"
was considered proof for HIV isolation.
In 1984 Gallo said that Montagnier's group data did not constitute
proof for isolation, and defined isolation as the detection of more than
one of the following:
"reverse transcriptase activity in supernatant fluids;virus observed
by electron microscopy [retroviral particles in the cultures];
intracellular expression of virus-related antigens detected with
antibodies from seropositive donors or with rabbit antiserum to
HTLV-III; or transmission of particles". By transmission of particles
was meant detection of reverse transcriptase or particles in cultures of
"human cord blood, bone marrow, or peripheral blood T lymphocytes",
cultured with concentrated fluids from the cell cultures from tissues
obtained from AIDS patients.
However:
1 As can be seen for Gallo et al, like for Barré-Sinoussi et al, the
detection of reverse transcription in two consecutive cultures is proof
for isolation, although a decade before the AIDS era Gallo himself
reported such activity in normal cell cultures. In the AIDS era such
activity was reported in the non "HIV" infected H9 cell line from which
Gallo "isolated" HIV as well as many other cell lines used to "isolate
HIV" and normal cell cultures.
2. Alternatively, according to Gallo's criteria, HIV can be
"isolated" in the absence of reverse transcriptase activity, considered
by Gallo to be the "sine qua non" of a retrovirus.
3. It is impossible for "rabbit antiserum to HTLV-III [HIV]" to
predate proof for the existence of, and pure HIV. It makes no sense at
all for Gallo to claim use of an antiserum to prove the existence of a
virus when the production of that antiserum is totally dependent on use
of the same, purified virus.
4. From the interaction of a protein with an antibody it is
impossible to determine the origin of the protein or the antibody. From
such a reaction one can determine the origin of only one of the
reactants, and then if, and only if, the origin of one of the reactants
is known and if there is proof that the interaction is specific. The
specificity of such reaction between the "HIV" proteins and antibodies
present in patient sera can be proven only by using HIV isolation,
purification as a gold standard. Gallo et al claim that the interaction
between proteins present in the cells and antibodies in the patient sera
proves not only that the proteins and antibodies are HIV protein and
antibodies, but the detection of such reaction together, for example
with reverse transcription proves HIV isolation. In fact, Gallo has
conceded that for him, an antibody test is the quintessence of "HIV
isolation". Interviewed in camera by Hugh Christie at the 1998 Geneva
AIDS conference he answered, "Sometimes we had Western blot positive but
we couldn't isolate the virus. So we got worried and felt we were
getting false positives sometimes so we added the Western blot [sic].
That's all I can tell you. It was an experimental tool when we added it
and for us it worked well, 'cos we could isolate the virus when we did
it". In other words, Gallo knew full well that to prove the specificity
of the antibody test it was essential to isolate the virus. When he saw
no correlation between antibodies and virus "isolation" Gallo resolved
the dilemma by defining virus "isolation" to include the Western blot
antibody test.
5. Both groups, Gallo’s and Montagnier’s, found proteins in
non-infected cells which reacted with sera from the AIDS, patients.
6. Gallo’s claim for proof of isolation that the findings of
particles in the culture supernatants of two consecutive cultures, or in
one culture together with reverse transcription or antigen/antibody
reactions is puzzling. A decade earlier, Gallo warned that "Release of
virus-like particles morphologically and biochemically resembling type-C
virus but apparently lacking the ability to replicate have been
frequently observed from leukaemic tissue", that is, these properties
are not proof for the existence of such viruses.
7. In the 1970s, such particles were frequently observed in human
leukemic tissues, cultures of embryonic tissues, and in the majority, if
not all, of human placentas. In the AIDS era retrovirus-like particles
have been revealed in non "HIV" infected H9 (the leukemic cell line
which Gallo used to "isolate" HIV), as well as other cell used for "HIV
isolation", CEM, C8166, EBV transformed B-cells and umbilical cord blood
lymphocytes.
8. HIV experts are unanimous that for infectivity, gp120 is
essential. Indeed, in 1988 your colleague JN Weber and you wrote, "The
first step in any viral infection is the binding of the virus particle
to a component of the host cell's membrane...For some time it has been
known that the binding takes place when CD4 interacts with an "envelope"
protein of the virus called gp120". However, Hans Gelderblom and his
colleagues at the Koch-Institute in Berlin, who have conducted the most
detailed electron-microscopy studies of "HIV particles" have shown that
the knobs on the surface of the particles, where the gp120 is found, are
only present in immature (budding) particles, which are "very rarely
observed". "Mature", cell-free particles do not have knobs, that is,
gp120.{Hausmann, 1987 #600 Thus it would impossible for Gallo to produce
"transmission by particles" by cell-free culture supernatants.
Surely, one would have to conclude, given the non specificity of
particles, reverse transcription (assumed to be due to reverse
transcriptase and no other enzyme activity) and antigen/antibody
reactions, Barré-Sinoussi's et al, Gallo's et al and Levy's et al data
do not prove the isolation of a retrovirus, even allowing your
definition.
When asked in 1997 by Djamel Tahi if Gallo purified HIV, Montagnier
replied "I don't believe so". He also added that when one uses leukemic
cell lives derived from patients with adult T-cell leukemia (as is the
case with the H9 cell line) which Gallo claims is caused by the
retrovirus HTLV-I and thus must be present in the culture, "You have a
mix of HIV and HTLV, it is a real soup". In other words, even if one has
proof for the isolation and the propagation of a retrovirus, it is not
proof that the retrovirus is HIV. It could very well be HTLV-I.
Montagnier forgot to mention that in the soup one could find at least
one more retrovirus, an endogenous retrovirus. The difference between
retroviruses and all other viruses is that while the finding of a virus
in a culture is proof that the virus has been introduced from outside
(the virus is exogenous), the finding of a retrovirus is not. You know
better than me that Varmus pointed out "one of the most striking
features that distinguish retroviruses from all other animal viruses is
the presence in the chromosomes of normal uninfected cells, of genomes
closely related to, or identical with those of infectious viruses". If
the finding of particles and RT activity in the "infected" cultures, and
proteins in the "infected" cells which react with sera from AIDS
patients is proof of HIV isolation, what does the detection of the same
phenomena in non-infected cultures and cells prove?
You also know, in fact you are among the many scientists who have
proven, that cultures of non-infected cells, sooner or later, begin to
release endogenous retroviruses. Their appearance can be accelerated and
the yield increased up to a million fold by stimulating the cultures
with mitogens, co-cultivation or by adding to the cultures supernatant
from normal, unstimulated cell cultures. Indeed, as far back as 1976
retrovirologists such as George Todaro recognised that "the failure to
isolate endogenous virus from certain species may reflect the
limitations of in vitro co-cultivation techniques". Montagnier et
al (as well as everybody else) employed at least two of the above
techniques. In fact, both Montagnier and Gallo concede that not one of
the phenomena which they claim prove the existence of HIV can be
detected unless the cultures are stimulated. In other words, while the
finding of a virus in culture is proof that the virus was introduced
from outside (infectious virus, exogenous virus ) the finding of a
retrovirus is not. Evidence exists that 70% of AIDS patients and those
at risk have antibodies to endogenous retrovirus. This means that even
if Barré-Sinoussi, et al Gallo et al and Levy et al, have all obtained
proof for the isolated (purification) of a retrovirus, even by your
definition, is not possible to claim that the virus is an exogenous
(infectious) virus. It could very well be endogenous and, as
retrovirologists have suggested, the result and not the cause of a
pathogenic process.
In 1997 in an article entitled "Current Problems and the Future of
Anti-retroviral Drug Trials", Joep Lange wrote: "There is also a
tendency to rapidly and widely publicise positive data and to delay or
refrain from publication of studies with negative outcome". In the case
of HIV, although both Montagnier's and Gallo's teams widely publicised
their claims of isolation (purification) of HIV, neither team published
electron micrographs of the material which in isopycnic sucrose
gradients bands at 1.16 gm/ml, the "purified HIV". At least in the case
of Montagnier's team (and according to Montagnier, Gallo's team as well)
this was because their results were negative. In scientific experiments
one manipulates the parameter whose effect is in question, executes
parallel control experiments with that parameter held constant, holds
other parameters constant throughout, replicates both the experimental
manipulation and the control experiment and obtains data. Given the fact
that retroviral phenomena are expected to arise spontaneously, let alone
be induced by the "experimental manipulation" absolutely essential to
obtain "HIV", in retrovirology controls constitute the quintessential
element. A common thread in "HIV" research is lack of controls. On the
rare occasions when authors do claim to use controls they are improper
and the experiments not performed blind. For example, "controls" consist
of cells cultured from healthy individuals, not sick individuals matched
to AIDS patients with respect to "other parameters". To date there is
only one exception and this from un-cultured tissue. In 1988 O'Hara and
his colleagues from Harvard reported "HIV particles" in 18/20 (90%) of
patients with enlarged lymph nodes attributed to AIDS and the identical
particles 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".
Molecular cloning cannot be considered proof for the discovery of a
retrovirus. To the contrary, cloning of the retroviral genome can only
be performed if and only if one first has a stretch of nucleic acid
which a priori has been proven to be the genome of a retrovirus. For
this one must first obtain particles in a purified form, or at least in
a material where there is not even a remote possibility of the presence
of an RNA apart from that contained in such particles. Then the
experimenter must show:
1. That the particles have all the morphological characteristics of
retroviruses;
2. That the particles are infectious;
3. Contain only RNA and not DNA;
4. The RNA codes for the particles' proteins.
To date there is not one single study proving even one of these
conditions, not to mention all of them.
Let us assume that HIV, unlike every other retrovirus or virus is, as
you say, a "virus without any proteins, particles etc.", that is, merely
a naked stretch of nucleic acid. If a stretch of RNA or DNA (the
provirus) is the genome of a unique retroviral particle then the most
basic requirement is proof for the existence of a unique molecular
entity. That is, all cultures and cells deemed infected must:
1. have a full length of the HIV genome, whatever that length is.
2. the stretch of DNA provirus, the genomes, must be identical.
To date the two "HIV DNA" or HIV DNA" of the same length have been
reported. Montagnier and his colleagues reported the "HIV DNA" to be 9 ±
1.5 Kb" whereas Gallo and his colleagues reported that "The overall
length of the HTLV-III provirus is approximately 10 kilobases". In the
1984 Levy and colleagues' first study of the "HIV genome", the "broad
band (> 15Kb) represents provirus integrated into host cell DNA". In
1995, Pasteur Institute researchers reported that "The complete
9193-nucleotide sequence of the probable causative agent of AIDS,
lymphadenopathy-associated virus (LAV) has been determined. 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".
In the same year, Gallo and his colleagues reported their results on the
"HIV" nucleotide sequences using clone BH10 but also added, "The
sequence of the remaining 182 bp of the HTLV-III provirus not present in
clone BH10 (including a portion of R, V5, tRNA primer binding site and a
portion of the header sequence) was derived from clone HXB2...Of note is
the presence of a fifth open reading frame (nucleotides 8,344-8991)
designated 3' orf, present in clone BH8 but truncated in BH10". They
concluded, "The complete nucleotide" sequence of two human T-cell
leukaemia type III (HTLV-III) proviral DNAs each have four long open
reading frames, the first two corresponding to the gag and pol genes.
The fourth open reading frame encodes two functional polypeptides, a
large precursor of the major envelope glycoprotein and a smaller protein
derived from the 3' terminus long open reading frame analogous to the
long open reading frame (lor) product of HTLV-I and -II...The HTLV-III
provirus is 9,749 base pairs (bp) long" In 1990 the HIV genome was said
to consist of ten genes. In 1996 Montagnier reported that HIV possesses
eight genes and Barre-Sinoussi, HIV has nine genes.
Man and chimpanzee DNA differ by less than 2% but variation in the
composition of the "HIV genome" (derived from analysis of "pieces"
measuring 2% to 30% of the presumed total) measures between 3-40%. For
comparison, two RNA containing viruses (polio and influenza, the latter
after 27 years of dormancy,) vary by less than 1% as do RNA molecules
self-assembled in test tubes denied the organising influence of living
cells.
Given that the DNA sequence determines the composition of a virus's
proteins, and the latter the physical, biochemical and biological
properties of a virus, how is it possible for such variation to
represent one and the same agent? For example, how is it possible that
HIV can induce the same antibodies which can be recognised in a
universal antibody test containing identical proteins? Since Peter
Duesberg reminds us, "there is a range, a small range, in which you can
mutate around without too much penalty, but as soon as you exceed it you
are gone, and you are not HIV any longer, or a human any longer...then
you are either dead or you are a monkey, or what have you", it is
evident that whatever the "HIV DNA genome" represents, it cannot be a
virus.
If the stretch of "HIV RNA" is the genome of a unique exogenous virus
which infects individuals with AIDS or those at risk, then this RNA (or
cDNA) should be present in fresh uncultured tissue from all these
individuals and in nobody else. Furthermore, if in these individuals
there is massive HIV infection, as some of the best known HIV experts
claim, Southern/Northern blot hybridisation should be more than
sufficient to detect it.
I have always found it extremely difficult to understand why neither
Montagnier's nor Levy's groups reported such experiments in 1984 when
they claimed to have identified, characterised and cloned the HIV
genome. Gallo did and reported "HTLV-III DNA is usually not detected by
standard Southern blotting hybridisation ...when it is, the signals are
often faint...the observation that HTLV-III sequences are found rarely,
if at all, in peripheral blood mononuclear cells, bone marrow, and
spleen provides the first direct evidence that these tissues are not
heavily or widely infected with HTLV-III in either AIDS or ARC". These
studies were confirmed by many other researchers. The finding that when
the results were positive the hybridisation bands were "faint", "low
signal" was interpreted as proof that HIV seropositive individuals
contain HIV DNA in small numbers of cells and at low copy numbers, as
interpretation which became generally accepted, although Gallo and his
colleagues had an alternative explanation: "Theoretically, this low
signal intensity could also be explained by the presence of virus
distantly homologous to HTLV-III in these cells". This alternative
explanation has been ignored by everybody, including Gallo. However, at
a 1994 meeting held in Washington sponsored by the US National Institute
of Drug Abuse, Gallo admitted "We have never found HIV DNA in the tumor
cells of KS...In fact we have never found HIV DNA in T-cells". Data
which has come to light since 1984 suggest that Gallo's and his
colleagues' alternative explanation may be a fact:
1. At present there is ample evidence showing that normal human DNA
contains sequences related to HTLV-I and HTLV-II;
2. As late as 1994, writing in "Harrison’s Principles of Internal
Medicine", Gallo (and Fauci) taught medical students, "...there are no
known human endogenous retroviruses". This means that by "virus
distantly homologous to HTLV-III" they could have meant none other than
the exogenous retroviruses Gallo claimed to have discovered earlier,
that is, HTLV-I and HTLV-II. However, at present even Gallo admits that
the human endogenous proviral sequences "comprise about one percent of
the human genome";
3. Some of the best known HIV experts including Montagnier, Blattner
and Gelderblom agree that the pol and gag genes "may be highly conserved
between subtypes of virus". In a paper published in 1996 by Reinhart
Kurth and his colleagues one reads: "Retrotransposons evolved in a
variety of organisms ranging from protozoa to human beings. In these
elements, RT genes are linked to genes that code for polyproteins with
the potential to self aggregate and to form core particles. These
proteins are the equivalents of the retroviral capsid proteins usually
designated group-specific antigens (gag)...They [retrotransposons] may
be either the derivative or predecessors of retroviruses. Retroviruses
differ from retrotransposons by the presence of at least one additional
coding region, the envelope (env) gene". In 1984, Gallo group reported
that the "HIV genome" hybridised with the "structural genes (gag. pol,
and env) of both HTLV-I and HTLV-II. Obviously, the finding of a
positive hybridisation "signal" at least with an "HIV" gag or pol probe
is no proof for the existence of the "HIV genome".
In fact, at present evidence also exists which shows the presence of
"HIV" sequences in non-infected tissues. A .few examples suffice to
illustrate this point:
1. Although it is no longer accepted that HIV is transmitted by or is
present in insects, in 1986 researchers from the Pasteur Institute found
HIV DNA sequences in tsetse flies, black beetles and ant lions from
Zaire and the Central African Republic.
2. DNA extracted from thyroid glands from patients with Grave's
disease hybridised with "the entire gag p24 coding region" of HIV".
3. In 1986 you published a paper entitled "Isolation of a retrovirus
from two patients with "common variable hypogammoglobulinaemia" (CVH).
Patients with CVH "are prone to certain bacterial and mycoplasma
infectious but not to opportunistic viral protozal, and fungal
infectious, such as one seen in patients with genetic defects in
cellular immunity ..Both patients sera were negative for HTLV-III [HIV]
antibodies". I found your paper very interesting for two reasons.
Firstly, for what you meant by retroviral isolation and secondly, your
Southern blots results. By isolation you meant: "Extensive syncytium
formation was seen to polybrene-treated co-cultures, which on electron
microscopy showed a retrovirus morphologically indistinguishable from
HTLV-III/LAV" (see figure) and animal lentiviruses. Supernatant from
this co-culture was positive for reverse transcriptase, and the cells
were positive by immunofluorescence with serum from a patient with AIDS
and with the anti-HTLV-III monoclonal antibodies, a-p24 and a-a-p19
(from Dr R C Gallo). Southern blots of restricted DNA from infected
cells were probed with ABH-10 (from Dr R C Gallo ), indicated that the
viral genome showed homology to HTLV-III/LAV but with restriction enzyme
sites distinct from the prototype isolates, HTLV-IIIB and LAV. In other
words in 1986 by isolation you did not mean propagation but detection of
totally non-specific phenomena. More importantly, while Gallo et al
using ABH-10 as a probe could not find in T-cells from AIDs patients
"HIV DNA" you found it in the T-cells of patients with CVH.
In the second half of the 1980, in order to rescue the concept of an
"HIV genome" extensive use was made of the polymerase chain reaction.
However, the results with this technique were not much better than with
Southern blot hydridisation, and like Gallo in 1984, were interpreted as
proof that "HIV infected" individuals contain "HIV DNA" in a small
number of cells. A most striking feature of the results "is the scarcity
or apparent absence of viral DNA in a proportion of patients" and when
found, the "signal is very low". In addition, the specificity of the PCR
has never been determined. In the only study in which an attempt was
made, using antibody tests as a gold standard (everyone should know that
these cannot be used as a gold standard), it was found that in "Seven
French laboratories with extensive experience in PCR detection of HIV
DNA", the concordance between HIV serology and "HIV DNA" varies between
40-100%. Even if the PCR were specific, with this technique one detects
only a small portion of the genome.
In the vast majority of cases the presence of the "HIV genome" is
proven by amplifying short" invariant regions" of a "viral gene",
usually of the gag gene. However, since it is accepted that a
significant proportion of the "HIV genomes" are defective, finding a
fragment of a gene is not proof of the existence of the whole gene and
even less so for the existence of the whole genome "HIV DNA" or HIV
RNA", a fact accepted by many HIV/AIDS researchers.
In yet another effort to rescue the "HIV genome", tests have been
developed which claim to measure the "HIV RNA" in plasma which in turn
is said to quantify the number of particles in blood, the "viral load" .
One does not need to enumerate the many problems of these tests, a
glance at the following table suffices to realise that such tests do not
exist.
|
HIV-1 STRAIN |
RT-PCR |
BDNA |
NASBA |
|
DJ258 |
<400 |
111,500 |
100,000 |
|
DJ263 |
<400 |
79,800 |
60,000 |
|
SF2 |
225,500 |
38,000 |
240,000 |
|
III-B |
54,000 |
17,000 |
360,000 |
|
ZAM18 |
78,300 |
70,000 |
66,000 |
|
ZAM20 |
178,800 |
125,800 |
420,000 |
|
UG270 |
179,800 |
29,200 |
170,000 |
|
UG274 |
320,000 |
41,400 |
32,300 |
|
CM241 |
18,800 |
72,800 |
35,000 |
|
CM235 |
4,700 |
52,000 |
15,000 |
|
163.3069 |
36,200 |
94,000 |
57,000 |
|
162.307 |
2,800 |
78,100 |
26,000 |
|
G98 |
254,700 |
269,000 |
<400 |
|
LBV21 |
184,500 |
295,000 |
<400 |
|
VI557 |
950,000 |
587,000 |
125,000 |
The three assays frequently used to quantify the "viral load" are
reverse transcription-polymerase chain reaction (RT-PCR), nucleic acid
sequence-based amplification (NASBA) and branched chain DNA (bDNA). To
assess the impact of the assays used and of "genetic variability in
HIV-1 RNA quantification", researchers from France "evaluated three
commercial kits by using a panel of HIV-1 isolates representing glades A
to H...These isolates were expanded in culture. Virus was collected by
ultracentrifugation and resuspended in HIV-seronegative plasma. To
standardize the quantities of virus to similar levels in each
preparation, the p24 antigen was determined and the volume adjusted so
that each specimen contained approximately 10pg of p24 antigen per ml".
Since all the samples had the same quantity of "HIV", of "HIV RNA", one
will expect all the number in the table to be similar if not identical.
Looking at the rows the only conclusion one can draw is that at least
two of the assays do not measure "HIV RNA". Similarly, from the columns
the only conclusion one can draw is that either no one of the test
measure "HIV RNA", and/or there is no such thing as "HIV RNA".
Rich et al state, "Plasma viral load ["HIV" RNA] assays are designed
for monitoring the effectiveness of antiretroviral therapies and for
measuring the quantity of virus in patients with confirmed HIV
infection, not for the diagnosis of HIV infection. Their performance in
patients who are not infected with HIV is unknown" and their use leads
to "Misdiagnosis of HIV infection".
The fact that patients where "viral load decreases to undetectable
level still develop AIDS" also means that either the test do not measure
"HIV RNA" or the cause of AIDS is not HIV.
In summary, unless one draws conclusion "beyond the validity of the
data", it is not possible to conclude that "Barré-Sinoussi et al Gallo
and Levy" have proven the isolation of a unique retrovirus, even by your
definition of isolation. Neither do the present data prove the existence
of a unique molecular entity "HIV DNA", which constitutes the genome of
a unique retrovirus, much less of a retrovirus which infects humans.
To answer the Continuum challenge regarding proof for the isolation
of HIV, and thus its existence, Edward King from AIDS Treatment Update
presented you the challenge. In the April 1996 where your comments were
published one reads: "Gene cloning techniques allow researchers to
extract the viral genes found in HIV-infected cells. When the complete
set of genes is re-introduced into healthy human cells in culture, the
cells produce HIV particles". There is no proof for the existence of the
"complete set of genes" that is of "HIV DNA" even in one cell of one
AIDS patient. The small number of "complete set of genes" reported so
far, all of which differ significantly from each other, are from
cultured immortal cell lines. Neither is there one single study which
proves that, "When the complete set of genes is re-introduced into
healthy human cells in culture, the cells produce HIV particles".
QUESTION 5
My question was:
You state: "When you have evidence of infection in culture,
purification is not particularly important". These researchers did not
know that their cultures were infected. This is what they were
attempting to establish. Surely you don't claim that electron
micrographs of some budding forms on the cell surface or some cell-free
particles in the culture supernatant which do not even have all the
morphological characteristics of retroviruses, are proof of infection?
Are you further arguing that, without isolation, that is, purification,
a scientist can obtain "HIV" proteins and RNA?
Your reply was:
Yes, I do claim that visualization of HIV by electron microscopy was,
in 1983/84, an important component of the collective data on virus
isolation. Taken together with virus propagation, reverse transcriptase
activity and enrichment of particles by isopycnic gradients, it
convinced me that HIV is a retrovirus. Even more so, it was Montagnier's
electron micrographs published in April 1984 and previously shown at
Cold Spring Harbor Laboratory in September 1983 that convinced me that
HIV was probably a lentivirus among retroviruses, as they resembled
particles of equine infections anaemia virus - a lentivirus first
propagated by inoculating a filtrate too small for bacteria to pass
through into horses and donkeys and causing disease. So yes, I am
definitely arguing that, disregarding your meaning of 'purification',
but with my meaning of 'isolation', you can make quite large amounts of
HIV proteins and smaller amounts of RNA.
My response:
In AIDS Treatment Update one reads: "other scientists have
highlighted the irrelevance of this insistence on purity if the HIV
particles themselves are clearly present, for example, it's like saying
that it is impossible to identify a German Shepherd dog by its unique
appearance, if it happens to be surrounded by a pack of poodles".
However, in the HIV cultures in addition to the myriad of other things
one could see a "zoo" of particles, looking more or less like one or
another type of retrovirus particles but no one having all the
morphological characteristics of retroviruses.
The correct analogy for HIV is a person with no knowledge of German
shepherds who possesses an aerial photograph of a zoo, expects to see
dogs (retroviruses) but all he sees is many objects some of which look
like animals (viruses) and decides that one of the objects is a dog, in
fact a dog with unique composition and behaviour without first showing
the object is (a) an animal; (b) the animal is a dog; (c) the dog is
unique.
It is interesting that you now claim in addition to electron
micrographs, "virus propagation, reverse transcriptase activity and
enrichment of particles by isopycnic gradients" are needed to convince
you that "HIV is a retrovirus". However:
1. "Virus propagation" presupposes you already know you have a virus,
therefore virus propagation can not be used to prove the existence of a
virus.
2. You agree that reverse transcriptase activity is present in all
cells (see my response to Answer 4). I will only add here that a decade
before Barré-Sinoussi and Jean Claude Chermann claimed proof for the
existence of HIV, they wrote:
"Since similar polymerase activity [reverse transcriptase activity]
has been found in normal cells, may be mainly ascribed to the cellular
enzyme. At the same time Gallo was proving the existence of RT activity
in PHA stimulated but not in unstimulated normal, non infected cells. In
his interview with Djamel Tahi, Montagnier initially insisted that this
activity was "truly specific of retroviruses," but later he said that it
was only "characteristic" of retroviruses. Yet while my medical students
and residents, and presumably their teachers, have been taught by
retrovirologists that reverse transcription is specific to retroviruses,
retrovirologists such as Montagnier and Gallo know differently.
3. "enrichment of particles by isopycnic gradients". Neither
Barre-Sinoussi, nor Gallo and Levy presented proof for any "isopycnic
gradients" including the 1.16 g/ml being "enriched" or even having one
retrovirus-like particle. According to Montagnier, such evidence was not
published because they (and in his view, Gallo's group as well) could
not find any retrovirus like particles in their "isopycnic gradients".
This fact alone proves beyond reasonable doubt they did not have a
retrovirus and that the RNA and proteins found at the 1.16g/ml band as
well as RT activity or any other effect induced by the material in the
band have nothing to do with HIV or any other retrovirus. To claim
otherwise is no different from me, as a surgeon, claiming to have a
patient’s gallstones isolated, that is, removed an in my hands, merely
because I have proven he or she has abnormal levels of liver enzymes in
his or her blood. May I repeat, to date nobody has published proof for
the existence in the "HIV" cultures, not to mention the 1.16 g/ml band
showing particles having all the morphological characteristics of
retrovirus particles.
You seemed to have misunderstood my question. I did not ask you what
amount of "HIV" proteins or DNA you can make. I am solely interested in
quality. Not quantity. Allow me to put the question differently: As far
as I know, one can claim that a protein or an RNA fragment belongs to an
object, for example either a human being or a virus particle, only if
proof exists that they come from the object. Do you disagree? In the
"isolate" (be it the culture supernatant or the 1.16 gm/ml band)
obtained by your "isolation" method, there is proof for the existence of
a myriad of non-retroviral objects containing proteins and RNA, but no
object which has even the morphological characteristic of retroviruses
not to mention the physical characteristics such as their density. How
it is possible then to prove that some of the proteins and some of the
RNA which banded at 1.16g/ml or present in the culture supernatant of
were "HIV" proteins and "RNA" as Montagnier and Gallo did?
QUESTION 6
My question was:
In your view is it scientifically valid to say on the one hand, as
Montagnier did, that the 1.16g/ml "material" did not have even particles
with the "morphology typical of retroviruses, while on the other hand,
asserting that the proteins and RNA were those of a retrovirus, HIV?
Your answer was:
Barré-Sinoussi et al published electron micrographs of early budding
forms of virus only, that were not immediately identifiable as
retrovirus particles. By September 1983, Montagnier's electron
micrographs looked more typical.
My response:
In the very first electron micrograph (published in May 1983),
Barré-Sinoussi, Montagnier et al not only immediately identified some
particles as retrovirus particles but they stated that: "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 et al 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." (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 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 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 and according
to non-morphological criteria. These taxonomical differences imply that
if HIV was a newly discovered mammal, it could have been either human,
or a gorilla or an orang-utan.
All this aside, you have not answered my question. Even if Montagnier
had electron micrographs typical of retroviruses, they were all from the
culture. As Montagnier acknowledged, no retroviruses were seen at the
1.16g/ml band. What I am interested in is how can anybody take some
proteins and RNA from the 1.16g/ml band where there are no proof of any
retrovirus-like particles and call them "HIV proteins" and "HIV
RNA"?
QUESTION 7
My question was:
What possible justification can there be for (a) using these proteins
as antigens in an antibody test to prove infection of millions of people
by a deadly virus? (b) using this RNA to prove not only infection but
also to quantify the viral load?
Your answer was:
There are many different tests for HIV-specific antibodies. Today's
commercial test kits are based on oligopeptides and on proteins
manufactured from cloned HIV DNA. No biological test for anything is
100% specific and 100% sensitive, but today's HIV tests are as good as
tests for any other human viral pathogen. Likewise, today's PCR primers
are highly specific and sensitive for the major strains of HIV in
developed countries. Some 'outlier' strains, especially in Gabon and
Cameroon are not picked up quite as sensitively and therefore estimates
of viral load with these 'outlier' infections should be interpreted
cautiously.
My response is:
Could it be there is no scientific justification for taking some
arbitrary RNA and proteins from a material in which there is no proof
for the existence of even retrovirus-like particles and calling these
"HIV RNA" and "HIV proteins"?
Above I have discussed the PCR and the "viral load tests". Here I
would like to add:
1. If the "viral load" test measures the number of HIV particles in
the blood and if there is a high level of such particles as it is
claimed, then it should be no problem to detect such particles using the
electron microscope. Yet to date, there is not even one electron
micrograph proving that such particles do exist in the blood. The only
electron micrographs published to date are from lymph nodes. In your
1993 review article in Science entitled "How does HIV cause AIDS?" you
state, "It has long been known from electron microscope and
immunofluoresence studies (24) that HIV is found in massive amounts in
the lymph nodes, even in the asymptomatic phase of infection". In ref.
24 you cite three papers, two by Tenner-Racz et al and one by Armstrong
and Horne (the latter authors are from the Royal Perth Hospital where I
work). In none of these studies is there evidence for "immunofluoresence
studies" of particles. The immunofluoresence studies of Tenner-Racz are
of lymph nodes. However, others report similar findings in patients who
suffer from a number of non-AIDS related diseases, and also healthy
individuals. In the first paper Tenner-Racz et al examined the lymph
nodes of 9 patients with persistent generalised lymphadenopathy and two
with Kaposi's sarcoma. In fig.2 where their results appear, there are
three electron micrographs. In the first two there is one "virus-like"
particle in each. The third shows one "Profile suggesting budding". In
the second paper there is one electron micrograph showing one particle.
It is interesting that without any proof the "virus-like" particles in
the first study become "retrovirus particles" and in fact "AIDS-related
virus" in the second, although even to a non-electron microscopist it is
obvious that the particles lack the appearances of the putative "HIV"
particle. In the Armstrong and Horne paper there are a few more
particles which are sometimes referred to as "virus-like" and at other
times retrovirus-like and whose "morphology conforms" to the type-C
retrovirus, not lentivirus as HIV is supposed to be. (Armstrong has
retired from the hospital but I contacted Horne who confirmed these were
indeed type-C particles). More importantly, particles with morphology
ascribed to "HIV" are found in the lymph nodes of non-AIDS patients.
2. The absolutely necessary, but not sufficient condition which one
must satisfy before using "PCR primers" in any test is to prove such
primers originate from a retrovirus-particle. Since no such proof exists
the only conclusion a scientist can draw is that nobody knows what a
positive "HIV PCR" is detecting. That this is the case is confirmed by
the test manufacturers themselves. For example, Roche states in their
package insert, "The AMPLICOR HIV-1 MONITOR Test is not intended to be
used as a screening test for HIV-1 or as a diagnostic test to confirm
the presence of HIV-1 infection" (Roche Diagnostics, Branchburg, New
Jersey, Art. 07 5623 7). HIV/AIDS experts agree. For example, Rich et al
state, "Plasma viral load ["HIV" RNA] assays are designed for monitoring
the effectiveness of antiretroviral therapies and for measuring the
quantity of virus in patients with confirmed HIV infection [positive
antibody test], not for the diagnosis of HIV infection. Their
performance in patients who are not infected with HIV is unknown" and
their use leads to "Misdiagnosis of HIV infection". Thus clinicians like
myself are left wondering how to reconcile statements such as "HIV RNA
(cDNA) is the RNA of a unique retrovirus HIV" and "today's PCR primers
are highly specific and sensitive" with statements such as HIV PCR is
"not for the diagnosis of HIV infection" because this will lead to
"Misdiagnosis of HIV infection". It does not make any sense that the PCR
results are confirmed by the antibody tests whose specificity has never
be determined, and vice versa that the specificity of the antibody tests
is confirmed by PCR whose specificity is unknown.
3. In my view the antibody tests are the most important aspect in
HIV/AIDS. This is because:
(i) you acknowledge that there are "naturally existing viruses"
(endogenous, non-infectious viruses) and there is a very high frequency
of recombination of the retroviral genomes. "HIV" has only been
"isolated" from cultures. As far back as 1988 the CDC researchers
pointed out that "the culture technique determines the ability of
infected cells to produce virus in vitro but does not necessarily
indicate the status of virus expression in vivo." This means that even
if one isolates a retrovirus from the culture, and even the isolation is
according to our terms, such finding is no proof for the existence of
this virus in vivo. The limited number of in vivo electron microscopy
studies, failed to prove even the existence of retrovirus particles in
AIDS patients, much less of a specific retrovirus. The vast volume of
genomic studies, failed to prove the existence in even one single AIDS
patient of the full-length "HIV genome". The existence of HIV in vivo
then rests with the antigen/antibody reactions.
(ii) the antibody tests are the only tests routinely used to prove
"HIV" infection.
(iii) the only way the proponents of the HIV theory of AIDS can
defend their position is to reassert the correlation between AIDS and a
positive antibody test. In your 1990 Nature publication with Harold
Jaffe where you "argued against Duesberg's view" you wrote, "The
evidence that HIV causes AIDS is epidemiological and virological, not
molecular...HIV is the singular common factor that is shared between
AIDS cases in gay men in San Franciso, well nourished young women in
Uganda, haemophiliacs in Japan and children in Romania orphanages".
However, correlation does not prove causation and any "correlation"
between "HIV" infection and AIDS is man made. Prior to 1987, one "HIV
specific" WB band was considered proof of HIV infection. However, since
15%-25% of healthy, no risk individuals have "HIV specific" WB bands, it
became necessary to redefine a positive WB by adding extra and selecting
particular bands, otherwise at least one in every seven people would be
diagnosed infected with HIV. (Notwithstanding, in the MACS, one band
remained proof of HIV infection in gay men until 1990). On the other
hand, although AIDS began to decline in 1987,this trend was countered by
the addition of more and more diseases and, most recently, mere
laboratory abnormalities to each revision (1985, 1987 and 1993) of the
first, 1982 CDC definition. The net effect of these changes was to
maintain a correlation between "HIV" antibodies and "AIDS" amongst the
"risk" groups while the risk of an HIV/AIDS diagnosis outside these
groups remained slight. This was further accentuated by avoiding testing
outside the risk groups. However, when such studies were performed, for
example, (a) amongst 89,547 anonymously tested blood specimens from 26
US hospital patients meticulously chosen to be at no risk of AIDS,
between 0.7% to 21.7% of men and 0-7.8% of women aged 25-44 years were
found to be HIV WB positive. (It is estimated that approximately 1% of
men are gay. Also, at the five hospitals with the highest rates of HIV
antibodies, one third of positive tests were in women. Yet men vastly
outnumber women as AIDS patients). (b) the US Consortium for Retrovirus
Serology Standardization reported that 127/1306 (10%) of individuals at
"low risk" for AIDS including "specimens from blood donor centers" had a
positive HIV antibody test by the "most stringent" US WB criteria (see
below). Thus the correlation between "HIV" antibodies and AIDS, which
experts accept as the only proof that HIV causes AIDS, is not a
statistic related to the natural, unbridled activity of a virus but is
instead a contrivance generated by mankind. Let me repeat, correlation
does not prove causation, and the artificiality of this particular
"correlation" severely compromises any scientific analysis.
Although the "antigens" used in the HIV antibody tests are said to
originate in a unique retrovirus HIV, it is not important if one has a
single or "many different tests" or what is used as antigen. Antigens
used in serological tests for syphilis and infectious mononucleosis do
not originate in the causative agents. However it is absolutely
necessary to have tests which are specific. That is, well before
introducing the test into clinical practice, the laboratory scientist
must prove that the tests are positive only in individuals infected. The
specificity of the "HIV" antibodies for proving HIV infection can be
determined only by using "HIV" isolation (purification) as a gold
standard. This has not been done and presently cannot been done because
nobody has purified "HIV". That this is the core, and that there is no
proof that "There are many different tests for HIV-specific antibodies"
is acknowledged by some of the best researchers in HIV testing and
HIV/AIDS such as Philip Mortimer and William Blattner. Even if one uses
your definition of isolation and purification it is still not possible
for anybody to have determined the specificity of the Western blot, the
antibody test used to "confirm" all other antibody tests. This is
because the WB is not standardised. The criteria used to define a
positive test varied with time (the US Food and Drug Administration have
had three so far) and vary between countries or even between
laboratories in the same country.
Space does not permit for me to cite the vast volume of data
regarding the non-specificity of the 'HIV antibody tests" but I am sure
you know where to find the relevant data. Because of this I will limit
the discussion to the basic problems associated with the definition of
the "HIV" antigens and antibodies. Barré-Sinoussi et al and Gallo et al
took the proteins which banded at 1.16g/ml, the "purified" virus and
reacted then with the sera from AIDS patients and those at risk. The
proteins which were found to most often react with some of the sera
sometimes were said to be "HIV" proteins and the reacting antibodies,
"HIV" antibodies. From such a reaction it is not possible to determine
the origin of one reactant, much less of both.
Let us consider a very ideal situation. Firstly, 75% of the material
which bands at 1.16g/ml is in the form of particles ("enriched") which
possess all the morphological characteristics of retroviruses. The
remaining 25% is cellular microvesicles and other cellular, bacterial
and viral constituents. Secondly, all of the many antibodies present in
AIDS patients and those at risk are "monospecific", that is, they react
with none other than the inducing antigen. A reaction between a protein
in the 1.16g/ml band and an antibody in the sera proves that the protein
is present in the individual and it is immunogenic. But it does not
prove the origin of that protein, that is, whether the protein is
retroviral, viral, bacterial or cellular. If we come closer to reality,
that is if you accept the proven fact that there are no such things as
"monospecific" antibodies, that all antibodies are "polyspecific", that
is, they cross-react, then, from such a reaction one cannot ever prove
that the protein is present in the individual or that the antibody was
directed against it. The reality, the truth, is that:
(a) Barré-Sinoussi et al and Gallo et al did not prove that their
1.16g/ml band contained even one single particle with the morphological
characteristics of retroviruses.
(b) The AIDS patients and those at risk have a plethora of antibodies
including auto-antibodies, all potentially cross-reactive. This means
that the most likely origin of the proteins which band at 1.16g/ml is
cellular or maybe bacterial/viral and the least probable retroviral. The
same is true for the antibodies. That both the proteins and the
antibodies are not retroviral has been proven by well known HIV
protagonists. Let us assume that although there is no proof that
Barré-Sinoussi's and Gallo's 1.16 g/ml band did contain retroviral
particles, it did contain some disembodied retroviral proteins. In this
case, if one compares the proteins which band at 1.16g/ml from the "HIV"
infected cultures, the "purified" virus, with the proteins which band at
the same density from non-infected cultures, the "mock" virus, we would
expect the "purified" virus to reveal its "extra" proteins.
In the well known Bess and co-authors 1997 Virology paper, the
authors had three HUT-78 (H9) cultures, two infected and one uninfected
control. The proteins from the banded material from all cultures
including the control (column A), which they called "mock virus", were
compared using electrophoresis. They stated that the only difference
between the three strips was that the infected strips contained major
bands of p24. But these same bands, although weaker, are present in the
"mock" virus protein strip whereas, to be HIV proteins, requires them to
be present exclusively in the "infected" strips. When asked for proof
that p24 etc in the strips B and C were HIV proteins their answer was
that the labels were added for the reader's convenience at the
suggestion of the reviewers. So Bess and his colleagues have shown that
the same proteins are present in the pure HIV and "mock" virus.
In their effort to develop a vaccine, and because humans cannot be
injected with either HIV or "mock" virus, Bess and his colleagues first
injected macaques with the "mock" virus. (This is culture fluids from
the uninfected H9 clone of the human HUT78 cell line "purified" as it
would be to obtain "HIV" or "SIV"). After the initial immunisation, the
animals were given boosters at 4, 8 and 12 weeks. At fourteen weeks, the
monkeys were challenged with intravenous SIV prepared from the same
human cells as "mock" virus and then monitored for seroconversion with
the SIV Western blot. According to the authors, the animal immunised
with "mock virus" "did not seroconvert to viral proteins after
intravenous challenge with SIV", and "These results are the first
demonstration that immunisation with purified cellular protein can
protect from virus infection...It has recently been suggested that
immunisation with alloantigens might serve as a vaccine to protect
against HIV infection. Our demonstration...support this concept".
The underlying principle of immunisation is its specificity. That is,
to protect against microbe 'X', the person or animal must be exposed to
material from 'X' in order that the immune system generates specific
antibodies. For example, immunisation with hepatitis vaccine does not
protect against poliomyelitis. Since monkeys immunised with proteins
derived from uninfected human cells are protected from infection with
'SIV' prepared from the same uninfected human cells, "mock" virus and
"real" SIV must be identical. If such "mock" virus and "SIV" are one and
the same we would expect that when "SIV" is prepared in
Home