The politics of AIDS in South Africa: beyond the controversies
BMJ 2003; 326 doi: https://doi.org/10.1136/bmj.326.7387.495 (Published 01 March 2003) Cite this as: BMJ 2003;326:495All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
Nicholas Bennett stated regarding critical 'AIDS' Analysts:
"There is no consistent view or aim, reflected in the regular
confused posts from newcomers to the dissident discussion boards.
Practically the only thing uniting them is a refusal to accept the
conventional thought."
On the contrary, critical 'AIDS' Analysts absolutely accept the
'conventional thought' (rules of virus isolation, etc), which is precisely
why we are questioning the proponents of the ‘HIV’ Hypothesis who
constantly ignore conventional thought about the practice of isolation,
etc.
It is precisely the total lack of "conventional thought" (and
conventional scientific practice) that mars the thinking of the proponents
of the 'HIV/AIDS' Hypothesis. For instance: when Koch’s Postulates, the
tried, trusted and ‘conventional’ method of proving the existence of a
pathogen were completely unfulfilled by 'HIV', the supporters of the 'HIV'
Hypothesis declared the Postulates to be rubbish.
Moreover, the 'conventional' rules for retrovirus isolation laid down
at a conference at the Pasteur Institute in 1974 were flagrantly ignored
by the scientific team working at the very same institute in 1983, who
claimed to have found a retrovirus in the tissues a homosexual man
suffering from lymphadonopathy merely by finding what they claimed to be
reversetranscriptase activity and other dubious surrogate markers.
However, when subsequently challenged, Luc Montagnier, the leader of the
team, admitted that they did not find or isolate any viral particles, and
despite heroic laboratory efforts - described by Montagnier, as "Roman
efforts" – no 'HIV' was found. If 'HIV' does not fit the conventional
rules, they rubbish those rules, move the goal posts and rewrite the rules
of the game – then shoehorn 'HIV' in as a 'killer pathogen' when in fact
it is nothing of the kind.
From the outset it was claimed, in order to explain the
embarrassingly elastic incubation period of 'HIV/AIDS' – said to be
anything from 10 to 30 years between putative 'infection' and onset of
disease - that 'HIV' was a lentivirus, a slow acting retrovirus. Yet now
we are told that 'HIV' causes 'AIDS' in a matter of months in Africa and
the Third World. Is 'HIV' a 'lentivirus' or not? As Peter Duesberg stated:
"There are no slow viruses – only slow virologists." Why is it that there
is still no heterosexual 'HIV' epidemic in the West whilst there is
allegedly a heterosexual 'HIV' epidemic in South Africa?
We are not 'dissidents' or 'denialists' but deconstructionists –
critical and autonomous 'AIDS' Analysts teasing out the absurdities,
anomalies, inconsistencies and contradictions of the redundant 'HIV'
Hypothesis.
It is the propagators of 'HIV' dogma who constantly and consistently
refuse to accept conventional thought (and practice) and merely make up
the rules as they go along – changing the rules virtually daily – to
patch up the tottering 'HIV' Hypothesis.
Competing interests:
None declared
Competing interests: No competing interests
Nick Bennett, yes, we're all individuals on the dissident side, with
many disagreements as well as many areas of agreement. So what? What does
that have to do with anything?
The point of my post was simply to point out to you a plausible
explanation for your assertion that Hiv negative people with the same risk
factors don't get lowered CD4 counts in some selected studies. We have
studies that show that psychological stress causes t-cell depletion. The
Hiv+ diagnosis goes well beyond stressful -- it is a hammerblow to the
psyche like no other, known to cause suicides, murders, and other
unpleasantries. Now that's a situation that should be studied further. I
would also theorize that the stressful effect is much worse in Third World
people than it is in, say, San Francisco gay men, who often accept the
diagnosis in a very blasé fashion since it is considered by many of them
to be an important component of gay identity.
For normal people in Thailand or Africa, it's quite different. To
them, the diagnosis is a life-ender. Just like that, you get pronounced
positive, and your life is over, your hope is gone. All your grand plans,
down the toilet. And not only will nobody sleep with you anymore, nobody
will want to come near you. They think they will get Aids just by touching
you. That's one of the lovely things the Aids establishment has done to
the simple people of the Third World by planting the panic of a deadly
germ in their minds. You don't need a pac-man virus eating your t-cells.
The gossip of your neighbors alone will do you in.
Would Hiv+ people get Aids if they didn't know they were Hiv+, didn't
do drugs, didn't have malnutrition, didn't drink from the same water they
defecate in? I don't think so. You'd probably consider it unethical to
deliberately withhold Hiv+ info from a person. Personally I think it would
be extremely ethical. Lots of people don't want to know their Hiv
"status." Why not enroll them in an experiment?
People are still presenting in "end stage Aids," are they? You mean
they are presenting, not having had a Hiv test? What percentage of people
are doing so, and which of the many criteria for defining "Aids" is being
used with each person? Which of the many criteria for diagnosing someone
"Hiv+" is being used in these end stage cases? I assume you must know they
are Hiv+, otherwise, how can you say they have "Aids?" Oh, except if they
are African, then under the Bangui definition you can say they have Aids
without a test! Or if they are Thai, you can call your "end stage"
presenters Hiv+, hence "Aids cases," if they have two positive Elisas from
a single blood sample. But they wouldn't be Aids cases in America or
Australia, would they? Because there you need to run the more specific
test, the Western Blot, as well (requiring four reactive bands for a
positive diagnosis in Australia, but only three in the US). Of course,
this wouldn't work in England, because there the WB is not considered
reliable!
Mr. Bennett, forgive me impertinence, but I suspect that many of your
never tested end stage Aids cases are just cases of tuberculosis and other
common diseases, relabeled as Aids. Even one of your Aids establishment
supporters, Daniel J. Ncayiyana, MD, Editor, The South African Medical
Journal, has said:
"I am quite confident in my own mind that many cases identified as
AIDS (according to their symptoms) are not AIDS...The numbers given must,
of necessity, include people who possibly have other conditions."
--Now Magazine, 9-15 March 2000
Why do you waste precious bandwidth debating whether we are
"skeptics," "dissidents," "denialists" or whatever. What does that have to
do with anything?
You say that "psychological impacts on physical health, while real,
don't result in pneumocystis pneumonia and KS!" Well, that sounds logical
re KS, which seems to be connected more to nitrite use than anything else
(though I know you guys have blamed it on a new virus, what a surprise!).
But couldn't depleted immune cells, caused by the overwhelming,
devastating, almost intolerably depressing knowledge that one possesses
the "deadly virus" -- that one is essentially a leper as far as the
community is concerned -- foster the conditions that might give rise to
pneumocystis pneumonia? Help me with that, I'm not a medical person.
I mean, you people have been saying for 20 years that you get
pneumocystis pneumonia because Hiv eats your t-cells, right? Why couldn't
you get it because stress and depression eat your t-cells?
We (groups like Alive and Well and others) have had many reports from
people who, immediately after their positive diagnosis, started getting
sick with diseases associated with Aids. It seems unlikely that the
slippery little lentivirus could have chosen that precise moment to do his
dirty work. It seems more sensible to conclude that such people are
suffering from psychological devastation. The fact that some of them then
had another test, which came back negative, upon which event their "Aids"
symptoms immediately ceased, would seem to strongly suggest that the
diagnosis caused their ailments. You have heard of the Nocebo effect, I
presume? Is that not a fairly well proven phenomenon?
Yes, as you say, "it seems simpler to invoke a single cause" just as
it is simpler to attribute Aids to God's wrath against the sexually
uninhibited, as many people do. Or to attribute misfortune to punishment
for sins committed in a previous life. But we're not looking for answers
that are simple, are we? We're looking for answers that are correct, and
can be validated by reference to the real world, not by high tech bean-
counting of t-cells, alleged Hiv proteins or other means that are fraught
with problems and create self-fulfilling prophecies.
Competing interests:
None declared
Competing interests: No competing interests
Marcel Giroidan can be forgiven for not realising that I've
previously mentioned psychological factors in HIV progression, in
particular depression. I've discussed these briefly in several posts last
year.
The simple fact is that psychological impacts on phsyical health,
while real, don't result in pneumocystis pneumonia and KS! The other
important fact is that people are, sadly, still presenting to doctors in
end-stage AIDS. Their first medical visit may be with pneumocystis
(typically) and CD4 counts under 100. It seems odd that to explain pre-
diagnosis AIDS the dissidents use drug use or lifestyle factors, and to
explain post-diagnosis AIDS they argue stress or antivirals. It seems
simpler to invoke a single cause, common to all cases - HIV infection as
judged by culture, viral load and serology in repeated matched cohorts
(i.e. tests were either consistently negative or positive, as one would
expect if they were all detecting the same thing in different ways).
Which neatly moves onto the point raised a few days ago about the aim
and nomencalture of AIDS dissidents. The term is arguably mis-applied,
similar to "religious fundamentalists" but has been in use for
considerable time. More recently some have preferred the term
"denialists" to more accurately reflect their approach to HIV/AIDS
science. In the same vein the conventional view has gone from being
referred to as "the orthodoxy" to "AIDS apologists".
The name "dissident" has been taken up as a battlecry by some groups,
such as the one previously mentioned several months back which waged a
campaign to shut down HIV/AIDS support groups online (Dissident Action
Group). The core dissenting website refers to those who question the
conventional view as "heretics" "skeptics" and "dissidents"
(virusmyth.com). It seems as if the name is entirely appropriate and
accepted by both sides.
The view however that these people somehow have a common way of
thinking is greatly misplaced. Some agree that HIV exists, some go
further and say it has been isolated. Some refuse to accept either. Some
admit the antibody tests reflect a risk factor but disagree that it is
HIV. Some consider the antibody tests useless predictors. Some think the
antivirals help due to non-HIV related effects, some that they do more
harm than good. Some do seem to genuinely believe they are preventing a
health catastrophe, some seem hell-bent on _causing_ a health catastrophe.
There is no consistent view or aim, reflected in the regular confused
posts from newcomers to the dissident discussion boards. Practically the
only thing uniting them is a refusal to accept the conventional thought.
That's how it appears to me from this "side" at least.
Nick Bennett njb35@cantab.net
Competing interests:
None declared
Competing interests: No competing interests
Nicholas Bennett wrote:
"I wonder though why Mr Tyler quotes from Des Jarlais but omits the
following:
""'We studied CD4 cell counts and percentages from 1984 to 1992 among
1,246 HIV-seronegative injecting drug users in New York City, a population
at very high risk for exposure to bloodborne pathogens. Severe CD4
lymphocytopenia was rare, and there was no evidence of an increase over
time. Of 229 subjects with longitudinal data, only four met the
surveillance definition for "idiopathic CD4 lymphocytopenia" (ICL).'
Hardly glowing evidence of support for the drug-AIDS hypothesis!
"The question dissidents have to answer is why these antibodies so
effectively predict the progression to fulminant immune failure. Why don't
HIV-negative people with the same risk factors have the same immune
decline?"
"Lang et al actually say:
"'The three groups were 37 HIV seroconverters, 304 prevalent HIV
seropositives remaining free of the acquired immunodeficiency syndrome
(AIDS), and 69 men who developed AIDS during observation. Six months
before seroconversion, CD4 levels were similar among HIV seroconverters
and 356 seronegative controls. Within 18 months of seroconversion, mean
CD4 levels fell to the level of the prevalent seropositives at study
entry.'
"I do not think these are very good arguments for the drug-AIDS
hypothesis. Lang et al actually is excellent evidence for HIV infection
leading to immune failure.
"The question dissidents have to answer is why these antibodies so
effectively predict the progression to fulminant immune failure. Why don't
HIV-negative people with the same risk factors have the same immune
decline?"
END OF BENNETT QUOTE
Nicholas Bennett blithely excludes a very important factor that
explains why the Hiv + group's CD4s decline: the tremendous psychological
stress and depression caused by the stigma "Hiv +" itself.
Dr. Matthew Irwin has written:
"Many of the symptoms of AIDS are either directly caused, or made
much worse, by the severe, chronic psychological stress, social isolation,
and negative beliefs created by the diagnosis."
"The [HIV] diagnosis itself can bring about a self-fulfilling
prophecy because of the powerful negative beliefs it creates. Stress,
social isolation, and negative beliefs can create the same type of
immunodeficiency that is commonly blamed on HIV."
"Being diagnosed HIV-positive is perhaps one of the greatest
stressors one can imagine. Not only does it raise the constant and extreme
fear of a relentless deterioration and death, but it also creates a social
isolation that pervades all aspects of people's lives. Social isolation,
alone, has been associated with a 100% to 200% increase in mortality in
several studies. The amount of psychological stress in people diagnosed
HIV positive is likely to be much greater than the stress in the people in
these studies."
"Studies...have shown that severe, chronic stress results in a
syndrome remarkably similar to AIDS...characterized by a reduction of the
number of T-lymphocytes, with special targeting of CD4, helper T cells.
Severe stress has also been linked to...AIDS defining conditions,
including pneumonia, tuberculosis, dementia, wasting, and death. Stress
has been demonstrated...to cause brain damage and neuronal atrophy,
resulting in a dementia that mirrors 'HIV dementia'..."
Preceding from "Aids and the Voodoo Hex," "Problems with Hiv
Science."
Dr. Lawrence Badgley has written:
"T4 white blood cell counts are intimately related to mental focus.
One of my patients was without symptoms and went to another doctor for an
'AIDS test.' The doctor did the test, which was positive, as well as the
T4 helper cell count, which was 494 and normal. Upon learning that his
antibody test was positive, the patient went into a tailspin of depression
and fear. One week later he returned to the doctor because of his anxiety,
and his T4 helper cell count was taken again. After one week of depression
and no other symptoms, his T4 cells count fell over 50% to 234."
"This intimate relationship of the mind and body raises a question
about the true nature of the AIDS epidemic. It is not far-fetched to
postulate that much of the immune system depression among AIDS-test-
positive patients might be the result of doctors telling them that it is
likely they will get AIDS and die. The brain is a giant immune system
gland that operates on hope, joy, and optimism. The gland turns off in
response to mental attitudes of fear and depression."
Preceding from "Healing Aids Naturally"
By pretending the psychological factor doesn't exist, those who
maintain that Hiv causes Aids ignore the self-fulfilling prophecy nature
of the diagnosis. Failing to take this factor into account invalidates a
great deal of "Aids Science." The mind-body connection is real; we are not
just vessels full of chemicals. The drug-Aids hypothesis also ignores this
very strong causative factor. Disease is multifactorial and the mental
component is very powerful.
Competing interests:
None declared
Competing interests: No competing interests
Dear Dr. Montagnier,
Thank you for sharing your remembrances of the discovery of HIV with
the readers of Science Magazine online.
http://www.aidscience.org/science/298(5599)1727.html
A continuing challenge to the methodology which led to the first
human retrovirus discoveries is discussed at some length (along with many
other facets of AIDS) on the British Medical Journal’s Rapid Response
series:
EDUCATION AND DEBATE:
Didier Fassin and Helen Schneider
The politics of AIDS in South Africa: beyond the controversies
BMJ 2003; 326: 495-497
http://bmj.bmjjournals.com/cgi/eletters/326/7387/495
As part of that challenge, a specific and apparently competing
protocol has been described in research proposals put forward in the South
African Presidential AIDS Advisory Report, March 2001.
It is my understanding that the provider of one portion of this
alternative protocol, Dr Etienne de Harven, has extensive experience and
impeccable credentials in the field of retrovirology as the result of his
involvement in work which led to the discovery of at least one retrovirus
in animals.
I would like to better understand what, if anything, there is about
the centrifugation, filtration, and EM confirmation process(1) described
by de Harven which places it in a competitive stance in regard to the
methods used to discover the first few human retroviruses.
Participants in the BMJ debate might be more accurately described as
combatants, and yet their one point of agreement seems to be that no human
retrovirus has ever been discovered using the techniques described by de
Harven, or at least that no material so obtained has been confirmed to be
a retrovirus by satisfying additional steps(2) described as originating
with Institut Pasteur.
One such additional step in the verification of material nominated as
retroviral is to confirm its ability to infect a new cell, which you
describe as the ability to “pass on” the virus in your interview with
Djamel Tahi.
If by “pass on” you are referring to transfection techniques, I can
understand the challenge to your proof of infectivity, but wonder if that
was a necessity imposed by the inability to solve the problem of achieving
physical separation of the retrovirus without damage to its structure.
That such a dilemma exists is suggested by supporters of your work who
have taken the position that absolute purification to the degree demanded
by your detractors would so physically damage the HIV particles as to
render them incapable of infection. I have not been able to discern
whether a solution to this problem was innovated, either by you and your
team at Institut Pasteur, or by Gallo and company at the Laboratory of
Tumor Cell Biology (LTCB), during production of material suitable for use
in determining the nucleotide sequence of the new retrovirus for the first
time.
In any event, there appear to have been two successive phases of
innovation necessary to adapt the protocol (whether or not it has been
accurately described here) used to discover animal retroviridae in order
to produce the first of our current list of human examples.
One such innovation you recount in your Science article. “In 1977,
as the viral oncology unit became interested in the action of interferon,
I had an illuminating idea: Perhaps we couldn't isolate retroviruses from
human cancers because their expression was inhibited by production of
endogenous interferon. If we could neutralize this effect by treating
cancer cells with antiserum against interferon, we might be able to detect
a human oncogenic retrovirus.”
You also mention a prior innovation of Gallo et al., presumably
employed during the discovery of HTLV-I: “We used the new T cell growth
factor (now called interleukin-2) discovered in Robert Gallo's laboratory
to make short-term T lymphocyte cultures from cancer patients”. However,
I assume interleukin-2 is but one of the novel elements which formed what
was essentially a new retroviral search protocol developed by the LTCB in
the service of their discovery of the first human retrovirus.
Given the significance of the protocol employed at the time of these
early discoveries of HTLV and LAI/LAV, it seems remarkable that a complete
description of those procedures isn’t commonplace. Perhaps they are, and
I do not know where to look.
Do you know of a published source for, or can you provide, a
comprehensive, step-by-step guide to the production of retroviral material
as accomplished during the period of the discovery of HTLV and LAV/HIV? I
am thinking of something as concise and as detailed as the isolation
procedure described by Dr Etienne de Harven below(1); the sort of
explanation which could be used by a group of graduate students to
recreate the procedure from scratch, right up to the point where the
sequencing process begins.
Any assistance you could provide is greatly appreciated.
Jeffrey Evans
(1) Low speed centrifugation to separate and discard erythrocytes,
leukocytes and platelets. Plasma samples (10 ml) diluted 1/1 with cold
heparinized Ringer solution. Filtration by aspiration through a Millipore
0.6u membrane. Collecting filtrate #1, and filtering it this time using a
Millipore 0.2u membrane. Collecting filtrate #2 and placing it in
appropriate Beckman tubes for ultracentrifugation in either a fixed angle
or a swinging bucket rotor, using the refrigerated ultracentrifuge to spin
the sample under 30.000g for 2 hours. Inspect the tubes for the likely
presence of extremely small pellets. Avoiding any risk of resuspending the
pellets, cover them with 1.5 % glutaraldehyde in 0.1M cacodylate buffer
(pH7) overnight at 0-4°C, rinsed with buffer and post-fixed with 1% osmium
tetroxide for 90 min. After rinsing, the pellets will be kept for several
hours in 0.5% uranyl acetate at 0-4°C, dehydrated in ethanol and propylene
oxide and embedded in Epon. Thin sectioning with diamond knives, staining
with uranyl acetate and lead citrate will be followed by examination under
the transmission electron microscope at initial magnification ranging
between 10.000 and 40.000x.
(2) 1. Culture of putatively infected tissue.
2. Purification of specimens by density gradient ultracentrifugation.
3. Electron micrographs of particles exhibiting the morphological
characteristics and dimensions (100-120 nm) of retroviral particles at the
sucrose (or percoll) density of 1.16 gm/ml and containing nothing else,
not even particles of other morphologies or dimensions.
4. Proof that the particles contain reverse transcriptase.
5. Analysis of the particles' proteins and RNA and proof that these are
unique.
6. Proof that 1-5 are a property only of putatively infected tissues and
can not be induced in control cultures. These are identical cultures, that
is, tissues obtained from matched, unhealthy subjects and cultured under
identical conditions differing only in that they are not putatively
infected with a retrovirus.
7. Proof that the particles are infectious, that is when PURE particles
are introduced into an uninfected culture or animal, the identical
particle is obtained as shown by repeating steps 1-5.
Competing interests:
None declared
Competing interests: No competing interests
Nassim C. Kamdar refreshingly stated regarding dumping the term
'AIDS' Dissidents:
"I think it is high time to review the term 'aids dissidents' which
puts one in the inadvertently similar position as the "insurgents" in
Iraq; A negative concept that automatically creates in the mind of those
with a herd mentality an emotional detachment from anything associated
with the "dissidents"; and artificially compartmentalises researchers in
this field. Since AIDS 'dissidents' are neither 'anti-government' nor
'anti-anything' can we, at least, avoid using the term in our own
discussions. To get the ball rolling, 'AIDS-theory analysts' which
recognises a common effort towards a common goal."
Kamdar is shrewd in adopting this strategy/tactic and we should
follow her stance and start using the term 'AIDS' Analysts or 'AIDS'
Critical Theorists or even 'AIDS' Deconstructionists since such analytical
-critical-intellectual terms lifts so-called 'dissenters' out of the
arbitrary binary opposition between 'them' and 'us': 'insiders' versus
'outsiders', 'establishment' versus 'dissident'.
We are not 'AIDS' dissidents but 'AIDS' Reappraisers and The Group
for the Scientific Reappraisal of the HIV-AIDS Hypothesis came into being
as a group of signatories of an open letter to the scientific community.
The letter (June 6, 1991) had been submitted to the editors of Nature,
Science, The Lancet and The New England Journal of Medicine. The
unpublished letter stated:
"It is widely believed by the general public that a retrovirus called
HIV causes the group diseases called AIDS. Many biochemical scientists now
question this hypothesis. We propose that a thorough reappraisal of the
existing evidence for and against this hypothesis be conducted by a
suitable independent group. We further propose that critical
epidemiological studies be devised and undertaken."
Many so-called 'AIDS' dissidents are well respected and 'established'
scientists, doctors, philosophers, cultural theorists, lawyers,
journalists, as well as Noble Laureates Kary B. Mullis (Nobel Prize in
Chemistry, 1993) and Walter Gilbert (Nobel Prize in Chemistry, 1980); and
Serge Lang, arguably one of the most brilliant mathematicians in the
United States; and not forgetting retrovirologist, Peter H. Duesberg,
Ph.D., professor of Molecular and Cell Biology at the University of
California, Berkeley.
Duesberg isolated the first cancer gene through his work on
retroviruses in 1970, and mapped the genetic structure of these viruses.
This, and his subsequent work in the same field, resulted in his election
to the National Academy of Sciences in 1986. Duesberg was also the
recipient of a seven-year Outstanding Investigator Grant from the National
Institute of Health.
Here are a few quotes from established 'AIDS' Analysts on the flawed
and failed 'HIV/AIDS' Hypothesis:
Prof. Serge Lang:
"For a decade, there has been increasing concern about 'AIDS,' and a
virus called 'HIV' which is said to cause 'AIDS'. Having named this virus
'HIV - Human Immunodeficiency Virus - contributes to making people accept
that 'HIV is the cause of AIDS'. However, to an extent that undermines
classical standards of science, some purported scientific results
concerning 'HIV' and 'AIDS' have been handled by press releases, by
misinformation, by low-quality studies, and by some suppression of
information, manipulating the media and people at large…A number of
scientists have questioned the established view that 'HIV is the cause of
AIDS,' and they have given evidence that this view - I call it dogma - may
be invalid."
- Serge Lang, HIV and AIDS: Have We Been Misled? Questions of
Scientific and Journalistic Responsibility, Yale Scientific, Fall 1994.
Kary Mullis, Ph.D:
"Where is the research that says HIV is the cause of AIDS? There are
10,000 people in the world now who specialize in HIV. None has any
interest in the possibility HIV doesn't cause AIDS because if it doesn't,
their expertise is useless...I can't find a single virologist who will
give me references which show that HIV is the probable cause of AIDS. If
you ask a virologist for that information, you don't get an answer, you
get fury."
- Kary Mullis, Ph.D. Nobel Prize in Chemistry, 1993, for inventing
the polymerase chain reaction [PCR].
Walter Gilbert, Ph.D:
"Duesberg is absolutely correct in saying that no one has proven that
AIDS is caused by the AIDS virus. And he is absolutely correct that the
virus may...not be the cause of AIDS."
- Gilbert, Ph.D., Nobel Prize in Chemistry, 1980.
Peter H. Duesberg, Ph.D:
"If you think a virus is the cause of AIDS, do a control without it.
To do a control is the first thing you teach undergraduates. But it hasn't
been done. The epidemiology of AIDS is a pile of anecdotal stories,
selected to fit the virus-AIDS hypothesis. People don't bother to check
the details of popular dogma or consensus views."
- Peter H. Duesberg, Ph.D., Professor of Cell & Molecular Biology
Member, National Academy of Sciences.
Competing interests:
None declared
Competing interests: No competing interests
Dear Editor,
I think it is high time to review the term "aids dissidents" which
puts one in the inadvertintly similar position as the "insurgents" in
Iraq; A negative concept that automatically creates in the mind of those
with a herd mentality an emotional detachment from anything associated
with the "dissidents"; and artificially compartmentalises researchers in
this field.
The Pocket Oxford Dictionary definition: disagreeing, especially with
the established government system.
Since AIDS "dissidents" are neither "anti- government" nor "anti-
anything"can we, at least, avoid using the term in our own discussions.
To get the ball rolling , "AIDS-theory analysts" which recognises a
common effort towards a common goal.
NC Kamdar
nckamdar@iafrica.com.
Competing interests:
None declared
Competing interests: No competing interests
It appears as if my point was made rather too obviously.
I chose to give examples of high-risk cohorts specifically because of
the simple fact that none of the HIV-negative members demonstrated a
chronic decline in immune function, or more specifically a chronic yearly
loss of CD4 T cells.
Mr Tyler asks "However, how could [Ascher] have known [drugs had no
effect] when all 'HIV' positives were gay men, and according to Table 2,
100% of these gay men were also either 'heavy' or 'light' nitrite users."
Firstly, as I think Ascher made clear in followup correspondance, the
"light" users did included a number of non-users. Secondly the light
users actually had worse CD4 T cell counts, as a group, compared to heavy
users, in direct contradiction to the drug-AIDS hypothesis. Thirdly,
epidemiology allows one to consider individual factors one at a time with
the factor-less group acting as a control. Only those with HIV had losses
in their CD4 counts.
The simple reason why "heavy" popper usage correlated with higher
rates of KS is as I've explained before, they have a far higher risk of
acquiring HHV8 due to the association with popper use and anal sex. The
relationship is not poppers ->KS but rather poppers -> anal sex -
> HHV8 -> KS. The missing link fits all the cases, including those
that aren't related to poppers, and therefore is a better explanation.
The reader should be reminded that lifestyle factors were considered
as a cause for AIDS until the point where low-risk individuals were found
to have AIDS - these included heterosexual partners of IV drug users and
the hemophiliacs. At that time a blood-borne sexually transmitted
infection was considered - the epidemiology simply didn't fit a lifestyle
cause. That's not to say that non-HIV factors can't contribute (e.g. high
risk sexual practises increasing the risk of infection) but they
themselves are not sufficient nor necessary.
The longitudinal studies are the most striking, because unlike a
chronic exposure, these demonstrate that individuals _start_ to lose their
CD4 T cells, after several years of normal levels, coincidentally at the
same time as they start to produce antibodies to HIV. One must presume
that the two events are linked.
For sure, some HIV-negative people will get AIDS-indicator diseases,
in the same way as some non-smokers get lung cancer. This is why
epidemiology teaches us the merits of Relative Risk. When deciding
whether a factor is or is not contributary to an outcome we judge how
frequent the outcome is with and without the risk factors. When
controlled for HIV status, drug use had no effect on whether or not
someone got AIDS. When controlled for drug use, HIV status had a large
effect (the only independant risk factor). Mr Tyler quotes some studies
apparently showing decline in CD4 T cell counts, but a count of 800 is
still in the normal range! Can he provide examples of HIV-negative people
with CD4 counts of 200 or lower? Also if an immune system is damaged by
some other factor (no-one is denying that it can happen) then an infection
with a virus will of course be at a higher rate. I'm not surprised that
people with lower CD4 counts prior to infection had a higher risk of
acquiring HIV - it is well established that immune responses can protect
against HIV infection even with multiple exposures (e.g. Kaul et al from
2000 and 2001)
I wonder though why Mr Tyler quotes from Des Jarlais but omits the
following:
"We studied CD4 cell counts and percentages from 1984 to 1992 among
1,246 HIV-seronegative injecting drug users in New York City, a population
at very high risk for exposure to bloodborne pathogens. Severe CD4
lymphocytopenia was rare, and there was no evidence of an increase over
time. Of 229 subjects with longitudinal data, only four met the
surveillance definition for "idiopathic CD4 lymphocytopenia" (ICL)."
Hardly glowing evidence of support for the drug-AIDS hypothesis!
Marion et al don't actually demonstrate any immune deficiency at all,
aside from lack of responses to DNCB (a chemical that can cause skin
reactions). Responses to TB protein, candida and trichopyhton were all
normal.
Lang et al actually say:
"The three groups were 37 HIV seroconverters, 304 prevalent HIV
seropositives remaining free of the acquired immunodeficiency syndrome
(AIDS), and 69 men who developed AIDS during observation. Six months
before seroconversion, CD4 levels were similar among HIV seroconverters
and 356 seronegative controls. Within 18 months of seroconversion, mean
CD4 levels fell to the level of the prevalent seropositives at study
entry."
I do not think these are very good arguments for the drug-AIDS
hypothesis. Lang et al actually is excellent evidence for HIV infection
leading to immune failure.
The question dissidents have to answer is why these antibodies so
effectively predict the progression to fulminant immune failure. Why
don't HIV-negative people with the same risk factors have the same immune
decline? They have to answer why these antibodies are associated with
standard assays of viral culture and PCR which cannot detect anything in
matched control subjects. They have to ask why they have to propose
multiple causes which make little biological sense to explain all of these
findings, when one (a retroviral infection) rather neatly explains them
all!
As regards the two women in question, the average time of progression
in untreated individuals is 8-10 years. They are still within normal
variation - they won't even qualify for long-term non-progressor status
(of which around 5% of HIV+ people will do) for another 7 years (the year
2012). This has been well known for over a decade, but the dissident
views are based upon Duesberg's comments along the lines of "Infections do
not cause illness after 10 years". If only that were true! Besides, Ms
Maggiore has said that she has also had HIV-negative and HIV-indeterminate
tests, so frankly one wonders which to believe.
Sadly I haven't the time to address the important points raised about
the viral load techniques, but judging by the quality of the points I have
got around to addressing so far, I do not think that there is much
substance to the concerns.
Nick Bennett njb35@cantab.net
Competing interests:
None declared
Competing interests: No competing interests
Dear Nicholas Bennett and everyone else,
I have been pondering on a few puzzles I have regarding
"immunosuppression"- CD4 levels in relation to HHV-8 incidence and the
incidence of Kaposi Sarcoma within various geographical areas or "risk-
groups" and I wondered if anyone from any "side" could please answer the
following questions for me. I would be most greatfull if anyone from any
"side" could provide me with any references/studies/answers to my
questions.
1.What is the average CD4 in post operative kidney transplant
recipients on "immunosuppressive therapies" ?
2. What is the average CD4 in post transplant liver transplant
recipients on "immunosuppresive therapies" ?
3.Is there any evidence/references/studies that show any geographical
differences in the level of "immunosuppression"-CD4 occuring in organ
transplants recipients on "immunosuppressive" therapies ?
4. Am I right in thinking that currentley it is claimed/believed that
the differences in geograpical rates of Kaposi Sarcoma occuring in organ
transplant recipients is due to the background incidence/seroprevelance of
HHV-8 ?
5.Am I right in thinking that currentley it is claimed/believed that
the differences in geographical and "risk-group" rates of occurance of
aids type KS is due to the background incidence/seroprevelance of HHV-8 ?
Thank you in advance.
Best Wishes
James J Whitehead
Clinical trials volunteer
Member www.altheal.org and www.aidsmythexposed.com
Competing interests:
Clinical trials volunteer
Member www.altheal.org
Competing interests: No competing interests
Reply to Bennett: 'HIV' Dogmatists negate 'conventional thought'
Nicholas Bennett stated regarding critical 'AIDS' Analysts:
"There is no consistent view or aim, reflected in the regular
confused posts from newcomers to the dissident discussion boards.
Practically the only thing uniting them is a refusal to accept the
conventional thought."
On the contrary, critical 'AIDS' Analysts absolutely accept the
'conventional thought' (rules of virus isolation, etc), which is precisely
why we are questioning the proponents of the ‘HIV’ Hypothesis who
constantly ignore conventional thought about the practice of isolation,
etc.
It is precisely the total lack of "conventional thought" (and
conventional scientific practice) that mars the thinking of the proponents
of the 'HIV/AIDS' Hypothesis. For instance: when Koch’s Postulates, the
tried, trusted and ‘conventional’ method of proving the existence of a
pathogen were completely unfulfilled by 'HIV', the supporters of the 'HIV'
Hypothesis declared the Postulates to be rubbish.
Moreover, the 'conventional' rules for retrovirus isolation laid down
at a conference at the Pasteur Institute in 1974 were flagrantly ignored
by the scientific team working at the very same institute in 1983, who
claimed to have found a retrovirus in the tissues a homosexual man
suffering from lymphadonopathy merely by finding what they claimed to be
reversetranscriptase activity and other dubious surrogate markers.
However, when subsequently challenged, Luc Montagnier, the leader of the
team, admitted that they did not find or isolate any viral particles, and
despite heroic laboratory efforts - described by Montagnier, as "Roman
efforts" – no 'HIV' was found. If 'HIV' does not fit the conventional
rules, they rubbish those rules, move the goal posts and rewrite the rules
of the game – then shoehorn 'HIV' in as a 'killer pathogen' when in fact
it is nothing of the kind.
From the outset it was claimed, in order to explain the
embarrassingly elastic incubation period of 'HIV/AIDS' – said to be
anything from 10 to 30 years between putative 'infection' and onset of
disease - that 'HIV' was a lentivirus, a slow acting retrovirus. Yet now
we are told that 'HIV' causes 'AIDS' in a matter of months in Africa and
the Third World. Is 'HIV' a 'lentivirus' or not? As Peter Duesberg stated:
"There are no slow viruses – only slow virologists." Why is it that there
is still no heterosexual 'HIV' epidemic in the West whilst there is
allegedly a heterosexual 'HIV' epidemic in South Africa?
We are not 'dissidents' or 'denialists' but deconstructionists –
critical and autonomous 'AIDS' Analysts teasing out the absurdities,
anomalies, inconsistencies and contradictions of the redundant 'HIV'
Hypothesis.
It is the propagators of 'HIV' dogma who persistently refuse to
accept 'conventional thought' (and practice) and merely make up the rules
as they go along – changing the rules of 'virtual virology' virtually
daily – to patch up the tottering 'HIV' Hypothesis.
Competing interests:
None declared
Competing interests: No competing interests