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
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When I stated that the murine retroviruses were "sexually and
horizontally transmissible" in my previous post, I did of course mean to
write "sexually and vertically transmissible", as stated in the paper
referenced by Mr Whitehead.
I apologise for any confusion that may have resulted!
Nick Bennett njb35@cantab.net
Competing interests:
None declared
Competing interests: No competing interests
I would like to echo Mr Whitehead, as I have mentioned previously, in
being in support of larger-scale investigations of the benefits of
treating antioxidant deficiencies. At some point it would be nice to
think I would be in a position to make a more practical contribution to
the idea!
As regards HHV8 and carcinogenesis, Mr Whitehead may have missed the
several posts I made previously highlighting the fact that HHV8 contains
various genes that are related to or can function similarly to human cell-
cycle regulators. HHV8 is not only epidemiologically associated with KS,
but can be detected in all forms of KS, from almost all samples, but not
from surrounding tissues. The fact that it contains genes that are
demonstrably and theoretically capable of causing cancer is enough for
most people.
The phrase "cutaneous lesions resembling Kaposi's Sarcoma" is about
as proof-positive as you'll ever get in a journal. It's tantamount to
saying "we created KS"! They can't of course say that because KS is a
naturally occuring disease, whereas this was "only" created by adding the
viral gene(s) artificially. As Yang et al [1] conclude for example:
"Here, we report that a single gene of HHV8 is sufficient to induce
in mice an angioproliferative disease that bears striking similarity to
human KS. Clinically, the lesions start as erythematous maculae or plaques
and progress to violaceous, purplish nodules and tumors that develop
predominantly in the skin and to a lesser extent in intestine, heart, and
skeletal muscle. Histologically and ultrastructurally, these lesions show
characteristics similar to those of human KS and Kaposiform
hemangioendotheliomas. Lesions within the skin developed and spread within
the dermis while sparing the overlying epidermis. Like KS, the nodular
angioproliferative tumors formed slit-like vascular spaces containing
erythrocytes and were surrounded by spindle cells and infiltrating
inflammatory cells. Finally, vGPCR, VEGF, and CD34, markers that have been
detected in KS, are also detected within these lesions."
One wonders what description of a lesion Mr Whitehead would consider
better than this, as evidence supporting HHV8 in causing Kaposi's Sarcoma?
He uses the phrase "at best" as if the findings somehow fall short of
meeting his expectations, whereas for me as a virologist they far exceed
my wildest expectations! For example, we cannot (yet?) induce an AIDS-
like illness by adding a single gene from HIV into an animal model. To do
this for HHV8 and KS is a holy grail of viral pathogenesis.
HHV8 alone is clearly not sufficient, due to the fact that most of
those infected with the virus do not get KS, but immune deficiency
increases the risk of KS. Also the model of Yang et al is obviously full
of caveats because it is a transgenic animal rather than a viral
infection. But still, it's striking enough.
The report of a possible mouse model of AIDS mentioned by Mr
Whitehead is interesting because it highlights the problem I previously
mentioned to Alex Russell some time ago, regarding the prolific number of
mouse retroviruses: both exogenous and endogenous. The followup papers to
that report clearly demonstrate the fact that this was the result of a
previously unknown retrovirus infection, which is sexually and
horizontally transmissible. Two endogenous retroviruses were activated
and the co-infection results in the disease process mentioned (a
lymphoproliferative condition and an autoimmune CD4 T cell depletion) [2].
This of course has several implications - the use of transgenic
porcine organs in human transplantations has had the worry of porcine
endogenous retrovirus activation for some time. An interaction between
one such virus and a human endogenous RV cannot be easily ruled out, nor
the outcome predicted. Additionally, while HIV sequences are not detected
in the human genome, HIV-like sequences have been detected in certain
cancers, which may implicate a new exogenous retrovirus. Recombination
between an ancestral SIV and another human RV may have resulted in the
formation of HIV. Such a theory is supported by the observation that in
this mouse model of co-infections, possible co-packaging of both virus
genomes within virions occured [2].
Mostly speculation, but this result highlights the fact that multiple
viral co-infections may have unpredictable outcomes.
Nick Bennett njb35@cantab.net
1. Yang et al J Exp Med. 2000 Feb 7;191(3):445-54. "Transgenic
expression of the chemokine receptor encoded by human herpesvirus 8
induces an angioproliferative disease resembling Kaposi's sarcoma."
2. Hook J Virol. 2002 Dec;76(23):12112-22. "Characterization of a
novel murine retrovirus mixture that facilitates hematopoiesis."
Competing interests:
None declared
Competing interests: No competing interests
Dear Eleni ,The Perth Group, Nicholas and all,
I would just like to say that I back this this request 100%.
It has been shown through out this debate that antioxidants ect can
significantly slow down disease progression, improve survival,and reverse
some "aids" defining diseases like wasting.
The only way to resolve this debate is through scientific experiments
and large scale clinical trials. With and with out combo.
It would be interesting to repeat these two expeiments again in
animals pre depleted by some GSH lowering agent/s.
but also try using antioxidants like NAC,SAG,ALA to name just a few
,I am sure All "sides" could come up with some good designes.
Where is the evidence that "HIV" is causally related to KS? 25 August
2004
Christopher J Noble,
postdoc
Australia
"There is a bit more than just the correlation of HHV-8 with KS. There is
temporal relation showing HHV-8 seroconversion before development of KS.
There are also animal models for HHV-8 and KS. Etiology and pathogenesis
of Kaposi's sarcoma., Injection of human herpesvirus-8 in human skin
engrafted on SCID mice induces Kaposi's sarcoma-like lesions. "
REPLY
HHV-8 and KS 18 October 2004
Eleni Papadopulos-Eleopulos,
Biophysicist
Department of Medical Physics, Royal Perth Hospital, Western Australia,
6001,
Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman
Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala
"
Christopher Noble gave us one paper which apparently he considers to
contain "extremely strong evidence for the causal role of HHV-8 in
Kaposi's Sarcoma". The paper by Nickoloff et al entitled: "Etiology and
Pathogenesis of Kaposi's Sarcoma" was published in Recent Results in
Cancer Research, Vol. 160, page 331-342; 2002.
In his rapid response: "KS and UV", 20 September, Nicholas Bennett
wrote: "I have previously supplied information that supports the premise
of HHV8 being an oncogenic virus epidemiologically associated with KS. The
simplest conclusion (Occam's Razor) being that it is the likely cause.
Other factors do not share the same association. The Perth Group say that
I have not done so, but I point them in the direction of the many
responses here on the BMJ Rapid Responses, in particular one by myself
dated 21st August. If the Perth Group choose to ignore them that is their
perogative, but they cannot say I did not answer their request. They have
clearly read it because it sparked the discussion regarding the
carcinogenic properties of water and semen. It contains references that
I'm sure will answer most or all of the questions regarding the
oncogenicity of HHV8 and epidemiology of KS (if not them directly, then
the references within)."
Epidemiological association is not proof for causation. Neither in
Christopher Noble's reference nor in any of Nicholas Bennett's references
is there any theoretical basis in respect of the claim that HHV-8 is
carcinogenic. Nor is there any experimental evidence that HHV-8 is
carcinogenic. All the researchers who have tried to induce KS by HHV-8
have reported that at best they could obtain, "cutaneous lesions
resembling Kaposi's sarcoma" or "Kaposi's sarcoma-like lesions". However,
"dramatic depletion of CD4-positive cells, progressive impairment of the
immune response, and Kaposi's sarcoma-like tumours or terminal B-
lymphomas", can be induced "by mating BALB/c female mice to C57BL/6 males
during 1-year period (7-10 allogenic pregnancies) followed by immunisation
with paternal lymphocytes".[1] "
1. Ter-Grigorov VS, Krifuks O, Liubashevsky E, Nyska A, Trainin Z,
Toder V. A new transmissible AIDS-like disease in mice induced by
alloimmune stimuli. Nat Med 1997;3:37-41.
Best wishes
James J Whitehead
Clinical trials volunteer.
Member www,altheal.org and aidsmythesposed.com
Competing interests:
Member www.altheal.org
Competing interests: No competing interests
Julian Turningheart has written:
> he regurgitates (without references!) the tired, Catholic-bashing canard of Conventional Wisdom that Galileo was “ostracized”...
That is correct, no reference was provided. mea culpa.
And then...
> Galileo was vehemently suspected of heresy, not “ostracized”...
For which, (perhaps as an example of what not to do?) Mr Turningheart hasn't, well, provided a reference.
Having an inconsistent and unscientific theory for which you have no evidence does not entitle you to wear the 'I AM LIKE GALILEO YOU'RE ALL PICKING ON ME' badge.
Competing interests:
None declared
Competing interests: No competing interests
Tony Floyd (8 February 2005) demonstrates the thinnest veneer of
superficial understanding when he regurgitates (without references!) the
tired, Catholic-bashing canard of Conventional Wisdom that Galileo was
“ostracized” by “religious rulers” because of the uncomfortable
ramifications of his scientific conclusions. Were he to investigate the
matter rather than accept the consensus of the scientific herd, Mr. Floyd
might discover that Galileo was vehemently suspected of heresy, not
“ostracized”; furthermore, the heresy accusation was simply the stick with
which Galileo’s scientific competitors delivered his smackdown.
Let’s see now….scientist raises uncomfortable questions challenging
prevailing orthodoxy…..mainstream scientific community contracts vaporous
outrage…..charges of heresy fly. Hmmmm, sounds familiar.
Competing interests:
None declared
Competing interests: No competing interests
If Mr Russell was referring only to oncoretroviruses (as I well knew)
then he should have said so. Such lack of clarity can only confuse the
issue further. Since he admits that he cannot extrapolate the work of De
Harven to other virus types, does he perhaps admit that to expect the same
of lentiretroviruses is (somewhat) unreasonable?
Additionally, one wonders if Mr Russell is aware that the De Harven
methodology, as I questioned previously [1], is not actually capable of
isolating pure virus? As with many of the early "oncogenic" viruses, the
virus was actually composed of a mixture of replication incompetant
transforming virus(es), and transformation incompetant replicating virus
[2]. Perhaps some other form of isolation should be performed, like
genetic cloning? Since we're on the topic of murine retroviruses, does Mr
Russell accept that these entities exhibit sexual horizontal transmission
with a preferential male to female spread, which he claims should not be
possible for HIV? [3]
Prof Mullis' remark clearly states that "quantitative PCR" is his
issue, rather than PCR detection per se. Since he did not invent
quantitative PCR it seems a fair enough comment to make - his method of
PCR was indeed largely non-quantitative unless you were to perform simple
limiting dilution assays. Other workers have taken his original idea and
drastically improved upon it, to the point where some of the latest
quantitative assays do not actually use the PCR reaction at all [4, 5]!
And as to who is in a better position to know X, Y or Z, I find it ironic
that Mr Russell of all people holds this position, since he is clearly
debating in a field of which he has no formal training whatsoever. I
don't find it a problem to disagree with Prof Mullis any more than Mr
Russell finds it a problem to disagree with Dr Bennett!
As I have stated here before [6], the amount of RNA in a virion is
tiny - even 1 trillion virions would hardly contain enough RNA to be
visible on an agarose gel without some form of amplification, and in order
to get that many virions from a peripheral blood sample you would need the
entire circulating volume from 200 people with viral loads of 1 million
per ml! Hardly feasible. Culture and PCR on the other hand provide a
standard scientific approach to amplifying what is already there to more
manageable levels. Does Mr Russell have issue with using telescopes to
amplify the sight of a distant star or planet? Why with PCR for HIV?
In addition, blood virus titre is not necessary to cause a disease,
and I refer Mr Russell to the aforementioned viruses (Influenza, Rabies,
Epstein Barr Virus, Human papilloma virus and Adenovirus) to ask if he can
cite papers of significant peripheral viral load, sufficient to cause
disease (no doubt by some arbitrary criteria of his own).
If I had access to an EM and a category 3 suite, suitable training in
EM preparation, and of course the time, I would be happy to attempt the
kind of experiments asked by Mr Russell. However, as Hans Gelderblom has
said, virus titres are likely to be too low unless a modified protocol is
used, but since isolation has been achieved for cultured HIV perhaps the
methods employed there might be transferable (rapid harvest, anion
exchange chromatography, Optiprep centrifugation etc).
When I'm in a position to perform such an experiment I will ensure it
is at the top of my agenda.
Nick Bennett njb35@cantab.net
Refs:
1. Nick Bennett, Rapid Response 20th Dec 2004
2. Ney and Andrea, BLOOD, 1 DECEMBER 2000 VOLUME 96, NUMBER 12
"Friend erythroleukemia revisited"
3. Portis et al, J Virol 1987 Dec:61(4):1037-1044. "Horizontal
transmission of murine retroviruses."
4. Versant HIV-1 RNA 3.0 assay (bDNA)
5. NucliSens HIV-1 QT assay
6. Nick Bennett, Rapid Response 28 June 2004
Competing interests:
None declared
Competing interests: No competing interests
Tony Floyd stated:
"These days you cannot just dismiss thousands of scientific papers
without being challenged and asked for references when you've quoted
someone. With so many precedents provided by the 'perth group' you surely
can't blame me for being suspicious as to whether or not arguments
presented here have a factual basis?"
You can "dismiss thousands of scientific papers" if they are all
based upon a mistaken premise that 'HIV' has been isolated. I wish Floyd
would be far more "suspicious" of the 'HIV/AIDS' hypothesis than being its
passive propagator. I would like to remind Tony Floyd that the peer review
system has completely broken down when it comes to publishing so-called
'HIV' research papers because there is no contesting counter-critique. As
the legendary mathematician Serge Lang observed:
"The peer review system at present is being abused to obstruct or
prevent scientific discussion, by Scientific American-Pour la Science, in
addition to the major international magazines such as Nature and Science,
and the funding agencies in the United States." Serge Lang: To the cc
list for the HIV-Pour la Science file. Serge Lang goes on:
"To an extent that undermines classical standards of science, some
purported scientific results concerning 'HIV' and 'AIDS' have been handled
by press releases, by disinformation, by low-quality studies, and by some
suppression of information, manipulating the media and people at large.
When the official scientific press does not report correctly, or obstructs
views dissenting from those of the scientific establishment, it loses
credibility and leaves no alternative but to find information elsewhere.."
Serge Lang, Challenges, Springer, 1998.
And Professor Gordon Stewart stated:
"...since 1990, Nature, Science, the New England Journal of Medicine,
the British Medical Journal and other mainline, peer-reviewed journals
have preferred to reject papers by others besides my colleagues and myself
containing verifiable data that throws doubt on the claim that AIDS is
capable of causing epidemics in general populations of developed
countries..."
Prof. Gordon Stewart, A paradigm under pressure, Index on Censorship,
Vol.28, No.3, May/June 1999.
As a student Tony Floyd should always be questioning current
scientific paradigms because consensus science is bad science and also
challenge his teacher's assumptions and propositions. Or as C.H.
Waddington; geneticist, stated:
"The most formidable barrier to the advancement of science is the
conventional wisdom of the dominant group".
Nicholas Bennett stated:
"I prefer to see it that we are supplying evidence that directly
counters the (worthless) logic behind Mr Russell's arguments. Many, myself
included, would reject an argument if it weren't supported by some
evidence. Such evidence includes a reasonably sound knowledge base of the
field (so that, for example, arguments that HIV virions MUST be isolated
from peripheral blood, prior to claiming causation, can be rejected out of
hand."
The logic behind my arguments are based upon deconstructing the
illogical 'HIV/AIDS' hypothesis.
There is no "reasonably sound knowledge" that 'HIV' has been isolated
from peripheral blood and Nicholas Bennett is not "supplying evidence" to
prove that 'HIV' exists but merely quoting reference papers which are all
based upon the mistaken premise that 'HIV' has been isolated. Nicholas
Bennett's so-called "supplying evidence" merely means reiterating (and
taking on trust) what Gallo, Montagnier or Ho happen to publish – and not
deconstructing their flawed logic.
Nicholas Bennett and Tony Floyd should be more critical and open
minded to the counter-evidence rather be mere protectors and propagators
of the flawed and failed 'HIV' hypothesis.
Competing interests:
None declared
Competing interests: No competing interests
There is an endless supply of unproven theories. They can't all be right merely because Galileo was right. In fact they can't all be right because they contradict each other, much the same as Duesberg's theory that HIV (which he has isolated) is a spectator virus can never fit with certain alt-AIDs theories that HIV doesn't exist at all.
Galileo and colleagues were mathematicians and scientists who were ostracized by the religious rulers of the time. These days you cannot just dismiss thousands of scientific papers without being challenged and asked for references when you've quoted someone. With so many precedents provided by the 'perth group' you surely can't blame me for being suspicious as to whether or not arguments presented here have a factual basis?
Competing interests:
None declared
Competing interests: No competing interests
Mr Russell ends his recent post with:
"Floyd (like Bennett, Noble and Flegg) likes to give the impression
of intellectual rigour by quoting us an endless list of (worthless)
references to authorise, sanction and legitimate his (lack of)
argument(s)."
I prefer to see it that we are supplying evidence that directly
counters the (worthless) logic behind Mr Russell's arguments. Many,
myself included, would reject an argument if it weren't supported by some
evidence. Such evidence includes a reasonably sound knowledge base of the
field (so that, for example, arguments that HIV virions MUST be isolated
from peripheral blood, prior to claiming causation, can be rejected out of
hand). There is neither precedent nor rationale for making the argument,
especially considering the supporting observations and results. Unless of
course, one prefers to ignore the (worthless) observations and results.
Nick Bennett njb35@cantab.net
Competing interests:
None declared
Competing interests: No competing interests
Can Bennett at last now isolate 'HIV' via de Harven's methodology?
Regarding my quest for Bennett to isolate 'HIV' he obfuscated yet
again:
"Additionally, one wonders if Mr Russell is aware that the De Harven
methodology, as I questioned previously is not actually capable of
isolating pure virus? Perhaps some other form of isolation should be
performed, like genetic cloning?"
Regarding "genetic cloning": I ask Bennett what is the use of cloning
something unless you are absolutely sure of what it is you are cloning? It
is imperative that isolation and purification has to precede genetic
cloning. Contrary to Bennett’s claim, Etienne de Harven's methodology is
far more rigorous at isolation/purification of virus than other methods
and all other indirect surrogate markers which are non-specific. I would
ask Bennett to take a look at the elctronmicrogrgraph published in the
paper by Etienne de Harven (1) and he will notice that de Harven uses
three arrows to indicate impurities. Now look at the elctronmicrograph by
Gelderblom et al (2) where three arrows arbitrarily point to questionable
particles identified as ‘HIV’. In all honesty Bennett, which of these two
electronmicrographs represents the more purified virus? The putative 'HIV'
is in fact a collection of endogenous microvesicles and cellular proteins
(which also never seem to form particles - so how can they be infectious)?
The very title of their paper gives the game away: Cell membrane vesicles
are a major contaminant of gradient-enriched human immunodeficiency virus
type-1 preparations; Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ.
(Virology, 230:125- 133, 1997).
Hence Gelderblom's images are mistakenly labelled as 'purified HIV'
but are in fact a compost heap of microvesicles and cellular debris. Three
arrows point to barely discernible dots alleged to be 'HIV'. Gelderblom’s
image shows three ambiguous particles in a swamp of microvesicles and
cellular debris– hardly isolated 'virus'! So how does Bennett explain all
the other gunge in the image? Isolation means – need I remind Mr. Bennett
– separation from everything else. As The Perth Group have rigorously
argued: the isolation of ‘HIV’ has never been achieved. Therefore we must
stop using the acronym ‘HIV’. In another paper in the same issue of
Virology by Bess et al., the authors admitted that all sorts of debris and
extraneous matter banded at the same level as retroviruses in the sucrose
medium, principally cellular microvescicles, something that Etienne de
Harven had observed even in the 1960's. Material that bands at 1.16 does
not represent purified retrovirus ('HIV'); therefore in examining the
proteins that make up this soup, which belong to 'HIV' and which are
merely cell debris etc? How can one derive a vaccine from all this stuff?
Bennett goes on:
"Culture and PCR on the other hand provide a standard scientific
approach to amplifying what is already there to more manageable levels.
Does Mr Russell have issue with using telescopes to amplify the sight of a
distant star or planet? Why with PCR for HIV?"
If you have to amplify the putative 'HIV' in the first place by using
PCR to show that it is there at all then there was obviously not enough
'virus' present to have any pathogenic relevance or even an infectious
relevance.
Bennett concludes:
"However, as Hans Gelderblom has said, virus titres are likely to be
too low unless a modified protocol is used, but since isolation has been
achieved for cultured HIV perhaps the methods employed there might be
transferable (rapid harvest, anion exchange chromatography, Optiprep
centrifugation etc)."
If virus titres are too low then obviously ‘HIV’ is not an infectious
agent and cannot be doing anything. Again I ask Bennett: if the alleged
virus titres are that low how can they have any pathogenic or even
infectious relevance? A virus that is not doing anything cannot be doing
anything.
Or as Peter Duesberg and Harvey Bialy wrote in Nature:
"...infectious units, after all, are the only clinically relevant
criteria for a viral pathogen."
Peter Duesberg and Harvey Bialy (Nature, 375, 1995, p. 197).
References:
1) PROBLEMS WITH ISOLATING HIV, Etienne de Harven, MD. Brussels –
European Parliament – December 08, 2003.
2) Cell membrane vesicles are a major contaminant of gradient-
enriched human immunodeficiency virus type-1 preparations; Gluschankof P,
Mondor I, Gelderblom HR, Sattentau QJ. (Virology, 230:125- 133, 1997).
PROBLEMS WITH ISOLATING HIV, Etienne de Harven, MD. Brussels –
European Parliament – December 08, 2003:
"To demonstrate the problem’s magnitude it appears necessary to
compare current results on HIV with those obtained, previously, in
experimental pathology, on another retrovirus known to be significantly
associated with a particular leukaemia of laboratory mice, the Friend
leukaemia. Both retroviruses, i.e. the Friend leukaemia virus, and the HIV
hypothetically related to AIDS, share extremely similar morphology under
the electron microscope, have identical diameters, and sediment at the
same density in sucrose gradients. A direct comparison between isolating
and purifying these two different retroviruses is, therefore, entirely
appropriate.
Mice suffering from the Friend leukaemia have considerable numbers of
retroviral particles in their blood stream. This phenomenon, described as
'Viraemia' in the past, would be called 'Viral load', in today ’s
terminology. From only a few ml of the blood plasma of leukaemic mice, the
viral particles could be readily separated by a simple technique of
ultrafiltration, then sedimented by high-speed centrifugation and finally
prepared for electron microscopy.
On this electron microscope image, a uniform population of virus
particles is clearly recognized. They all have the same diameter and
morphology, and one has to look very carefully to identify rare, non-viral
structures, attesting to the high degree of purification of these
retroviral particles. Such samples of purified retrovirus were
successfully used to identify viral proteins and to extract viral RNA. The
method applied to achieve this purification of a typical retrovirus is
rapid, inexpensive and highly reproducible.
Most surprisingly, nobody has ever succeeded in demonstrating HIV
particles in the blood of any AIDS patient by this simple method, even
though patients were selected for presenting a so-called high 'Viral load'
as determined by PCR methods. This embarrassing lack of electron
microscope evidence for substantiating the nature of the so-called viral
load in AIDS patients was first reported during an important AIDS
conference that took place in Pretoria, S.A., in May 2000. None of the
AIDS experts present at that conference could demonstrate the presence of
retroviral particles in the blood of AIDS patients."
Competing interests:
None declared
Competing interests: No competing interests