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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Forgive me if I find it quite ironic that a writer/artist/philosopher (Russell) suggests to a postdoctoral PhD fellow in Infectious Diseases (Bennett) that he should sadly obtain "some form, any form, of education in the field" in order to appreciate that HIV does not exist, while quoting a "virologist" (Lanka) who believes that "viruses which are claimed to be very dangerous in fact do not exist at all" as the source for his evidence.
Competing interests:
None declared
Competing interests: No competing interests
Alexander Russell writes:
What isolated evidence does Nicholas Bennett have that
'retroviruses' really exist?
and
Sadly if Bennett had some form, any form, of education
in the field he would know better and realise that
'retroviruses' do not exist.
The Friend murine leukemia virus is a retrovirus or should
I write a 'retrovirus'.
Make up your mind! Did de Harven record electron
micrographs of Friend leukemia complex or not?
Competing interests:
None declared
Competing interests: No competing interests
Regarding 'endogenous entities' and 'epiphenomena' Peter Morrell
stated:
"I thank Alex Russell for explaining what 'epiphenomenon' and
'endogenous entity' mean in regard to HIV…However, he has not said if this
theory proposes that ALL viruses should be regarded as 'epiphenomena,'
'disease markers' and 'endogenous entities,' or whether this idea should
be confined solely to the so-called retroviruses?"
I thought it was blatantly obvious that not all 'viruses' are an
'epiphenomena,' 'disease markers' and 'endogenous entities'. I was writing
specifically about 'HIV' and 'retroviruses' which are these
'epiphenomena', 'disease markers' and 'endogenous entities' - and which
were wrongly classified as 'viruses'.
Peter Morrell concludes: "Can Alex Russell please therefore also
explain what makes this theory of AIDS superior to the standard HIV
theory? In particular, can he state what specific facts of the disease
this theory explains better, more clearly and neatly than the standard HIV
hypothesis? Or, to put it another way, what facts of the disease are not
satisfactorily explained by the HIV hypothesis that the epiphenomenon idea
explains better? I thank him in advance for these further clarifications."
All Peter Morrell's questions are best answered by Peter Duesberg's
superior drug/AIDS hypothesis which better explains 'AIDS' than does the
redundant 'HIV/AIDS' hypothesis. All the predictions based upon the
'HIV/AIDS' have been proven wrong. We have also had thousands of 'HIV' -
free 'AIDS' cases therefore 'HIV' fails to meet Koch's first postulate.
Duesberg's first three parts to his theory rely on Koch's 1st, 2nd,
3rd postulates: (1) free virus is not detectable in most cases of AIDS;
(2) virus can only be isolated by reactivating virus in vitro from a few
latently infected lymphocytes among millions of uninfected ones; (3) pure
HIV does not cause AIDS upon experimental infection of chimpanzees or
accidental infection of healthy humans.
The standard and simplistic 'HIV' theory also does not explain why
'AIDS' is solely restricted to specific 'high-risk groups' proving also
that 'HIV' is not an STD: there is no white heterosexual 'HIV' epidemic in
the West.
We must go back just before 'AIDS' was invented to1981 when five
young homosexuals, who were previously healthy, were diagnosed as having
Pneumocystis carinii pneumonia (PCP). Soon after these cases another
twenty-four young homosexuals were diagnosed as having Kaposi's sarcoma
(KS) and these cases initiated the term 'Gay Related Immune Deficiency',
or 'GRID'. In all these cases all the young homosexuals were heavy
recreational drug users, particularly 'poppers' (amyl nitrites) and the
correlation between KS and popper-use is 100%. Why is it that only
homosexuals who use poppers get KS? It is as absurd as saying that they
all drank cyanide but only died because they had 'HIV'.
To try and blame KS on a novel herpes virus is ludicrous because you
cannot have a herpes virus restricted to one group of people. By the early
1980s it was not seen as 'politically correct' to state that recreational
drugs cause immune damage and premature death so 'HIV' was soon invented
to take the blame (and the heat off the homosexuals) and the dangers of
recreational drug-use were tragically ignored and soon forgotten. Hence:
'HIV' was purely an invention of 'politcal correctness' and the social
construction of an 'equal opportunities disease'.
It must be remembered that all the first 'GRID' and 'AIDS' cases were
heavy consumers of recreational drugs and the 'AIDS' establishment at the
time saw the 'drug/AIDS' hypothesis as a viable contributory explanation
of these early cases.
Recreational drugs are known to cause endogenous 'HIV' expression. A
recent 'scare story' from New York alleging a new 'super strain' of 'HIV'
was (mis) 'diagnosed' from a man in his mid forties who took crystal
methamphetamine. Crystal methamphetamine is oxidative, it depletes
glutathione and induces apoptosis/cell death and depletes CD4's and
cultures and activates endogenous 'HIV' expression.
Crystal methamphetamine, an addictive stimulant, itself depletes the
immune system (not 'HIV'). Regarding this spurious 'super strain' of
'HIV', a cynical Dr. Robert Gallo stated: "The odds are enormous that it
is not going to go anywhere."
Here is a summary of Peter Duesberg's drug/AIDS hypothesis which
should answer Peter Morrell's questions neatly and eloquently.
The AIDS Dilemma: drug diseases blamed on a passenger virus, by Peter
Duesberg & David Rasnick, Genetica 104: 85-132. 1998:
Almost two decades of unprecedented efforts in research costing US
taxpayers over $50 billion have failed to defeat Acquired Immune
Deficiency Syndrome (AIDS) and have failed to explain the chronology and
epidemiology of AIDS in America and Europe. The failure to cure AIDS is so
complete that the largest American AIDS foundation is even exploiting it
for fundraising: 'Latest AIDS statistics 0,000,000 cured. Support a cure,
support AMFAR.' The scientific basis of all these unsuccessful efforts has
been the hypothesis that AIDS is caused by a sexually transmitted virus,
termed Human immunodeficiency virus (HIV), and that this viral
immunodeficiency manifests in 30 previously known microbial and non-
microbial AIDS diseases.
In order to develop a hypothesis that explains AIDS we have considered ten
relevant facts that American and European AIDS patients have, and do not
have, in common:
(1) AIDS is not contagious. For example, not even one health care
worker has contracted AIDS from over 800,000 AIDS patients in America and
Europe.
(2) AIDS is highly non-random with regard to sex (86% male); sexual
persuasion (over 60% homosexual); and age (85% are 25-49 years old).
(3) From its beginning in 1980, the AIDS epidemic progressed non-
exponentially, just like lifestyle diseases.
(4) The epidemic is fragmented into distinct subepidemics with
exclusive AIDS-defining diseases. For example, only homosexual males have
Kaposi's sarcoma.
(5) Patients do not have any one of 30 AIDS-defining diseases, nor
even immunodeficiency, in common. For example, Kaposi's sarcoma, dementia,
and weight loss may occur without immunodeficiency. Thus, there is no AIDS
-specific disease.
(6) AIDS patients have antibody against HIV in common only by
definition-not by natural coincidence. AIDS-defining diseases of HIV-free
patients are called by their old names.
(7) Recreational drug use is a common denominator for over 95% of all
American and European AIDS patients, including male homosexuals.
(8) Lifetime prescriptions of inevitably toxic anti-HIV drugs, such
as the DNA chain-terminator AZT, are another common denominator of AIDS
patients.
(9) HIV proves to be an ideal surrogate marker for recreational and
anti-HIV drug use. Since the virus is very rare (< 0.3%) in the
US/European population and very hard to transmit sexually, only those who
inject street drugs or, have over 1,000 typically drug-mediated sexual
contacts are likely to become positive.
(10) The huge AIDS literature cannot offer even one statistically
significant group of drug-free AIDS patients from America and Europe.
In view of this, we propose that the long-term consumption of
recreational drugs (such as cocaine, heroin, nitrite inhalants, and
amphetamines) and prescriptions of DNA chain-terminating and other anti-
HIV drugs, cause all AIDS diseases in America and Europe that exceed their
long-established, national backgrounds, i.e. >95%. Chemically distinct
drugs cause distinct AIDS-defining diseases; for example, nitrite
inhalants cause Kaposi's sarcoma, cocaine causes weight loss, and AZT
causes immunodeficiency, lymphoma, muscle atrophy, and dementia. The drug
hypothesis predicts that AIDS:
(1) is non-contagious;
(2) is non-random, because 85% of AIDS causing drugs are used by
males, particularly sexually active homosexuals between 25 and 49 years of
age, and
(3) would follow the drug epidemics chronologically
Competing interests:
None declared
Competing interests: No competing interests
Regarding the Ho paper I cited (Ho et al NEJM 1989 321:pp 1621-1625
"Quantitation of human immunodeficiency virus type 1 in the blood of
infected persons." [1]) Mr Russell confuses the issue by talking about
viral load. This particular paper was in fact measuring the number of
infected cells in the periphery. 3,500 per ml. This corresponded to 1 in
400 peripheral mononuclear cells (of which only a subset will be CD4 T
cells, around 10% in healthy people as I recall).
He is right in that peripheral viral load over-estimates cell-free
infectious virions by around 60,000 fold (I've admitted as much here
previously) but as Panteleo et al clearly state in their 1993 Nature
paper:
"The peripheral blood does not accurately reflect the actual state of
HIV disease, particularly early in the clinical course of HIV infection."
[2]
They show 10-100 fold higher levels of virus in the lymph nodes, a
concept I have been trying hard for some time to put across. To argue
that there isn't enough HIV in the blood stream to cause AIDS is a bit
like arguing there isn't enough influenza in tears to cause the flu.
Viral load is a surrogate marker of viral replication, NOT the entire
viral infection.
His comments regarding the use of uninfected controls are quite
right, which is why the data of Hellerstein [3] and Morhi [4] is
important. They measure peripheral T cell replication and death rates in
treated and untreated HIV+ people, and uninfected controls. They support
the initial conclusions of Ho and others, despite the fact that Ho didn't
perform as complete an analysis.
Hellerstein:
Healthy non-HIV infected: CD4 T cell halflife of 87 days.
HIV+ untreated: CD4 T cell halflife of 24 days. T cell replacement
rates UNCHANGED despite increased loss.
HIV+ treated: CD4 T cell halflife initially dropped further, then
recovered to normal over time (published in a later paper). Replacement
rates increased.
Mohri: Normal T cell replication: 0.004 per cell per day
HIV+ T cell replication 0.025 (over 6-fold higher)
Treated HIV+ 0.010 (steady decline over several months after
treatment initiation)
Cell death rates were also affected: 0.044 per cell per day in
uninfecteds versus 0.129 in untreated HIV patients.
Of interest are the other cell types. CD8 T cells also demonstrated
(as previously known through other methods) high levels of replication
(0.003 versus 0.023) but unlike CD4 T cells cell death rates were only
slightly increased (0.043 versus 0.050). Monocyte kinetics were entirely
unaffected by HIV infection. These findings, to me, rather neatly rule
out the non-specific causes of AIDS proposed by Duesberg and others.
Critics like Craddock, Duesberg and Bialy (and I would add, Russell!)
would prefer us to reject any less-than-perfect analysis (a fact I find
ironic considering that in Duesberg's 2003 paper he tries to argue using
HIV prevalence figures misrepresented as incidence [5], among other
errors). In truth, what one should do is take such results in the setting
of other findings and then come to a conclusion. Certainly one should
await clarifying work before deciding to reject (or accept of course) any
unclear results: but absence of evidence is not evidence of absence.
Regarding PCR, Mr Russell seems unable to comprehend the sheer
smallness of viruses. The titres of even an extremely high viral load
test are still 10,000 times lower than what Gelderblom estimates would be
necessary to perform EM from plasma samples. What method other than PCR
would Mr Russell like to see used? In my mind there is no philosophical
difference between "amplifying" virions per visual field by centrifugation
and amplifying virion genomes per test tube by PCR. There are several non
-PCR quantification methods (he mentions the branched chain DNA assay),
but I wonder if it's just the amplification step per se he objects to. A
virus, ANY virus, requires amplification steps in order to detect it.
Such steps include centrifugation, enzyme-linked antibody assays, PCR-
based assays. Microscopy itself is an amplification step! Powerful EM's
can even visualise the diploid RNA genome of HIV, never mind the virion,
but that doesn't mean we should spend weeks scouring microscope slides for
such things when we can PCR them up and detect them in a morning's work.
I note that Mr Russell ignores my points regarding DNA virus
replication in the nucleus (despite the fact that this puts a hole in his
world view on virus replication) and he then goes on to state that all
retroviruses are endogenous! Having spent some time studying genetics as
well as virology I can attest to the fact that the endogenous phenomenon
are well understood and quite distinct from the exogenous viruses. I also
find it rather amusing that in one fell swoop Mr Russell has obliterated
all of Duesberg's work and that of De Harven, since presumably the viruses
they isolated and characterised didn't exist either.
Retroviruses likely evolved from the endogenous entities, that much
is suggested from phylogenetic analysis, but Mr Russell's esoteric
"epiphenomenon" explanation as to why these sequences magically appear in
certain cells that just happen to carry a membrane receptor that this
viral agent uses to enter the cell, but in no other cell types, makes no
sense. Those are the findings for an exogenous virus. Such sequences
should be present in all cell types at all times. The HERV-W virus
responsible for Syncytin for example is present in all cells, even though
it is only expressed in the placenta. THIS is an endogenous
epiphenomenon. HIV is not.
I also note the following quotes, both from Mr Russell.
"No photograph of an isolated 'HIV' particle has ever been
published."
But in response to my statement that HIV has been isolated from
cultures he says "Precisely."
In addition, HIV has certainly been grown outside of co-cultures,
separately from virally-transformed cells, AND in the presence of viral
inhibitors [6]. This after all is how the antivirals are developed!! I
have never claimed that HIV has been isolated from peripheral blood or
semen (so Mr Russell is badly misrepresenting me there), whereas he HAS
just claimed that HIV is "never" grown in pure culture. Similarly to the
way he claimed that retroviruses were never passed on sexually and that
even so such an STD would be spread equally between the sexes. He was
wrong on both counts. [7]
If Mr Russell's world view of virology and genetics were supported by
the evidence he would have a point to make.
Nick Bennett njb35@cantab.net
1. Ho et al NEJM 1989 321:pp 1621-1625 "Quantitation of human
immunodeficiency virus type 1 in the blood of infected persons"
2. Pantaleo et al Nature. 1993 Mar 25;362(6418):355-8. "HIV infection
is active and progressive in lymphoid tissue during the clinically latent
stage of disease."
3. Hellerstein, M. et al Nature Medicine (01/99) Vol. 5, No. 1, P.
83; "Directly Measured Kinetics of Circulating T Lymphocytes in Normal
and HIV -1-Infected Humans"
4. Mohri et al J Exp Med. 2001 Nov 5;194(9):1277-87. "Increased
turnover of T lymphocytes in HIV-1 infection and its reduction by
antiretroviral therapy."
5. Duesberg et al J Biosci. 2003 Jun;28(4):383-412. "The chemical
bases of the various AIDS epidemics: recreational drugs, anti-viral
chemotherapy and malnutrition.
6. Smith et al J Virol. 1987 Dec;61(12):3769-73. "Resumption of virus
production after human immunodeficiency virus infection of T lymphocytes
in the presence of azidothymidine."
7. Portis et al. J Virol. 1987 Apr;61(4):1037-44. "Horizontal
transmission of murine retroviruses."
Competing interests:
None declared
Competing interests: No competing interests
Bennett stated: "RNA viruses (with the exception of the retroviruses
which must integrate) do largely replicate in the cytoplasm, since this is
far easier than trying to enter the nuclear membrane and there are
reasonable numbers of free ribonucleotides in the cytoplasm."
What isolated evidence does Nicholas Bennett have that 'retroviruses'
really exist?
Dr. Stefan Lanka, virologist and molecular biologist, stated:
"I already had a somewhat critical attitude when I started studying
molecular genetics, so I went to the library to look up the literature on
HIV. To my big surprise, I found that when they are speaking about HIV
they are not speaking about a virus. They are speaking about cellular
characteristics and activities of cells under very special conditions. I
was so deeply shocked…So for a long time I studied virology, from the end
to the beginning, from the beginning to the end, to be absolutely sure
that there was no such thing as HIV. And it was easy for me to be sure
about this because I realized that the whole group of viruses to which HIV
is said to belong, the retroviruses - as well as other viruses which are
claimed to be very dangerous - in fact do not exist at all."
(Stefan Lanka interviewed by Mark Gabrish Conlan, Zenger's Magazine,
San Diego -October 1998).
What we are wrongly calling 'retroviruses' are in fact the body's own
creation: what I nominate as 'endogenous entities' or an 'epiphenomenon'.
Sadly if Bennett had some form, any form, of education in the field he
would know better and realise that 'retroviruses' do not exist. No
photograph of an isolated 'HIV' particle has ever been published and yet
Bennett 'believes' it has but without offering us the evidence.
Competing interests:
None declared
Competing interests: No competing interests
Regarding David Ho's debunked 'virological mayhem model' Nicholas
Bennett stated:
"Ho et al found 3,500 tissue-culture infectious doses of HIV per
milliliter of peripheral blood. How much HIV would Mr Russell like?"
The 'gung-Ho' theory purporting to show 'high viral titres' was
completely demolished within a very short time, not least by a letter from
Peter Duesberg and Harvey Bialy grudgingly published in Nature (375, 1995,
p. 197). It is worth quoting at length:
"The senior researcher [George Shaw] of the Wei et al paper has
previously claimed that the method they used overestimates by at least
60,000 times the real titre of infectious HIV [Piatak et al, Science, 259,
pp 1749-1754, 1993]. 100,000/60,000 is 1.7 infectious HIV's per ml ...
Further, Ho and a different group of collaborators have just shown [Cao,
et al New Eng. J. Med 332, pp 201-208, 1995] that more than 10,000 'plasma
virions', detected by the branched-DNA amplification assay used in their
Nature paper, correspond to less than one (!) infectious virus per ml. And
infectious units, after all, are the only clinically relevant criteria for
a viral pathogen.” [my emphasis]
Moreover, David Ho's mathematical calculations have been challenged
by Prof. Serge Lang, the greatest mathematical mind in America, as being
rubbish, a typical example of a gigo – 'garbage in, garbage out' - Lang
stated:
"Ho and Shaw (among other authors) engage in the practice of throwing
math and statistics at people, pretending to give a mathematical model for
HIV infection and its purported effects, namely the destruction of CD4 T-
cells. There is developing a substantial history of criticisms of these
papers. We have already mentioned some criticisms in the preceding
section, concerning control groups. We now list other criticisms which
have developed over the last five years." (The Case of HIV: We Have Been
Misled, Sege Lang, Yale Scientific, Spring 1999, Volume 72, Nos. 2 &
3, pp. 9-19).
According to Mark Craddock, (School of Mathematics, University of New
South Wales, Sydney), the Nature papers (12 January, 1995) by Wei et al
(Viral dynamics in human immunodeficiency virus type 1 infection ) and Ho
et al (Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1
infection) should have failed peer review for the following reasons alone:
1) Obvious mathematical errors,
2) Unjustified assumptions unrelated to the empirical data,
3) Lack of control groups: (a) "Neither group compared the rate of T4
cells generated in the HIV positive patients with HIV negative controls",
(b) "It must surely be admitted that the system they are trying to study,
namely the interaction of HIV with T4 cells, might behave substantially
differently in people who are not being pumped full of new drugs, in
addition to 'antiretrovirals' like Zidovudine?"
Yet these flawed papers got past the peer reviewers and instigated
the fatal consequences of 'early intervention' ('hit early, hit fast')
which translated is a cynical marketing strategy for the 'anti-retroviral'
drug pharmaceuticals. It could be argued that David Ho's 'virological
mayhem model' was only ever devised to hard-sell 'anti-retroviral' drugs
in asymptomatic patients.
Here is Mark Craddock's crique of the Ho and Shaw Nature papers:
"The logic [of Ho and Shaw] here is remarkable. It is claimed that
HIV sends the immune system into overdrive as measured by a supposedly
accelerated production of T4 cells...But where are the healthy controls?
How can this production of T cells be ascribed to HIV if there is no
comparison made with healthy people? And even if there were a comparison,
how can the production be unambiguously attributed to the ‘battle’ with
HIV?...Does what Shaw and Ho say actually make sense?... Is their
mathematical analysis sound?...As a mathematician, I was intrigued by the
claim of John Maddox, editor of Nature, that the new results provide a new
mathematical understanding of the immune system. Unfortunately, my
confidence in this claim was badly shaken when it turned out that on the
very first page of the Shaw paper (Wei et al., p 117) they make an
appalling mathematical error. And in the same paragraph make an assumption
which turns out, by their own admission to have no basis in observation,
and which they give no justification for...They are trying to estimate
viral production rates by measuring viral loads at different times and
trying to fit the numbers to their formula for free virus. But if their
formula is wrong, then their estimates for viral production will be wrong
too..." ('HIV: Science by Press Conference', AIDS - Virus or Drug
Induced?', Kluwer Academy, 1996).
Craddock concludes in his analysis of the flawed Ho and Shaw papers:
"Ho uses the analogy of a sink with water pouring into it but the
drain is open. He argues that the virus is killing slightly more cells
than the body can replace and so you get a slow decline in T cells. In
terms of his analogy, the water flows out of the sink slightly faster than
it flows in. A better analogy would be that as the water level drops, the
drain gets bigger. So the process speeds up. Ho and Shaw’s data if you
read it correctly predicts that AIDS should develop in a matter of days
after infection or at most a few months. This is what exponential growth
is all about. The virus grows exponentially, doubling in number every 2
days in the absence of an immune response they say. So when the immune
response is weakest, before antibody production, it should kill every T
cell in the body quickly. This does not happen. I wonder how they explain
this?" (Analysis of the Ho and Shaw Papers, Mark Craddock PhD, School of
Mathematics, University of New South Wales, Australia).
If Ho and Wei were correct, it would be possible to pellet down
virions from fresh plasma taken from a person who has had a recent 'high
viral load' test result, and to see tightly packed identical viral
particles using EM, but so far this has never been achieved with HIV'. And
again: if Ho's 'viral mayhem model' was correct, why, in the previous
decade of 'HIV' research, did no one ever see these alleged 'high viral
titres'? More importantly, why, in the presence of these teeming
quantities of putative 'virus' did they need to amplify it using PCR to
find it at all – especially if 'HIV' is deemed to be at such high titres?
Bennett concludes: "HIV has certainly been isolated to extraordinary
levels of purity from lab cultures of peripheral blood and lymph nodes."
Precisely - but never in pure culture, always in co-culture,
utilising cell lines which are themselves suspected of harbouring virus.
It is also worth remembering that cultures exclude anything resembling an
immune response or any form of viral inhibitor. Cultures produce artefacts
which are very easily misinterpreted – "To culture is to disturb"!
Contrary to Bennett's unfounded claim, 'HIV' has never been recovered and
purified from a fresh blood or semen sample. 'HIV' has certainly not been
truly isolated.
As Peter Duesberg stated in 1987, 'HIV' is restricted to virtually
complete latency by antibodies and a latent 'virus' cannot cause a
disease.
Competing interests:
None declared
Competing interests: No competing interests
I thank Alex Russell for explaining what 'epiphenomenon' and
'endogenous entity' mean in regard to HIV. However, as I do not feel he
has explained enough of the aspects of the notion to my own satisfaction,
I must probe further. As I understand the concept being described, it
raises further questions.
From what he says, it is clear that Alex Russell does regard [some?]
viruses merely as 'associative factors' and as *effects* of a disease
process rather than the *cause* of a disease process. That to me is an
important distinction, and is as I originally assumed it to be from
reading his previous posts on this topic.
However, he has not said if this theory proposes that ALL viruses
should be regarded as 'epiphenomena,' 'disease markers' and 'endogenous
entities,' or whether this idea should be confined solely to the so-called
retroviruses?
Then, of course, running on with this notion to its logical
extensions, one needs to ask what proposed lifestyle factors, immune
system degradations or deeper organism derangements, for example, might
then be adduced as the suspected or proven causes that induce 'normal
cells' to then embark upon this deranged pattern of prolific virus
manufacture? Also, for example, does Alex Russell regard this idea as a
much more general theory of disease?
None of these points seem very clear to me even though the notion
seems essentially and intrinsically no more outrageous or outlandish than
the flawed and simplistic HIV theory. Can Alex Russell please therefore
also explain what makes this theory of AIDS superior to the standard HIV
theory?
In particular, can he state what specific facts of the disease this
theory explains better, more clearly and neatly than the standard HIV
hypothesis? Or, to put it another way, what facts of the disease are not
satisfactorily explained by the HIV hypothesis that the epiphenomenon idea
explains better? I thank him in advance for these further clarifications.
Competing interests:
None declared
Competing interests: No competing interests
I simply had to write upon reading Mr Russell's statement that:
"Most viruses replicate in the cytoplasm."
Sadly if he had some form, any form, of education in the field he
would know better.
RNA viruses (with the exception of the retroviruses which must
integrate) do largely replicate in the cytoplasm, since this is far easier
than trying to enter the nuclear membrane and there are reasonable numbers
of free ribonucleotides in the cytoplasm. RNA viruses also tend to encode
their own polymerases, and so can make mRNA's or rough equivalents without
using the cellular RNA polymerase II. The cell is there largely as an ATP
supply and source of amino and nucleic acids, and membrane (as
appropriate).
DNA viruses on the other hand require considerable quantities of
deoxyribonucleotides and furthermore often use the cellular DNA
polymerase, making nuclear entry a paramount feature of their replication
strategy. They also need some way to make mRNA, and RNA pol II is only in
the nucleus. Such viruses include adenovirus, papilloma virus, the herpes
viruses, parvovirus etc. Since the nuclear membrane is removed during
mitosis, and deoxyribonucleotide production is increased, many DNA viruses
induce cell cycling - this is why they are more frequently associated with
cancers.
The one exception, which is an exception to most "rules" of virology,
is the pox virus family. These behemoths are DNA viruses but encode their
own DNA and RNA polymerase and an entire deoxyribonucleotide production
plant, and so can replicate in the cytoplasm.
Nick Bennett njb35@cantab.net
Competing interests:
None declared
Competing interests: No competing interests
Peter Morrell stated: "Several times in his recent posts Alex Russell
has referred to HIV as "an epiphenomenon" and the viruses purportedly
involved as 'endogenous entities.' Can he please explain in greater detail
what he means by these terms?"
An epiphenomenon is an associative factor found in a disease which
cannot be shown to be either causative or contributory to said disease. –
association is not proof of causation.
Morrell continues: "For example, as I provisionally grasp this idea,
does he mean to say that viruses are simply random products of deranged
cells?"
In some cases, yes, they are - where viral proteins can be shown to
originate in the nucleus of the cell. Most viruses replicate in the
cytoplasm.
"Does he then further mean to say that such 'endogenous entities'
cannot realistically be regarded as the *causes* of a disease process, but
that they might be better understood as mere 'associative factors' or even
products of a disease? It would be very helpful if Alex Russell could
clarify these points."
It would seem that endogenous viruses are activated or released in
response to a prior disease condition. This may be the case with hepatic
viruses which are released by the liver and subsequently interpreted to be
the cause of the liver disease: i.e: hepatitis. In other words the liver
becomes diseased for other reasons - pathogenic assault, alcoholism, etc.
and then may release endogenous virus particles in response to the disease
rather than instigating the disease. However, hepatitis viruses when
generated replicate at a huge rate and massive titres are recorded; this
has never been the case with 'HIV'.
It is high time that many of the cherished assumptions about virology
be re-examined – not least assumptions concerning so-called
'retroviruses'. For instance is 'HIV' a lentivirus or not? If 'HIV' is
never found at a sufficient titre in vivo to be considered an infectious
dose – some 200 particles or more per ml of blood etc. - then it is
unlikely to be transmitted horizontally or only with the greatest
difficulty, as shown by the studies of Padian and others.
Traditionally, as Peter Duesberg reminds us, retroviuses are
transmitted vertically from female to offspring. The idea that highly
infectious 'HIV' is teeming in the blood and semen of infectees, and
therefore very easily spread, has never been demonstrated and is
completely false.
It is my hypothesis that what we are calling 'HIV', assuming it to be
an exogenous, infectious virus, is merely an over-interpretation of the
antibodies raised against a constellation of hitherto unobserved
endogenous proteins expressed by perturbed cells.
The Perth Group have dealt with each of the 'HIV' proteins in turn
showing them all to be standard cellular proteins; indeed they argue that
all data presented so far are consistent with the 'HIV' proteins being
cellular. Using 'HIV' antibodies as probes, 'HIV'proteins have been
identified in the tissues of persistently HIV-negative, healthy
individuals, including in blood platelet and skin cells, thymus, tonsil
and brain. (1).
Reference:
1) Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. (1993),
"Is a positive Western blot proof of HIV infection?", Bio/Technology
11:696-707.
Competing interests:
None declared
Competing interests: No competing interests
Re: When "HIV antibodies" are not "HIV" antibodies
The Perth group ask me: “How does a person develop “HIV-antibodies” apart from being infected with “HIV”?”.
To clarify matters for them, HIV antibodies are always induced by HIV infection. I am not claiming that a positive anti-HIV ELISA test is proof positive of HIV antibodies (and therefore HIV infection), it merely indicates a positive test.
The tests for HIV antibody are not 100% specific, since the assays used may rarely be reactive (positive) in the absence of specific HIV antibody. In the field of laboratory diagnostics this is what is known as a “false positive test”.
This is why a single positive HIV antibody test should not automatically be assumed to indicate an HIV diagnosis or infection.
They also ask: “When was the last time Peter Flegg told a patient of any description with “HIV-antibodies” he is not infected with “HIV”?”
I do encounter patients whose HIV antibody tests are falsely positive. The last occasion was about 6 months ago in a patient with acute hepatitis B, whose HIV screening test was reactive (but negative using confirmatory assays and negative 2 weeks later).
Perhaps I can ask the Perth group some questions in turn concerning the tests.
(1) Why do so many individuals whose lifestyles put them at risk for “oxidative stress” have negative HIV antibody tests?
(2) Why do these HIV-seronegative individuals not develop profound, clinically-relevant immunodeficiency?
(3) Why is it only those who are HIV seropositive who develop profound, clinically-relevant immunodeficiency?
Competing interests:
None declared
Competing interests: No competing interests