HIV; Reality
or Artefact?
By Stefan Lanka
An error can
never become true however many times you repeat it.
The truth can never be
wrong, even if no one ever hears about it.
Mahatma Gandhi
For the past 10 years or so it has been the
accepted wisdom that the human immuno-deficiency virus, HIV, causes
AIDS. It supposedly occurs in many body fluids, and its transmission
especially in semen and blood to a new host, triggers a slow but
inexorable progression to AIDS and ultimately death. To infect another
cell, HIV must at some stage in its life cycle exist as a separate and
identifiable entity.
What has been ignored and kept from public
awareness is, that there has never been a workable HIV test and that
the definition of 'positive' has always changed according to the views
of different organisations dealing with it, changed also according to
the kind of tests used and changed from laboratory to laboratory
performing the tests:
".. Its techniques have not been
standardised, and the magnitude and consequences of interlaboratory
variations have not been measured. Its results require interpretation,
and the criteria for this interpretation vary not only from laboratory
to laboratory but also from month to month .."(1)
The dispute over who discovered HIV (2), was a
distraction from the question of whether the virus actually exists at
all. The public was impressed that if a President and a Prime Minister
(3) had to meet to resolve attribution, then the thing they were
negotiating about must be real.
In 1993 a research group from Perth, Australia
succeeded in publishing a paper on the HIV test.(4) Since then anybody
could have read for him or herself that no AIDS test could ever work,
because HIV has never been isolated nor even shown to exist. Since
AIDS research and the media have largely ignored any critique of
HIV=AIDS, especially the essential question of whether HIV really does
exist, it is time to call again for a reappraisal of the whole
HIV/AIDS hypothesis. In going back to the origins of HIV virology and
telling the HIV story, a view will be presented which will make clear
that HIV itself, the very object of this Manhattan Project of modern
medicine, AIDS research, does not exist.(5)
A little virology
Viruses are essentially just packages of genetic
information enclosed in a coat which consists of proteins. They can
reproduce themselves only by infecting a suitable host cell and
appropriating the chemical machinery they find there. The proteins
making up the viruses are characteristic for each species of virus.
Apart from enveloping and transporting the genetic information intact,
the composition of proteins for a given virus results in a specific
shape for the virus particle.
This much is generally known. Less well-known is
the existence of other particles which look like viruses but aren't,
and are nonchalantly referred to as "virus-like" particles.
Such particles are far from rare, found, for example, always in
placentas, and very frequently in the artificial environment of
laboratory cell cultures. They have served to muddy the waters
considerably as far as AIDS research is concerned, because particles
just like these have been called HIV. To date, none of these has been
characterised and shown to exist as an entity which one may
justifiably call a virus.
One root of the belief in the
AIDS virus
In classical theory DNA encodes the genetic
material of heredity, which is then transcribed into messenger RNA
which in turn specifies the assembly of amino-acids to construct the
proteins of all living beings. In 1970 an enzyme (biological catalyst)
was discovered in extracts of certain cells which was capable of
converting a molecule of RNA into DNA. This was a revolutionary
discovery, because it overturned a fundamental tenet of molecular
genetics, namely, that the flow of information was strictly one-way
and never reversed. It had hitherto always been thought that DNA was
transcribed (converted) into messenger RNA and that the reverse
process from RNA to DNA was impossible. The enzyme responsible became
known as reverse transcriptase (6) and a lot of new myths arose.
An error of the past: cancer
caused by viruses.
It was believed that the new enzyme was a marker
for a virus, because the cells in which it was detected, and which
were used to study cancer (7), were thought to have become cancerous
through being infected by a virus. New to the idea of cancer viruses
(8) was that nucleic acid, when in the form of RNA could be converted
into DNA by the enzyme, thus providing a mechanism for viral nucleic
acid to be inserted anywhere in the chromosome of the cells.(9) These
"new" viruses became known as retroviruses.(10) The
insertion of certain retroviral genes was thought to trigger cancer.
The idea that these postulated viruses caused
cancer quickly became "hot news" the world over, but did not
survive investigation (11) and other explanations were sought.(12) The
theory did not predict or explain the dramatic increase in cancer
cases, cancer could not be shown to be transmissible, nor could it
suggest any remedy in the form of a vaccine.(13) Interestingly, the
spread of cancer viruses was blamed on homosexuals, prostitutes and
black people, just as AIDS came to be 13 years later.(14)
Whenever and wherever reverse transcriptase
activity was detected it was rashly assumed that retroviruses were at
work. This turned out to be a grave error, because it was later found
that the enzyme occurred in all living matter, proving that reverse
transcriptase activity had nothing to do with retroviruses per se.(15)
Repetitive elements
Further research showed that at least 10% of
mammalian DNA was composed of repetitive sequences which were referred
to as "nonsense genes", parts of which, nonetheless, were
described as "retroviral genes". They exist in their
hundreds if not thousands. Some of them can even replicate
independently and jump within and between chromosomes, and for this
reason became known as retrotransposons.
In the laboratory they can be made to migrate,
and when this happens reverse transcriptase is invariably detected,
which underlines the fact that reverse transcriptase activity has
nothing to do with retroviruses as such.(16)
LAV, HTLV-III, HIV and all
that
Because all this was already well known in 1983
it is incomprehensible that Francoise Barre-Sinoussi, a member of
Montagnier's group, as well as Gallo's group itself in 1984, claimed
to have discovered a new virus, when all they did was to demonstrate
reverse transcriptase activity, and to publish photographs of cellular
particles without proof that they were viruses. They could neither
isolate them nor show that they were responsible for creating the
observed reverse transcriptase activity nor the tissue abnormalities
from which they were obtained.(17) They concluded: "the role of
the virus in the aetiology of AIDS remains to be determined".(18)
What makes a virus new?
The isolation and purification of a real virus
is a straightforward matter, because unlike cells, viruses of one
species are always of the same size and shape, and can be readily
separated from other cell components by standard techniques. A control
experiment is to try an isolation with putative non-infected material
in exactly the same way as the supposedly infected material. Nothing
should be isolated in this case.
To identify a virus definitively, a first and
simple step is to photograph isolated particles of it in an electron
microscope, and they must look like the viral particles observed in
cells, body fluids or cell cultures to distinguish them from other
cellular particles which look like viruses, but are not. Proteins
making up the viral coat must then be separated from each other and
photographed. This produces a pattern which is characteristic of the
species of virus. A similar separation and identification procedure
must be gone through for the DNA or RNA of the virus. Only after the
viral proteins and nucleic acid components have been properly
identified, is it legitimate to speak of a new virus.
No evidence for the existence
of HIV
Such evidence has up till now never been
produced for HIV. No photograph of an isolated HIV particle has ever
been published nor of any of its proteins or nucleic acids. No control
experiments as mentioned above have been published to date. What has
been shown are photographs of virus-like particles in cell cultures,
but none of isolated viruses, let alone of a structure within the
human body having the shape ascribed to HIV. What the whole world has
seen are models representing HIV with dish aerials, said to be
receptors with which the virus attaches itself to cells.
The existence of HIV is inferred from an
antibody test, but how this is supposed to work, when the virus has
never been shown to exist and obtained free of contaminants, remains a
mystery.
The AIDS Test
Let us recall that the AIDS test is supposed to
detect antibodies produced by the immune system in response to
infection by the virus. This is routinely done by layering proteins
ostensibly from the virus in the wells of a plastic rack and adding
blood serum to be tested to each. If antibodies are present, they bind
to the proteins, and when this happens sophisticated staining
procedures can make this visible. But, because no proteins which are
viral and free from contaminants, have ever been obtained, one cannot
be sure what the antibodies are that bind to the proteins.
This is the crux of the problem facing all HIV
(AIDS) tests. The inability to isolate a viral entity, and to
characterise its constituent proteins unambiguously means that the
evidence for the existence of HIV using antibodies is just arguing in
a circle. Antibodies that are detected, are due to other causes.
Why no HIV test is ever able
to work
It is consequently quite illogical to claim that
a positive test results from prior contact with the virus.(19) Because
various ill-characterised proteins are involved, every test kit
manufacturer applies his own arbitrary criteria, and no two kits ever
give the same result. It makes no difference that learned committees
set standards to decide which tests should be regarded as
"positive" and which not, because this merely skirts round
the problem, namely, to what are antibodies actually being detected in
the AIDS test? It is of no help that nowadays "second" and
"third" generation tests exist using synthetic proteins
which give greater consistency and comparability, because only by an
unscientific stretch of the imagination are they viral proteins!
Neither fudging the true identity of the
proteins, nor advocating two kinds of test - reassuringly but
mistakenly described as "search" and
"confirmatory" tests - resolves this difficulty.
The ELISA test is used to screen for antibodies,
which is "confirmed" by the more specific Western Blot. The
dilemma cannot be stated more poignantly than by quoting from the
leaflet accompanying one such test kit:
"The test for the existence of antibodies
against AIDS-associated virus is not diagnostic for AIDS and AIDS-like
diseases. Negative test results do not exclude the possibility of
contact or infection with the AIDS-associated virus. Positive test
results do not prove that someone has an AIDS or pre-AIDS disease
status nor that he will acquire it".(20) Quite.
The direct proof of HIV
Some HIV researchers have tried to circumvent
the problem by pointing to something called "direct"
evidence for the virus. All that this meant, though, was arbitrarily
selecting a protein of a certain size which happened to coincide with
that shown in HIV models. The delusion of such "evidence"
was illustrated when the protein later turned out to be of human
origin! (21)
How the genetic information
of HIV was manufactured through ...
Despite this deplorable state of affairs the
majority of AIDS researchers still cling to the authenticity of HIV,
because a genetic sequence for it has been published. Moreover,
genetic procedures now exist, which, unlike antibody tests, attempt to
identify the presence of HIV more or less immediately, instead of only
weeks later when antibodies are formed. The fact that the genetic
tests (PCR)(22) do not give the same results as the antibody tests is
simply ignored.
Since no virus has been isolated, it follows
that no nucleic acid has been isolated from it either. Complicated
procedures are even so described in the literature, at the end of
which something is produced which is called the nucleic acid of
HIV.(23)
...a test tube
HIV and its DNA can allegedly be made by the
"bucketful" (24), but under very surprising conditions
which, inter alia, entail the use of extracts from plants and other
oxidising chemicals, which could not possibly exist in vivo.
Immortalised cell lines devised (and later patented) by the Montagnier
and Gallo groups are co-cultured with extracts from human cells or the
cells themselves. At the end of it all HIV itself is not actually
obtained - only reverse transcriptase activity is shown to occur -
which is taken to imply that the DNA that is found, must have been
viral in origin.
The real explanation of what happens is as
follows. In the mixture of cell cultures and stressed human cells, RNA
and reverse transcriptase come to be produced in large amounts,
because the cells have been specially selected and treated to do this.
The RNA is transcribed into DNA by reverse transcriptase, and long
pieces of DNA are produced which are said to be viral DNA. In fact
they are composed of unrelated pieces of expressed cellular RNA,
transcribed into DNA and linked together by a process of
"template switching" (a well-characterised property of
reverse transcriptase).(25) This misleads ordinary researchers into
believing that they have actually produced viral DNA.
It is said that this linear DNA is the free or
the non-integrated form of HIV, which furthermore is said to be a
unique feature of HIV, because a lot of detectable free linear DNA has
not been suggested in any other models of retroviruses.
...and a selecting process
The resulting pieces of DNA too, are necessarily
both shorter and longer than the "correct" length of HIV.
Pieces corresponding to the "correct" length of HIV must be
selected for size, because otherwise the purported DNA preparation
would be a mixture of various lengths, which would violate a cardinal
rule of virology that all nucleic acid of a particular virus be
identical in size.
...and a detecting process
Having artificially prepared DNA pieces of
uniform length, they are still not ready for presentation, because
they consist of a mixture of all kinds of RNA fragments transcribed
into DNA and thus cannot be shown to represent unique viral DNA.
Accordingly, the mixture is subjected to a kind of lock-and-key
detection process called hybridisation, whereby pieces of DNA are
detected which complement more or less a probe of that which it is
desired to be shown to have been prepared.
...and choosing a desired
probe
Since no DNA from HIV existed to hybridise with
the prepared DNA, Gallo and Montagnier simply used stretches of DNA
from what they said was specific to HTLV-I, a retrovirus Gallo had
earlier claimed to have discovered, and which they deemed suitable for
this purpose. The DNA detected in this way was replicated and certain
stretches of it cloned and declared to be the DNA of HTLV-III (later
to be called HIV).
To summarise, the purpose of the exercise is to
grow HIV, but it actually produces a mixture of different lengths of
DNA, contrary to theory which says they should all be identical, and
no virus at all. It is then claimed that the "correct" DNA
has been prepared by finding certain strands in this heterogeneous mix
by hybridising them with an HTLV-I DNA probe whose sequence is known
and defined to be similar to HIV. However, non-hybridising strands of
DNA should not be there at all, and the fact that they are, proves
that a complete rag-bag of DNA has been prepared, without any
indication of what it is made up of.
It follows that "HIV" DNA must just be
a laboratory artefact constructed to a preconceived idea of what
retroviral DNA should be, and this assessment does not even raise the
question why no virus can be obtained, whatever the experimental
conditions.
Gallo and Montagnier's cloned
HIV DNA
One cannot help asking why no-one had not long
ago spotted the flaw in the techniques employed by the Gallo and
Montagnier groups. After defining some segments of DNA to be
"HIV"-specific, every researcher in the field worked
exclusively with short, cloned sequences (never the whole strand) on
the reasonable assumption that the original characterisation had been
correctly performed. From the isolation and identification procedure
described above, it follows that the resultant sequences vary widely
from one preparation to the next, which sequence analysts
misinterpreted as the legendary capacity of HIV to mutate. A computer
simulated phylogenetic tree was constructed, which established
precisely what its designer sought to prove.(26)
Some history
(I) Perhaps one reason for this calamitous state
of affairs is that HTLV-III was presented to the world as the cause of
AIDS at a historic press conference on April 23, 1984 (a patent for an
antibody test was applied for on the same day!), instead of making the
evidence for it available beforehand, as correct science demands. The
undue haste may be explained by the fact that both the National Cancer
Institute and the Centers for Disease Control (CDC) had actually one
day earlier in a lengthy front page article in The New York Times on
April 22 come out in favour of the French claim for priority.(27)
(II) Even so, one must admire Gallo's audacity,
because using the same technique he claimed in 1975 to have discovered
the first human retrovirus (HL23), but which turned out to be nothing
more than pieces of DNA from three different sources of
contamination.(28) Nowadays, even an undergraduate would know that if
you added DNA to a cell culture, part of the DNA would be incorporated
into the cells without any virus being involved.
What does the AIDS test
actually test for?
Since "HIV" has been shown to be a
laboratory artefact it must be assumed that, when not just
cross-reacting with other known antibodies, the "AIDS" test
detects antibodies against proteins produced in the procedure itself.
They must be of human origin because the cells used originated from
leukaemic patients. Test positivity, logically, results from
immunological contact with them. However, since positivity actually
correlates with otherwise unrelated factors such as rheumatism and sun
bathing, no specificity can be ascribed to the test.(29) Whether
antibody positivity really correlates with disease as is commonly
supposed, remains to be determined by a critical re-evaluation of the
data. Condoms, therefore, serve only to protect against venereal
diseases and as contraceptives, and worse lull the user into a false
sense of security by ignoring real dangers he may be exposing himself
to.
Re-direction of AIDS research
AIDS research is therefore back at square one
and not at Basic Science as suggested elsewhere.(30) The main players
have since 1993 begun to slink off, arguing that the virus having
mutated so much is now no longer detectable. AIDS has therefore to be
explained "in the absence of further whole virus".(31) Apart
from the shortcomings of the antibody test, other misconceptions such
as T-cell counting exist, which mean that the whole concept of AIDS
needs to be completely revised.(32) It must be shown that there is any
point in renaming a collection of known diseases as AIDS, just because
someone is positive in the antibody or genetic (PCR) tests. Leaving
HIV out of the picture explains why the epidemiological projections,
which years ago had forecast a world-wide epidemic, have been a
complete failure. Africa in 1986 was held up as a dire warning of what
would befall the Western world. There, AIDS was diagnosed by a
combination of clinical conditions (33) such as chronic fevers,
diarrhoeas, coughs and weight loss, all symptoms of the diseases of
poverty, without testing for HIV antibodies.(34) It should hardly come
as a surprise that an entirely different definition produced a
different outcome.
Finally, the effect of a positive test result on
mental and physical health needs to be considered and
investigated.(35)
Anti-virals
Whatever happens, the use of AZT and other
"anti-virals" which are supposed to target HIV replication,
but actually kill cells indiscriminately (and ultimately the whole
body), must be stopped immediately. It is especially distressing to
note that AZT and its analogues preferentially attack those cells
which divide most rapidly, namely, cells in the intestines causing
diarrhoea and malabsorption of food, and in bone marrow, ironically,
the primary production site for cells of the immune system.(36)
The people who need
enlightenment
The most important and delicate task is to
convince HIV positives that their test result is not a death sentence,
to be generally supportive of them, to assuage their anxiety, and to
help them understand that with appropriate treatment of any specific
disease, they have a good chance to retain or regain their health. The
large number of long-term positives, whose condition cannot be
explained by conventional AIDS theory, as well as the phenomenon of
sero-reversion (return to negative test status), provide eloquent
testimony to this. HIV/AIDS researchers and health officials are
herewith called upon to debate the whole subject of HIV/AIDS openly
and humanely, and to recognise the mistake that immune deficiency was
acquired by an infectious agent.
The future
To be able to live a fuller life we have first
to regain and then retain autonomy over our bodies and health from
self-appointed experts, who have dispossessed us of it.(37)
If we refuse to learn from what has happened in
AIDS research and related medical policies, then worse is on the way,
some of it is, indeed, here already.(38) The genetics agenda begun in
the 1860's (39) and a primitive genetic determinism have become
established through the availability of genetic sequences and the
ability to manipulate them easily, which are, in fact, pure
fantasy.(40) Furthermore, all models of genetics and associated
technologies, e.g. genome therapy, are based on a one-dimensional,
static model of genetics which is a crass oversimplification, not
defensible even when Mendel first proposed it.(41) *
Health as a Virtue (Ivan
Illich):
Health designates a process
of adaptation. It is not the result of instinct, but of an
autonomous yet culturally shaped reaction to socially created
reality. It designates the ability to adapt to changing
environments, to growing up and to ageing, to healing when damaged,
to suffering, and to the peaceful expectation of death. Health
embraces the future as well, and therefore includes anguish and the
inner resources to live with it.
Health designates a process
by which each person is responsible, but only in part responsible to
others. To be responsible may mean two things. A man is responsible
for what he has done, and responsible to another person or group.
Only when he feels subjectively responsible or answerable to another
person will the consequences of his failure be not criticism,
censure, or punishment but regret, remorse, and true repentance. The
consequent states of grief and distress are marks of recovery and
healing, and are phenomenologically something entirely different
from guilt feelings. Health is a task, and as such is not comparable
to the physiological balance of beasts. Success in this personal
task is in large part the result of the self-awareness,
self-discipline, and inner resources by which each person regulates
his own daily rhythm and actions, his diet, and his sexual activity.
Knowledge encompassing desirable activities, competent performance,
the commitment to enhance health in others - these are all learned
from the example of peers or elders. These personal activities are
shaped and conditioned by the culture in which the individual grows
up: patterns of work and leisure, of celebration and sleep, of
production and preparation of food and drink, of family relations
and politics. Long-tested health patterns that fit a geographic area
and a certain technical situation depend to a large extent on
long-lasting political autonomy. They depend on the spread of
responsibility for health habits and for the socio-biological
environment. That is, they depend on the dynamic stability of a
culture. The level of public health corresponds to the degree to
which the means and responsibility for coping with illness are
distributed among the total population. This ability to cope can be
enhanced but never replaced by medical intervention or by the
hygienic characteristics of the environment. That society which can
reduce professional intervention to the minimum will provide the
best conditions for health. The greater the potential for autonomous
adaptation to self, to others, and to the environment, the less
management of adaptation will be needed or tolerated.
A world of optimal and
widespread health is obviously a world of minimal and only
occasional medical intervention. Healthy people are those who live
in healthy homes on a healthy diet in an environment equally fit for
birth, growth, work, healing, and dying; they are sustained by a
culture that enhances the conscious acceptance of limits to
population, of ageing, of incomplete recovery and ever-imminent
death. Healthy people need minimal bureaucratic interference to
mate, give birth, share the human condition, and die. Man's
consciously lived fragility, individuality, and relatedness make the
experience of pain, of sickness, and of death an integral part of
his life. The ability to cope with this trio autonomously is
fundamental to his health. As he becomes dependent on the management
of his intimacy, he renounces his autonomy and his health must
decline. The true miracle of modern medicine is diabolical. It
consists in making not only individuals but whole populations
survive on inhumanly low levels of personal health. Medical nemesis
is the negative feedback of a social organization that set out to
improve and equalize the opportunity for each man to cope in
autonomy and ended by destroying it.
Acknowledgements:
This article is dedicated to Ivan
Illich and Thomas McKeown: had their writings been taken more
seriously the world would have been spared the AIDS panic as well as
other perversions. I would also like to thank Volker Gildemeister (Meditel,
London) for translation and constructive criticism, and of course, my
family, Hans-Walter Wiegand and other friends too numerous to list,
for all their support.
References
1 Klemens B. Meyer and Stephen G.
Pauker. 1987. Screening for HIV: Can we afford the false positive
rate? NEJM 317: 238-241. See also: Marsha F. Goldsmith.
1985. HTLV-III testing of donor blood imminent; complex issues
remain. JAMA 253: 81-86, 173-175, 179-181.
2 John Crewdson. The Great AIDS
Quest. Special report. Nov. 19. 1989. Chicago Tribune.
3 Frankel, Mark; Mary Hager, Theodore
Stanger. July 25 1994. The End of a Scientific Feud. Newsweek.
4 Eleni Papadopulos-Eleopulos,
Valendar F. Turner, John M. Papadimitriou. 1993. Is a positive
Western Blot proof of HIV infection? Bio/Technology 11: 696-707.
5 A similar article was published in a
German monthly: Stefan Lanka. 1994. Fehldiagnose AIDS?
Wechselwirkung, Aachen, December, 48-53.
6 Temin H.M. and Mizutani. 1970.
Viral RNA-dependent DNA-polymerase. Nature 226: 1211-1213. Temin
H.M. and Baltimore D. 1972. RNA-directed DNA synthesis and RNA tumor
viruses. Adv Vir Res 17: 129-186.
7 Gerald B. Dermer. 1994. The
Immortal Cell: Why Cancer Research Fails. Avery Publishing Group,
Garden City Park, NY. Gerald B. Dermer. 1994. Another Anniversary
for the war on Cancer. Bio/Technology 12: 320.
8 Gye W.E. and W.J. Purdy. 1931. The
cause of Cancer. Cassell, London.
9 Weiss R. et al. 1982. RNA Tumor
Viruses. Cold Spring Harbor Laboratory. Cold Spring Harbor, New
York.
10 Bishop J.M. 1978. Retroviruses.
Ann. Rev. Biochem. 47: 35-88. Bishop J.M. 1983. Cellular oncogenes
and retroviruses. Ann. Rev. Biochem. 52: 301-354. Doolittle R.F.
et al. 1989. Origins and evolutionary relationships of retroviruses.
The Quarterly Review of Biology 64: 1-30. Varmus H. and Brown P. 1989.
Retroviruses. In: Mobile DNA: 53-108, eds.: Berg E. and Howe
M.M. American Society for Microbiology. Washington D.C. Coffin J.M.
1990. Retroviridae and their replication. In: Virology. Fields
B.N. ed., New York. Doolittle D.F. et al. 1990. Retrovirus
Phylogeny and Evolution. Current Topics in Microbiology and
Immunology 157: 1-18.
11 Why we will never win the war on
AIDS. Ellison B.J. & Duesberg P.H. 1994 Inside Story
Communications, El Cerrito CA
12 John Higginson, Calum S. Muir,
Nubia Munoz. Human cancer: epidemiology and environmental causes.
Cambridge University Press. Samuel S. Epstein. 1992. Profiting from
Cancer. Vested Interests and the Cancer Epidemic. The Ecologist
22: 233-240. Samuel S. Epstein. 1993. Evaluation of the National
Cancer Program and proposed reforms. International J. Health
Services 23: 15-44.
13 Tim Beardsley. 1/1994. A war not
won. Scientific American 70: 118.
14 see ref 11
15 Malcolm A. Martin et al. 1981.
Identification and cloning of endogenous retroviral sequences present
in human DNA. PNAS 78: 4892-4896. T.I. Bonner et al. 1982. Cloned
endogenous retroviral sequences from human DNA PNAS 79: 4709-4713.
Callahan R. et al. 1982. Detection and cloning of human DNA
sequences related to the mouse mammary tumor virus genome. PNAS
79: 5503-5507. Temin H.M. 1985. Review: Reverse Transcription in
the Eukaryotic Genome: Retroviruses, Pararetroviruses,
Retrotransposons, and Retrotranscripts. Mol. Biol. Evol. 2:
455-468. Harold Varmus. 9/1993. Reverse Transcription.
Scientific American 257:48
16 Dixie L. Mager and Paula S.
Henthorn. 1984. Identification of a retrovirus-like repetitive
element in human DNA. PNAS 81: 7510-7514. Catherine O'Connell et
al. 1984. ERV3, a full-length human endogenous provirus:
chromosomal localization and evolutionary relationships. Virology
138: 225-235. Baltimore D. 1985. Retroviruses and Retrotransposons:
The Role of Reverse Transcription in Shaping the Eukaryotic Genome.
Cell 40: 481-482. Paulson K.E. et al. 1985. A transposon-like
element in human DNA. Nature 316: 359-361. Callahan R. et al.
1985. A new class of endogenous human retroviral genomes.
Science 228: 1208-1211. Weiner A.M. et al. 1986. Nonviral
retrotransposons: Genes, pseudogenes, and transposable elements
generated by the reverse flow of genetic information. Ann. Rev.
Biochem. 55: 631-61. Dixie L. Mager and Douglas Freeman. 1987. Human
endogenous retroviruslike genome with Type C pol sequences and gag
sequences related to human T-Cell Lymphotropic viruses. J Virol.
61: 4060-4066. Shih A. et al. 1989. Detection of multiple, novel
reverse transcriptase coding sequences in human nucleic acids:
relation to primate retroviruses. J Virol. 63: 64-75. Krause H. et
al. 1989. Molecular Cloning of a Type D Retrovirus from Human Cells
(PMFV) and its Homology to Simian Acquired Immunodeficiency Type D
Retroviruses. Virology 173: 214-222. Wilkinson D.A. et al. 1990. Autonomous
expression of RTVL-H endogenous retroviruslike elements in human cells.
J Virol. 64: 2157-2167. Banki K. et al. 1992. Human T-cell
lymphotropic virus (HTLV)-related endogenous sequence, HRES-1, encodes
a 28-kDa protein: A possible autoantigen for HTLV-I gag-reactive
autoantibodies. PNAS 89: 1939-1943. Horwitz M.S. et al. 1992. Novel
Human Endogenous Sequences Related to Human Immunodeficiency Virus
Type 1. J Virol. 66: 2170-2179. Maizels N. and Weiner A.M. 1993. The
Genomic Tag Hypothesis: Modern Viruses as Molecular Fossils of Ancient
Strategies for Genomic Replication. In: The RNA World. Gesteland
F. and Atkins J.F. eds. Cold Spring Harbor.
17 Robert C. Gallo et al. 1984.
Frequent detection and isolation of cytopathic retroviruses (HTLV-III)
from patients with AIDS and at risk for AIDS. Science 224: 500-503
18 Francoise Barre-Sinoussi et al.
(including. L. Montagnier). 1983. Isolation of a T-lymphotropic
retrovirus from a patient at risk for Aquired Immune Deficiency
Syndrome (AIDS). Science 220: 868-871. Robert C. Gallo et al.
1983. Isolation of Human T-Cell Leukemia Virus in Acquired Immune
Deficiency Syndrome (AIDS). Science 220: 865-867.
19 see ref 4
20 Bio-Rad, 1989.
21 see ref 4
22 Just how little confidence is
placed in the validity of such tests is revealed by the caveats in the
leaflet accompanying one of them: "The Amplicor HIV-1 PCR test
has been tested using whole blood specimens only. Performance with
other specimens has not been evaluated and may result in false
negative or false positive results... Detection of HIV-1 may be
dependent on the amount of proviral DNA in the specimen. This may be
affected by specimen collection methods and patient factors such as
age, disease status and risk factors etc. As in any diagnostic test,
results from Amplicor HIV-1 test should be interpreted with
consideration of clinical and laboratory findings." It will
become clear later why whole blood rather than serum is used for this
test, all the more so as the purpose of the test is to detect
transmissible virus particles which should not have anything to do
with the presence or absence of blood cells. This all the more
significant, since a major form of HIV transmission is supposed to be
via Factor 8 given to haemophiliacs, where blood cells are absent. The
implication is that without blood cells no "viral" DNA would
be detected!
23 Beatrice H. Hahn et al. (incl.
Robert C. Gallo). 1984. Molecular cloning and characterization of
the HTLV-III virus associated with AIDS. Nature 312: 166-169. Shaw
G.M. et al. (incl. Robert C. Gallo). 1984. Molecular
Characterization of Human T-Cell Leukemia (Lymphotropic) Virus Type
III in Acquired Immune Deficiency Syndrome. Science 226:
1165-1171. Marc Alizon et al. (including. Luc Montagnier). 1984. Molecular
cloning of lymphadenopathy-associated virus. Nature 312: 757-760.
Wain-Hobson S. et al. 1985. Nucleotide Sequence of the AIDS Virus,
LAV. Cell 40: 9-17. Ratner L. et al. 1985. Complete nucleotide
sequence of the AIDS virus, HTLV-III. Nature 313: 277-284.
24 Tedder R.S. UCL Medical School
London, 1994 Personal communication
25 Guangxiang Luo and John Taylor.
1990. Template Switching by Reverse Transcriptase during DNA
Synthesis. J Virol 64, 4321-4328. Goodrich D.W. and Duesberg P.H.
1990. Retroviral recombination during reverse transcription.
PNAS 87: 2052-2056.
26 Hahn B.H. et al. 1986. Genetic
Variation in HTLV-III/LAV Over Time in Patients with AIDS or at Risk
for AIDS. Science 232: 1548-1553. Alizon M. et al. 1986. Genetic
Variability of the AIDS Virus: Nucleotide Sequence Analysis of Two
Isolates from African Patients. Cell 46: 63-74. Yasuo Ina and
Takashi Gojobori. 1990. Molecular Evolution of Human T-Cell
Leukemia Virus. J Mol Evol 31: 493-499. Balfe P. et al. 1990. Concurrent
Evolution of Human Immunodeficiency Virus Type 1 in Patients Infected
from the Same Source: Rate of Sequence Change and Low Frequency of
Inactivating Mutations. J Virol 64: 6221-6233.
27 Barbara J. Culliton. 1990. I: Inside
the Gallo Probe. Science 248: 1494-1498. Ellis Rubinstein. 1990.
II: The Untold Story of HUT78. Science 248: 1499-1507. Barbara
J. Culliton. 1992. NIH report vindicates Gallo on conduct of AIDS
research. Nature 357: 3-4. John Maddox. 1992. More on Gallo and
Popovic. Nature 357: 107-109. Jon Cohen. 1993. HHS: Gallo
Guilty of Misconduct. Science 259: 168-170.
28 Steve Connor. 1987. AIDS:
Science stands on trial. New Scientist 12.2., 49-58.
29 see ref 4
30 Fields B.N. 1994. AIDS: Back to
Basic Science. Nature 369: 95.
31 Laurie Garrett. 1993. Seeing the
Light; AIDS scientists shift their focus. Newsday, September 6.
Charles A. Thomas, Jr., Kary B. Mullis, Bryan J. Ellison, and Phillip
E. Johnson. Why there is still an HIV controversy. October 20,
1993. Cited as reference 72 in Richard Strohman (37). Nature,
submitted in November 1993; rejected December 1993, manuscript
available upon request (RS).
32 J.S. Goodwin, 1981. A Piece of
My Mind: OKT3, OKT4, and All That. This article is a diatribe
against the measurement of T-cell subsets in human diseases. JAMA 246:
947-948. Caspar G. Schmidt, 1984. The group fantasy origins of AIDS.
J. Psychohistory 12: 37-78. Peter H. Duesberg, 1987. Retroviruses
as Carcinogens and Pathogens: Expectations and Reality. Cancer
Research 47: 1199-1220. AIDS - A different View. Abstracts.
International Symposium 14.-16. May (Amsterdam). Eleni
Papadopulos-Eleopulos, Valendar F. Turner and John M. Papadimitriou,
1992. Kaposi's sarcoma and HIV. Med. Hypotheses 39: 22-29.
Peter H. Duesberg and Jody R. Schwarz, 1992. Latent viruses and
mutated oncogenes: no evidence for pathogenicity. Prog. Nucleic
Acid Res. Molec. Biol. 43: 135-204. Peter H. Duesberg, 1992. AIDS
acquired by drug consumption and other noncontagious risk factors.
Pharmac. Ther. 55: 201-277. Eleni Papadopulos-Eleopulos, Valendar F.
Turner and John M. Papadimitriou, 1992. Oxidative stress, HIV and
AIDS. Res. Immunol. 143: 145-148. John Lauritsen, 1993. The
AIDS War. Propaganda, Profiteering and Genocide from the
Medical-Industrial Complex. Asklepios, New York. Eleni
Papadopulos-Eleopulos, Valendar F. Turner and John M. Papadimitriou,
1993. Has Gallo proven the role of HIV in AIDS? Emergency
Medicine 5: 113-123. Serge Lang, 1994. HIV and AIDS: Have we been
misled? Questions of Scientific and Journalistic Responsibility.
Yale Scientific, New Haven. Neville Hodgkinson, 1994. Paradigms Lost.
Continuum 2/5&6, London. Eleni Papadopulos-Eleopulos, Valendar F.
Turner, John M. Papadimitriou and David Causer, 1995. Factor VIII,
HIV and AIDS in haemophiliacs: an analysis of their relationship. Genetica.
Eleni Papadopulos-Eleopulos, Valendar F. Turner, John M. Papadimitriou,
David Causer, Bruce Hedland-Thomas and Barry A.P. Page, 1995. A
critical analysis of the HIV-T4-cell-AIDS hypothesis. Genetica.
33 Chirimuuta R.C and Rosalind J.
Chirimuuta 1989. AIDS, Africa and Racism. Free Association
Books, London.
34 Eleni Papadopulos-Eleopulos,
Valendar F. Turner, John M. Papadimitriou and Harvey Bialy, 1995. AIDS
in Africa. Distinguishing fact and fiction. World Journal of
Microbiology and Biotechnology 11.
35 Hassig A. Research paper, 1993.
Study Group on Nutrition and Immunity. Neuroendocrine causation of
CD4/CD8 shift 3066 Stettlen, Switzerland.
36 John Lauritsen. 1990. Poison by
Prescription. The AZT Story. Asklepios, New York. John Lauritsen,
1993. The AIDS War. Propaganda, Profiteering and Genocide from the
Medical-Industrial Complex. Asklepios, New York.
37 Ivan Illich. 1990. Limits to
Medicine. Medical Nemesis: The expropriation of health. Penguin.
Thomas McKeown The Role of Medicine - Dream, Mirage, Nemesis 1979
Princeton University Press. Robert S. Mendelsohn. 1979. Confessions
of a Medical Heretic. Chicago.
38 Ruth Hubbard and Elijah Wald with
Nicholas Hildyard. 1993. The Eugenics of Normalcy. The Politics of
Gene Research. The Ecologist 23: 185-191. Ruth Hubbard and Elijah
Wald. 1994. Exploding the Gene Myth: How Genetic Information is
Produced and Manipulated by Scientists, Physicians; Employers;
Insurance Companies, Educators, and Law Enforcers. Beacon. R.C.
Lewontin. 1994. Women Versus the Biologists. The New York
Review of Books, April 7. Steven Rose. 1995. The rise of
neurogenetic determinism. Nature 373: 380-382.
39 D.J. Weatherall. 1991. Ethical
issues and related problems arising from the application of the new
genetics to clinical practice. In: The New Genetics and Clinical
Practice. D.J. Weatherall (ed.). Oxford University Press.
40 Theodore Friedmann. 1994. The
promise and overpromise of human gene therapy. Gene Therapy 1:
217-218.
41 John Rennie. 3/1993. DNA's New
Twists. Scientific American 260: 88. and most important: Richard
Strohmann. 1994. Epigenesis: The Missing Beat in Biotechnology?
Bio/Technology 12: 156-164.
Published in
Continuum April/May 1995
