The Isolation Question
Does HIV exist? Do HIV tests indicate HIV infections?
Here's why some scientists say no.
By Paul Philpott
How an Australian biophysicist and her simple observations have taken center
stage among AIDS reappraisers.
Of course HIV exists--I've seen pictures of it in text books and on
the news--and scientists work with it every day. How could there be HIV
tests if there's no HIV? What those tests detect, that's HIV...
So goes the typical response from physicians, biologists,
and AIDS activists when faced with a very simple question: Does HIV exist?
But like all questions fundamental to the HIV/AIDS model, nobody asked
this in 1984, the year Robert Gallo published a group of four papers in
Science (224:497-508, May 4) proclaiming the existence of a unique
retrovirus, HIV, that causes AIDS.
Gallo's HIV-AIDS model stood unquestioned in the
medical literature for three years, until 1987, when UC-Berkeley retrovirologist
Peter Duesberg published the first academic paper contesting the notion
of pathogenic retroviruses (Cancer Research 47: 1199-1220). Although
disputing the infectious AIDS model, Duesberg accepted Gallo's claim of
having prepared isolates of a unique retrovirus, HIV, and having
abstracted from them proteins needed to construct tests for identifying
people and cells infected with it.
By 1987 the plasma and T4 cells of thousands of
AIDS patients had been tested for evidence of the proteins and genetic
material from Gallo's "isolates." The AIDS reappraisal movement grew out
of Duesberg's critique of these data. HIV exists, but the blood contains
so little of it, and it infects so few T4 cells, and replicates--harmlessly--in
vitro with so much difficulty, and so many patients test negative for
it altogether, that it is just too ineffectual, inactive, and imperfectly
correlated with AIDS to explain AIDS.
Out of Australia: Questioning HIV's existence
Before Duesberg's 1987 paper made it to press, a second academic, authoritative
deconstruction of HIV had already been submitted for publication in another
journal. This one was written by Eleni Papadopulos-Eleopulos, a medical
physicist at Australia's Royal Perth Hospital. In 1988 France's Medical
Hypotheses (25:151-162) published her paper, "Reappraisal of AIDS:
Is the Oxidation Induced by the Risk Factors the Primary Cause?" Papadopulos
had independently reached many of Duesberg's conclusions, but ultimately
had quite a different take on Gallo's claims: "Unlike other viruses [HIV]
has never been isolated as an independent stable particle."
What she meant was this: Electron microscope pictures, micrographs
, of samples Gallo calls "HIV isolates"--and of all "HIV isolates" produced
before by Luc Montagnier of France, or since by other scientists--show
some objects that look like retroviruses (the "HIV") plus lots of other
things, including things that clearly aren't viruses. So there's no way
to identify the origin of the "HIV" proteins and genetic material abstracted
from these samples. Do the proteins come from the objects that look like
retroviruses? Or do they represent some of the contaminants?
And what about those retroviral-looking objects? Papadopulos pointed
out that among the microbial objects that look like retroviruses are (1)
microvesicles: non-infectious, unstable organelles that bud from cells;
and (2) endogenous retroviruses: non-infectious, unstable retroviruses
coded for by healthy human DNA. She noted that this presents a special
problem for the objects called "HIV." They can be observed only in cell
cultures that have been stimulated by agents that induce the production
of microvesicles and endogenous retroviruses.
Without true isolates of the objects declared "HIV," there really is
no way to determine if they constitute what HIV is claimed to be: a retrovirus
of exogenous origin (an autonomous entity unaccounted for by a person's
inherent DNA library). There is no way to pull proteins and genetic material
out of a heterogeneous sample and know that they came from one group of
particular looking objects rather than another, or simply from the surrounding
Oxidative stress: Unifying AIDS, its causes, and "HIV"
In addition to introducing an HIV critique based on the principal of
viral isolation, Papadopulos also unveiled in her 1988 paper an explanation
for AIDS based on the process of oxidative stress. According to Papadopulos,
the stimulants used to induce "HIV" phenomena (retrovirus-looking objects
plus certain proteins that may or may not be affiliated with those objects)
in cultures are oxidizing agents . As are the factors uniting American
AIDS patients, including street drugs, hemophilia treatments, and rectally
deposited semen. Papadopulos proposed that both "HIV" phenomena and AIDS
conditions are consequences of these and other stressors she would introduce
in later papers (such as blood transfusions, anti-AIDS pharmaceuticals
including AZT, and antibiotics).
Duesberg drew on the 1988 Papadopulos paper (and even earlier writings
by John Lauritsen in the gay press) in formulating his 1992 treatise "AIDS
Acquired by Drugs and Other Non-contagious Risk Factors" (Pharmacology
& Therapeutics 55:201-277). In that paper, Duesberg added to his
HIV critique alternative explanations for AIDS. He agreed with Papadopulos
that street drugs and hemophilia treatments caused AIDS, but dismissed
rectal insemination as inconsequential. His 1992 paper was the first to
implicate "anti-HIV" drugs such as AZT, and Papadopulos subsequently adopted
them into her oxidative stress model.
That same year, 1992, Papadopulos formed a writing team with two University
of Western Australia physician-professors, Valendar Turner of the Department
of Emergency Medicine, and John Papadimitriou, Professor of Pathology.
Together they published "Oxidative Stress, HIV, and AIDS" (Res-Immunol.
143:145-148), which restated her Unified AIDS Theory.
Virus tests without virus isolation?
In 1993 Papadopulos finally caught the attention of AIDS reappraisers.
"Is A Positive Western Blot Proof of HIV Infection?" appeared in Bio/Technology
(11:696-707), a major medical journal and sister publication of Nature.
The article debunked the validity of "HIV tests" on several grounds:
(1) that they are constructed from the constituents of heterogeneous samples
rather than true viral isolates; (2) that proponents of the purported virus
(HIV) claim to observe it only in stimulated cultures, as opposed to fresh
patient plasma; (3) that accuracies for these tests are established without
an independent gold standard (isolation from fresh patient plasma);
and (4) that these tests are assumed to be equally accurate for people
with and without the risks associated with, and the conditions classified
as, "AIDS," a syndrome the purported virus supposedly causes.
Isolation, Papadopulos explains, is the only sure proof that a virus
is present--the only direct, unambiguous evidence of a virus. And isolation
from uncultured patient plasma is the only sure proof that a person
harbors an active infection-- the only sort of infection
that can cause disease. She points out that the accuracy for even a properly
constructed viral test (one made from true viral isolates) can be established
only by answering the following question: In what fraction of people who
test positive can the virus be isolated from their fresh (uncultured) plasma?
Instead, "HIV" test accuracies are established using circular logic;
"accuracy" for HIV ELISAs is taken as the fraction of positive people who
subsequently test HIV Western blot positive. And "accuracy" for HIV Western
blot tests is nothing more than reproducibility (the fraction of positive
people who test positive when retested).
These pseudo accuracies--each over 99%--are assumed for all people,
even those free of the risks and symptoms associated with the syndrome
that the purported virus supposedly causes. Yet among risk group members
with blood that reacts with these tests--those who test positive--pseudo
isolations ("HIV" phenomena in stimulated cultures) are achieved for only
some of those with AIDS conditions, and for only a few who are symptom-free.
For example, of risk group members (gay men, drug injectors, and blood
recipients) testing "HIV-positive":
(1) Gallo achieved pseudo "HIV" isolations in 26 of approximately 63
(41%) patients with AIDS conditions (this is a generous figure that assumes
Gallo's isolations involved only the 88% of his 72 AIDS-diagnosed patients
who tested positive) ;
(2) Piatak reported (a) "infectious HIV" (according to some of the
same criteria as pseudo isolations) in only 29 of 38 (76%) patients with
AIDS conditions and in only two of 21 (10%) patients with no AIDS conditions
(Science 259: 1749-1754, 1993); and (b) in one of six (16%) symptom-free
patients (Lancet 341: 1099, 1993);
(3) Daar reported "infectious HIV" in none of four symptom-free patients
(NEJM 324:961-964, 1991);
(4) Clark reported "infectious HIV" in none of three symptom-free patients
(NEJM 324:954-960, 1991); and
(5) Cooper found "infectious HIV" in neither of two symptom-free patients
(Lancet 340:1257-1258, 1992).
So among people with AIDS risks, using pseudo isolations from stimulated
cultures as an independent standard, HIV antibody tests are between 41%
and 76% accurate for people with AIDS conditions, and between 0% and 16%
accurate for those with no symptoms, a far cry from the 99% accuracies
established using reproducibility and cross-checking.
What about people without AIDS risks? No one has compiled even pseudo
isolation data for drug-free, blood product injection-free heterosexuals
who test positive. HIV researchers simply assume that the data from risk
group studies apply for everyone.
And what about the real accuracy of HIV tests? That is, accuracy
established using the only valid gold standard: isolation from fresh plasma.
The Australians reason that since isolation from fresh plasma has not been
achieved under any circumstance, then the true accuracy for all
"HIV tests" should be considered zero , and all positive results
should be regarded as false. There is no basis for thinking that a virus
observed only in stimulated cultures exists in the plasma of any humans,
even those who test positive for it as determined by antibody, antigen,
"viral load" or any other assay.
"HIV": Normal cellular residents?
In the Bio/Technology paper, Papadopulos examined what are accepted
as substitutes for true HIV isolation. These include "HIV proteins" (gp160,
gp120, gp41, p32, p24, and p17), reverse transcriptase, "HIV" DNA and RNA,
and retrovirus-looking objects. She suggests that they are each cellular
constituents, some normal, some produced in response oxidative stress.
(1) HIV existentialists--those who think HIV exists--hypothesize that
gp160 is made of gp120 stuck to gp41, and it decorates HIV, with gp41 embedded
in the outer membrane envelope, anchoring gp120, which protrudes outward,
ready to latch onto T4 molecules; Papadopulos cites references showing
that gp160 and gp120 are oligomers of gp41 (four gp41s stuck together make
gp160; three make gp120), and that gp41 might be the ordinary cellular
protein actin. (She also cites references showing that cell-free objects
considered to be HIV contain no gp120, and thus have no infectious capability,
just like endogenous retroviruses.)
(2) The existentialists hypothesize that p17 lines the inside of the
envelope, and p24 forms the hollow core; Papadopulos cites references showing
that p24 and p17 might be the two constituent globs that form the ordinary
cellular protein myosin.
(3) The existentialists hypothesize that p32 decorates HIV's envelope,
along with gp160; Papadopulos cites references showing that p32 is the
"Class II histocompatibility DR" marker found on all human T immune cells.
(4) The existentialists hypothesize that reverse transcriptase is a
constituent of HIV, and is used to make HIV DNA from HIV RNA; Papadopulos
cites references showing that this enzyme is a normal constituent of all
human cells, and even some ordinary viruses, like hepatitis viruses, which
are common in AIDS patients.
(5) Papadopulos shows that no complete "HIV" RNA molecule or DNA genome
has ever been identified, that what is claimed to be the "HIV" genome represents
bits and pieces of genetic sequences cobbled together, that the "HIV" RNA
and DNA haven't been shown to code for what are claimed to be the HIV proteins,
and that all the "HIV" genes are very similar to genetic sequences common
to all humans.
(6) The existentialists hypothesize that the retrovirus-looking objects
in electron micrographs of heterogeneous samples from AIDS patients are
identical retroviruses, HIV, that consist of the "HIV" proteins and RNA
abstracted from those samples; Papadopulos explains that since those samples
are heterogeneous, there's no way to match the retrovirus-looking objects
to any material abstracted from the samples, that retrovirus-looking objects
are common products of stimulated T-cells, and that such objects are not
necessarily viruses of any sort and can be proven to be so only when examined
HIV antibodies as autoantibodies
Although the "HIV proteins" haven't been shown to be constituents of
a virus, they are the constituents of the ELISA and Western blot
antibody tests for HIV. If Papadopulos is correct that these are ordinary
cellular proteins, why would humans express antibodies against their own
cellular proteins, a condition called autoimmunity ? And why would
such antibodies correlate (however imperfectly) with AIDS conditions and
The Bio/Technology paper argues that antibodies against actin,
myosin, and p32 indicate exposure to those proteins donated by other people
via injected blood products, unsterile needles, and rectally deposited
semen. These factors nearly unify all American AIDS patients, and
they are oxidative stressors. So Papadopulos proposes that oxidative stressors
cause AIDS conditions and positive HIV tests, thus explaining the
correlation between AIDS conditions and positive HIV test results.
(Which is not to say that every positive "HIV antibody" test indicates
autoimmunity or oxidative stress, or that autoimmune phenomena always cause
disease, or that oxidative stress always causes "HIV" phenomena or AIDS
In non-industrial regions such as those in Africa where lots of AIDS
patients reside, Papadopulos shows that HIV antibody tests (the only sort
of HIV tests used there) cross-react with antibodies against numerous ordinary
microbes and parasites that are rampant there due to extremely impoverished
living standards. AIDS conditions in these regions, she says, result from
those cross-reacting infections, other infections common among impoverished
people, and poverty itself.
Proving causation: another need for isolation
Papadopulos' group published another 1993 paper, "Has Gallo Proven
The Role of HIV in AIDS?", in the Australian journal Emergency Medicine
(5:113-123). This paper presented much of the same data and arguments about
the lack of HIV isolation offered in the Bio/Technology paper. But
where that paper examined the absolute requirement of viral isolation for
constructing and validating viral tests, this paper examined the absolute
requirement of viral isolation for demonstrating a causal relationship
between a virus and a disease.
The Australians focused here on Gallo's 1984 papers, which they characterized
as the most thorough to date. They argued that a virus can only be considered
causal for a disease if:
(1) It can be isolated in every case of the disease from fresh (uncultured)
plasma. Yet Gallo claimed to isolate HIV only from cultures, and only after
stimulation with agents that cause inactive viral DNA (provirus) to produce
viruses that might not be present in vivo . Furthermore, Gallo could
only claim HIV isolation in 34% of the AIDS patients tested, and even then
these claims were based not on real isolation, but on the observation of
certain proteins, reverse transcriptase, and retrovirus-looking particles,
though usually not all at the same time.
(2) Adding isolates of the virus to cultures of cells of the type affected
in the disease in question results in behavior consistent with the disease.
In the case of AIDS, that would mean adding HIV isolates to cultures of
T4 cells and looking for either cell death (predicted by the original killer
HIV model) or high rates of HIV activity (predicted by the new hyperactive
HIV "viral load" model). But Gallo found neither. Cells declared "HIV-infected"
lived happily ever after, and would produce HIV indicators only when prodded
by artificial stimulants.
The Australians emphasized that no researcher since 1984 has improved
on Gallo's very weak case for HIV as a cause of AIDS.
All antibodies non-specific
The Bio/Technology paper presented a long list of non-HIV agents
that can cause positive reactions on HIV ELISA and Western blot antibody
tests. This is very bad news for those tests.
HIV antibody and antigen tests are constructed from heterogeneous samples
rather than isolates, and validated against each other rather than the
isolation gold standard. Therefore their validity requires that HIV proteins
and the antibodies against them be specific . That is, the proteins
must be exclusive to HIV, and the antibodies that react with them must
react with no other proteins.
Gallo and the other existentialists, Papadopulos explains, simply assume
that their "HIV proteins"--and antibodies against them--always indicate
a virus made from those proteins, and nothing else. They base this assumption
on no data, and no wonder. Only isolation--which none of them has achieved--can
demonstrate this sort of specificity. Furthermore, Papadopulos' list of
cellular sources for each "HIV protein," and her list of non-HIV entities
that cause reactions with "HIV" antibody tests, absolutely falsify the
specific antibody ideal for HIV.
Papadopulos explains that there is no such thing as specific antibodies
against any microbial agent. All viral tests (including properly
constructed ELISAs and Western blot tests for properly characterized viruses)
"cross react" with entities other than their intended targets.
This is why test accuracies must be established for different groups
(those with and without symptoms and risks associated with the virus) using
the gold standard (virus isolation from fresh plasma).
Properly validated virus tests are not undermined by a list of cross-reacting
entities. If the virus can be isolated from the fresh plasma of 99% of
the people with certain symptoms who test positive in validation studies,
then physicians would have a 99% certainty that a patient with those symptoms
who tests positive has an active infection.
The existence of cross-reacting entities becomes important only in
circumstances of low accuracy. In the world of properly constructed and
validated viral antibody tests, that means symptom-free people, and people
who have been exposed to cross-reacting factors.
Virus isolations are rarely achieved in symptom-free people who test
positive, which means the accuracy is low for apparently healthy people.
The only sensible interpretation for positive results in healthy people
is that these people have experienced, sometime in the past, an infection
that is no longer active (and is thus inconsequential), or they were exposed
to cross-reacting proteins.
Before the introduction of HIV science, physicians did not test healthy
people for viral infections, except for people with certain risks, such
as recent exposure to someone with a confirmed infection. Validation studies
can show a relatively high accuracy for positive tests in symptom-free
people with such a risk. So it is rational to test such people. HIV tests
are the only viral tests administered routinely to healthy people with
In the strange case of HIV and AIDS, though, even testing people in
the AIDS risk groups is a dubious enterprise. This is because the official
risks that define these groups (rectal intercourse, unsterile needle use,
blood product injections, residency in impoverished nations), involve exposure
to non-HIV factors that cause cross-reactions with these tests.
Virologist Lanka supports Papadopulos
The Bio/Technology paper influenced most reappraisers to question
the validity of "HIV" tests, mostly on the grounds of cross-reactivity.
Few seemed to appreciate that the isolation question was the real crux
of the matter. The question of HIV's actual existence seemed just too big
for most reappraisers to tackle. Then along came a young German virologist,
Stefan Lanka, co-author of an academic paper that properly established
the existence of a marine virus, ectocarpus siliculosis .
The British AIDS reappraisal magazine Continuum published in
its April/May 1995 issue Lanka's exposition, "HIV: Reality or Artifact?"
This was the first article for a popular audience explaining Papadopulos'
contention that HIV simply does not exist, and that the phenomena considered
to indicate its presence have non-viral explanations, such as artifacts
of the lab procedures applied to cultures made from the blood of AIDS patients.
The next issue (June/July) included a fiery and detailed exchange between
Lanka and Steven Harris, a physician who advocates the HIV-AIDS model.
That article displayed two electron micrographs of properly isolated viruses:
Lanka's ectocarpus siliculosis, and adenovirus type 2 (which cause common
colds). Those two micrographs exclusively contained identical virus-looking
objects. Harris presented a micrograph of what he called an "HIV isolate."
Lanka pointed out that this micrograph contained, in addition to retrovirus-looking
objects labeled "HIV," lots of microvesicles and "macromolecular debris."
Therefore it was not an isolate.
This exchange created such interest--and Continuum 's editor-ial
board was so persuaded by Lanka's argument--that the magazine in its January/February
1996 issue posted a 1,000 "Missing Virus Reward" for anyone who could produce
a micrograph of a proper "HIV" isolate.
Papadopulos answers the first challenge
In April, 1996, the National AIDS Manual (NAM) Treatment Update
published an editorial answering the Continuum challenge. NAM
made no claim on the prize, conceding an absence of the micrograph specified
by the reward. Instead, NAM argued against the need for such a requirement
in establishing the existence of a virus.
Specifically, NAM rejected the Papadopulos/Lanka objections
to contaminating material in the available "HIV" micrographs. "...It's
like saying that it is impossible to identify a German shepherd dog by
its unique appearance," the article reasoned, "if it happens to be surrounded
In the May/June issue of Continuum , Papadopulos' team responded
to the NAM critique with a remedial lesson in microbiology: "The
analogy with HIV is more like someone who does not know what a German shepherd
is but who looks at an aerial photograph of a zoo," and notes that some
of the objects look like dogs, then "mince[s] up all the objects in the
zoo," and presumes to know which teeth, claws, hair, hearts, and stomachs
came from the objects that looked like dogs, and claims that those objects
are some new breed deserving of a new name.
Instead, German shepherds have been carefully studied on their own,
which is why they can be identified merely by their image, even in the
midst of other dogs. Certainly a new breed of dog could not be declared--and
identified by aerial photographs (the human scale equivalent of an electron
micrograph)--without first studying one up-close (the human scale equivalent
of viral isolation).
If isolates were obtained of the objects labeled "HIV" in micrographs
of heterogeneous samples, and those isolates were shown to consist of a
unique, exogenous retrovirus, then there would be a basis for pointing
out these objects in heterogeneous samples and declaring them to be "HIV."
Until then, nobody knows what the objects purported to be "HIV" are
in any of the "HIV micrographs."
Duesberg demurs, Lanka descries
By the July/August issue, Continuum 's reward had increased
to 25,000, and none other than Peter Duesberg wrote in to claim the prize.
Conceding that there existed no such micrograph as that sought by Papadopulos
and Lanka, Duesberg argued that existing data "exceeded the [Papadopulos/Lanka]
criteria" for virus isolation: the isolation of "infectious full length
HIV DNA" from "HIV-infected cells," and the detection of this DNA in some
T4-cells of nearly 100% of people who test positive for "HIV antibodies,"
but in nearly 0% of those who test negative.
In the same issue Continuum published rebuttals by both Lanka
and the Australian team, which now included a fourth member, David Causer,
Senior Physicist at the Department of Medical Physics at the Royal Perth
Lanka surprised everyone with his "Collective Fallacy: Rethinking HIV."
Leaving it to "the distinguished Australians" to provide "a detailed reply
to the Duesberg claim," he leaped past that dialogue and into a novel assertion:
all retroviruses are fictions, artifacts of the contrived laboratory
conditions invariably used to find them. He described Duesberg as:
limiting his objections to the relatively minor aspect of whether
HIV could cause AIDS or not, whereas he really ought to have smelt a rat
regarding the whole concept of retroviruses. ...Indeed, the extraordinarily
artificial and circumscribed conditions under which reverse transcription
could be induced in the laboratory should have alerted everyone to the
extreme improbability of such exclusively laboratory conditions having
any bearing whatsoever on naturally occurring phenomena .
The Papadopulos treatise
Papadopulos' rebuttal was an exhaustive exposition entitled "The Isolation
of HIV: Has It Really Been Achieved? The Case Against," included as a 24-page
supplement. She asserted that until a virus has been isolated according
to the criteria required by the Continuum reward, its constituents--including
genetic material and proteins--cannot be cataloged. So there is no basis
for a viral explanation for this correlation.
Yet Duesberg has a point. How can Papadopulos and Lanka explain the
high correlation between particular proteins (and antibody reactions to
them) and the detection of particular DNA/RNA sequences? This can not be
a chance occurrence.
Papadopulos agrees. But she points out that isolating DNA does not
equal isolating a virus, and certainly does not "exceed the criteria" specified
by the reward, which represent, in fact, an official standard procedure
for retroviral identification which was discarded only to accommodate "HIV."
Logically, there is no basis for concluding that an RNA molecule abstracted
from a heterogeneous sample (even one containing retrovirus-looking objects),
or a strip of corresponding chromosomal DNA, originates from a retrovirus.
Such an assumption can only apply to RNA abstracted from a retroviral isolate
(and only if that RNA is shown to code for the proteins abstracted from
the same isolate).
To explain the "HIV" protein-RNA/DNA correlation, Papadopulos referenced
studies showing that the correlation between the proteins and the genetic
material was not quite as high as in the study Duesberg cited. Then she
proposed that the "HIV DNA" in cellular chromosomes might result from the
rearrangement (transposition) of a few normal cellular DNA sequences in
response to oxidative stress caused by both the AIDS risks (street drugs,
etc.) and the laboratory agents required to observe "HIV" phenomena.
Duesberg says this would require an improbable number of nucleic acid
rearrangements ("recombinations"), one for each of the 9,150 bases said
to constitute the HIV genome. Papadopulos says the number of required rearrangements
is actually much lower, since each of the supposed HIV genes are already
very similar to recognized normal human genetic sequences.
Is Papadopulos certain that oxidation-induced recombination explains
the HIV protein-RNA/DNAcorrelation? No. She's simply convinced that this
is more likely than the Duesberg-Gallo explanation, which is that the "HIV"
genetic sequences originate in a retrovirus that carries with it the "HIV
To her, the viral explanation is fatally undermined by several facts:
(1) heroic attempts to isolate such a virus always fail, de-spite huge
financial incentives and numerous attempts to do so by an enormous army
of scientists dedicated to "HIV," whereas far less interesting viruses
are routinely isolated by much smaller, less-funded groups of virus hunters;
(2) what is called HIV RNA and DNA comes in many sizes and varieties that
always differ from each other (no two are alike, even when abstracted
from the same patient ), whereas viral RNA and DNA should be of uniform
length and composition; (3) the lethargy that characterizes what is considered
"HIV replication" excludes the possibility that replicative mutation can
explain the wide HIV genetic variation; and (4) no one has produced a whole
"HIV RNA" molecule or a complete "HIV DNA" strip, offering instead as the
"HIV genome" cobbled together bits of genetic material.
Papadopulos notes that when "HIV DNA" shows up, it does so in only
a tiny fraction of T4 cells. Duesberg's explanation is that this means
HIV simply infects too few cells to explain any disease. But if HIV is
so lethargic as to infect only a few cells, how can its amazing variability
be explained? Papadopulos' hypothesis predicts wide variability: if "HIV
DNA" originates from the rearrangement of normal cellular DNA sequences,
then each one originates independently and separately in each cell where
it is found. Various points of origin would result in a variety of recombination
products: DNA strips of varying lengths and composition, and corresponding
RNA molecules transcribed from that DNA.
Papadopulos stresses that her argument against the existential hypothesis
of HIV does not require that her alternative hypothesis be correct. Since
the existence of HIV is not a default hypothesis, we are not obligated
to assume that HIV exists in the absence of a better explanation. To the
contrary, until unambiguous evidence is provided for HIV--in the form of
a proper viral isolate--explanations for the data are open to suggestions.
As far as the Australians are concerned, the viral model has been thoroughly
examined, and it comes up empty. It's time to propose and study some new
The Duesberg-Papadopulos dichotomy
Papadopulos' advocacy of a non-viral explanation for microbiological
phenomena labeled as "HIV" remarkably resembles Duesberg's advocacy of
a non-HIV explanation for pathological phenomena labeled as "AIDS": (1)
Duesberg explains that the HIV-AIDS correlation is not as high as it's
made out to be; Papadopulos makes the same claim about the HIV protein-DNA/RNA
correlation; (2) Duesberg shows that the microbiological data unqualifiedly
exclude a role for HIV; Papadopulos shows that the microbiological data
unqualifiedly exclude definitive evidence of a virus; (3) Both say we should
therefore consider non-viral explanations; and (4) Duesberg says that even
if the alternative hypotheses are ultimately falsified, the HIV-AIDS model
is not consequently resurrected, because it fails all on its own; Papadopulos
says the same thing about the HIV existential model.
The February/March 1997 Continuum carried a second appeal from
Duesberg responding to the Papadopulos and Lanka rebuttals. The editors
entitled the article, "Near Enough Is Good Enough?" reflecting their
sympathy for the non-existentialist position. Duesberg restated his conclusions
that rearrangement of normal chromosomal DNA sequences was less likely
than the viral explanation, and that the traditional virus isolation requirements
advocated by Papadopulos and Lanka were outdated and, in any case, less
rigorous than those which he said had been achieved by HIV.
This defense of HIV's existence recalls the arguments used against
Duesberg's own proposal that HIV is harmless. Within that discussion, Duesberg
shows that HIV fails to meet the traditional and logical standards of microbiology,
including Koch's postulates. Advocates of the HIV-AIDS model respond by
proclaiming those criteria are outdated, and offer new criteria which accommodate
the HIV-AIDS model.
The Australian response is summarized in the title, "Why No Whole Virus?",
and reemphasized points made in their previous exposition.
More interesting was Lanka's second rebuttal to Duesberg, which included
some new insights. Lanka expounded on the implications of a lack of "HIV
isolates" despite dogged efforts. This should not be so for a virus that
exists. Lanka writes:
It has been long known that what "AIDS" researchers have presented
as photos of "HIV" show normal cellular [microvesicles]... As those particles
are designed, in contrast to viruses, for cellular use only, they are very
unstable when removed from their context, and not able to be isolated and
photographed in an isolated state. Viruses are stable because they have
to leave cells or even the organism in order to infect other cells or organisms
anew. Using centrifugation techniques it is no problem to separate viruses
from all contaminating components and in doing so to isolate them--then
photograph them, then represent their proteins and genetic substance in
a direct way... Genuine viruses are so stable that it is easy... to photograph
them directly as three dimensional particles in the [scanning] electron
microscope without prior chemical fixation. In contrast [microvesicles]
are so unstable they can only be photographed [with a transmission electron
microscope, which requires they be] in a chemically fixed state... in very
thin sections. All that have been shown to us as [micrographs of] "HIV"
are ultrathin sections [that include what are agreed to be] cellular particles.
Sure enough, the micrographs of proper viral isolates presented by Lanka
in his rejoinder to Steven Harris were photographed with the scanning electron
microscope, and thus showed--with high resolution and three-dimensional
relief--the outer surfaces of the viruses. In contrast, the purported "HIV"
micrograph presented by Harris was photographed by the transmission electron
microscope in "ultrathin sections," producing flat, transparent, cross-sectional
images with no surfaces and poor resolution. According to Lanka, viruses
are hardy enough to be photographed either way, and ought to be, since
one reveals the surface in great detail, and the other reveals important
But there exists no published scanned micrograph of anything claimed
to be "HIV." Since there are billions of dollars and tens of thousands
of scientists annually devoted to the study of "HIV," it seems improbable
that this could indicate an oversight. More likely the retrovirus-looking
objects called "HIV" are, like microvesicles, simply too unstable for scanned
electron microscopy and procedures that could otherwise separate them from
all other objects into pure samples, which is to say--in Lanka's opinion--they
are too unstable to be viruses.
(Instability, by the way, gives the objects labeled "HIV" both the
characteristics Papadopulos assigns endogenous retroviruses, the other
being non-infectivity in their cell-free form.)
"'HIV' has never been identified as a secure biological entity," he
concludes. "The logical explanation given that all the characteristics
ascribed to 'HIV' are well-known cellular entities and characteristics,
is that 'HIV' never was, and the claim of the existence of 'HIV' is not
On hemophilia-AIDS, T4 counts, and African AIDS
Papadopulos' contribution to the AIDS reappraisal movement transcends
the discussion of HIV's existence. Remember that she unifies all the proposed
causes of AIDS, and even the agents required for "HIV" expression, by a
common denominator: they all cause oxidative stress. She also shows that
oxidation is a logical source of many diseases, including all that qualify
In 1995 her team published a lengthy consideration of "AIDS" in hemophiliacs,
"Factor VIII, HIV and AIDS: An Analysis of Their Relationship" (Genetica
95: 25-50). To their assertion that factor VIII contaminants cause AIDS
conditions in both HIV-positive and -negative hemophiliacs, they also stress
a point promoted by no other reappraising scientists: that there is not
even a basis for HIV transmission via Factor VIII injections--or any other
mechanism, for that matter--since what is called cell-free "HIV" is bare
of the surface protein (gp160) supposedly required for infection.
The Australians have also advanced--with Bruce Hedland-Thomas and Barry
A. P. Page joining Papadopulos and Causer from the Medical Physics Department
at Royal Perth Hospital--another novel hypothesis, this one refuting the
role of lost T4 cells in AIDS. In "A Critical Analysis of the HIV-T4-cell-AIDS
Hypothesis," they argue that the progressive drop in T4 counts observed
in many AIDS patients does not reflect a loss of T4-cells. Rather, it indicates
the conversion of many T-cells from producing T4 surface markers to producing
T8 markers instead. Thus there is no need to propose a T4-specific factor,
such as HIV, to explain AIDS.
Then there is the issue of AIDS in Africa, where the symptoms and proposed
causes are often quite different than in the industrialized world. In 1995
the Papadopulos team published "AIDS in Africa: Distinguishing Fact and
Fiction" (World Journal of Microbiology and Biotechnology 11: 135-143),
co-authored by PhD biologist Harvey Bialy, research editor of Bio/Technology
who has spent a great deal of time in Africa. This paper attributes AIDS
cases there to the same thing that causes identical symptoms (persistent
fever, wasting, and diarrhea) in Africans who test negative: extreme poverty,
featuring subsistent diets and rudimentary or nonexistent sanitation.
The paper also explores the implications of the very poor heterosexual
transmission rate (one per thousand unprotected contacts with a positive
person) assigned to HIV in the face of high fractions of African heterosexuals
testing HIV-positive. Either African heterosexuals are much more promiscuous
than their American counterparts, or HIV tests are especially problematic
The Australians show that problematic testing is the more likely explanation.
Malaria, tuberculosis, and other tropical microbes that are widespread
in Africa feature proteins that elicit the same antibody response as some
of the "HIV proteins." HIV proponents have not accounted for this in any
of their experiments. They simply assume that Africans who test positive
are indeed infected by HIV, when these tests may instead be indicating
very common and conventional infections.
Gordon Stewart joins Papadopulos
"It seems tragic," Duesberg said in one of his Continuum papers,
"that over 99% of the AIDS researchers study a virus that does not cause
AIDS and that the few who don't are now engaged in a debate over the existence
of a virus that doesn't cause AIDS."
Charlie Thomas, the retired biochemistry professor who used to teach
at the medical schools at Harvard, John Hopkins, and the University of
Michigan, takes a more popular view. "The debate over HIV's existence instigated
by the Australians," he has said, "is the only issue of high scientific
interest that has emerged from this HIV/AIDS mess."
The "HIV non-existentialists," as Duesberg calls them, acquired an
important endorsement this year from the eminent British epidemiologist
and physician Gordon Stewart, who is emeritus public health professor at
the University of Glasgow in Scotland. Stewart co-authored the Australians'
latest paper, "HIV Antibo-dies: Further Questions and a Plea for Clarification"
(Current Medical Research and Opinion 13:627-634), which argues
that "the evidence for the existence of HIV and its putative role in AIDS
must be reappraised."
Voltaire, though, might side with Duesberg on this one. He said, "To
not be occupied and to not exist amount to the same thing." And Duesberg
and Papadopulos do agree on one thing. There is no HIV occupied with AIDS-causing