By Paul Philpott

Reappraising AIDS, June, July, Aug. 1997

Does HIV exist? Do HIV tests indicate HIV infections? Here's why some scientists say no. 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 molecular soup.

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[14]:961-964, 1991);

(4) Clark reported "infectious HIV" in none of three symptom-free patients (NEJM 324[14]: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 as isolates.

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 AIDS risks?

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 conditions.)

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.

False positives

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 no risks.

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 by poodles."

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 Hospital.

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 proteins."

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 ideas.

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.

Electron microscopy

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 cross-sectional information.

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 sustainable."

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 as "AIDS."

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 in Africa.

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 activities. *