WHERE HAVE WE GONE WRONG?
By Valendar Turner
Continuum Spring 1998
The real purpose of scientific method is to make sure Nature hasn't misled you into thinking something you don't actually know There’s not a mechanic or a scientist alive who hasn’t suffered from that one so much that he’s not instinctively on guard. That’s the main reason why so much scientific and mechanical information sounds so dull and so cautious. If you get careless or go romanticising scientific information, giving it a flourish here and there, Nature will soon make a complete fool out of you. It does it often enough anyway even when you don’t give it opportunities. One must be extremely careful and rigidly logical when dealing with Nature: one logical slip and an entire scientific edifice comes tumbling down. One false deduction about the machine and you can get hung up indefinitely.
-- Robert Pirsig. Zen and the Art of Motorcycle Maintenance
Over the seventeen years since the beginning of the AIDS era our small group in Perth, Western Australia have researched and written considerable amounts detailing why currently it is not possible to accept the HIV theory of AIDS.(1-16) Indeed, the cruelest irony of the AIDS era is that, right from the very beginning, armed with a few, simple biological facts, it was possible to foresee that cell cultures derived from AIDS patients and those at risk would evince the very phenomena erroneously inferred as proving the existence of a unique, exogenously acquired retrovirus. The problem that has developed from these data, that is, the HIV theory of AIDS, stems from the fact that these phenomena, while characteristic of retroviruses, are not specific to retroviruses. The truth of this statement is obvious from an appreciation of basic science and was astonishingly confirmed quite recently by none other than the discoverer of HIV, Professor Luc Montagnier from the Pasteur Institute.(17) Interestingly, in Djamel Tahi’s monumental interview, Professor Montagnier gives on one hand while taking with the other. Having conceded the non specificity of reverse transcription, viral-like particles and protein/antibody reactions for retroviruses, he then claims that "it was the assemblage of such properties [in cell cultures] which made me say it was a retrovirus". This is analogous to claiming that since your newborn baby has red hair, fair skin and a beguiling smile, she must be a girl. Or more precisely, that a febrile, asthenic, lifetime heavy smoker coughing up blood must have lung cancer when he might just as well have tuberculosis or a pulmonary abscess. In fact, well before the time of Montagnier’s discovery of what has been called HIV, it was well known that the collective phenomena ascribed as retrovirus could even arise spontaneously in normal tissue cultures derived from healthy animals, and that certain stimuli and culture conditions considerably accelerate this process. Significantly, these are the same factors that operate in AIDS patients and are obligatory accompaniments for HIV to "appear" in cultures regardless of their origin from the tissues of AIDS patients. In fact, according to the distinguished retrovirologist George Todaro, if a researcher had sufficient time and ingenuity he could make retroviruses appear in any uninfected cell culture.(18) These retroviruses, that have no parents and materialise from nowhere, are indistinguishable from exogenous retroviruses and owe their existence to latent, DNA genomes in animal cells being handed down to offspring via the germ (sex) cells of parents. They are not introduced into the cells by the action of an external particle. When such endogenous DNA is copied into RNA and the RNA translated into proteins, ultimately leading to the assembly and release of particles (known in virological jargon as viral expression), the particles are called endogenous retrovirus. No data ever obtained in the AIDS era excludes the "assemblage of such properties" known as HIV, if a retrovirus, as being endogenous. Well before the AIDS era, to explain endogenous retroviruses, retrovirologists claimed that pathogenic processes including diseases may cause retroviruses and not vice versa. No data in the AIDS era precludes a similar genesis for all the phenomena adduced as HIV including HIV DNA. Despite the fact that the cell theory of biology transcends all species, as recently as 1994 neither Gallo nor Fauci accepted that what readily took place in animal cells could occur in normal or sick human cells and manifest as human endogenous retroviruses.(19) Nowadays it is known that endogenous retroviral genomes constitute at least 1% of the human genome and are present "in all of us" in an amount of DNA 3000 times the size of the HIV genome.(20) It was from a prolonged, intense study of retroviruses, combined with our hypothesis that the common link amongst those with AIDS or at risk is cellular oxidation (this prediction is now well established by numerous papers), that we came to our theory which explains both AIDS and "HIV" (although at the beginning it was politically impossible to argue outright there was no proof for the existence of HIV. Even to accept the existence of HIV but to question a pathogenic role provoked the ire of editors and reviewers and posed more than enough difficulties publishing). The fact is, that at very best, Montagnier’s assertion translates to circumstantial evidence for the existence of a unique retrovirus in AIDS patients and as such his ultimate conclusion warrants the strongest rejection. This is especially so given the existence of the method, blessed with imprimatur of the Pasteur institute,(21,22) which leads to unambiguous and direct proof for the existence of a retrovirus. This was well established at least a decade before the discovery of HIV and why it was never used for proving the existence of HIV is one of the many great AIDS mysteries. Perhaps this enigmatic omission will one day serve as a memorial to the rapidity with which the clever age forsook reason under the alluring, imperious cloak of late twentieth century technology.
It is all too easy, and all too human, to get carried away with a host of non-scientific speculation as to why the HIV theory of AIDS is seriously adrift. Thus we have the Russians, the CIA, Africans eating dead monkeys, nepotism at the Centers for Disease Control, the AIDS industry, the seductiveness of the germ theory of disease, self seeking, self aggrandising government and non-government individuals and organisations and profit motives for avaricious biotechnology and pharmaceutical companies, perhaps incorporated into a flavour of the month conspiracy theory. Some of these make exciting reading but in my experience, given the choice of a conspiracy theory or human foibles, it is a far better bet to opt for the latter every time. To hypothesise that one day in the early 1980s a group of scientists colluded with divers others to deliberately mislead the rest of the world strains belief. There is no need to invoke these kind of agencies in order to point a stolid finger at the problems with the HIV theory. There are abundant scientific reasons why HIV cannot presently be accepted as the cause of AIDS. And in my view, and as is the purpose of this article, the central problem, that is, HIV itself, can be relatively easily explained. To paraphrase Cassius, the fault, lies not in our stars but in our scientist selves. Given the truth of the arguments below, if and when HIV is finally discredited, it will not be for HIV that the bell tolls. It will be for science and those science is meant to serve.
There are several scientific issues we could consider and for the previous readers of Contiuum most of these ideas are not new. However, it may unmuddy the waters for us all to collect and arrange these into more manageable chunks. The seminal argument is this: For an HIV theory of AIDS we must begin by proving we have HIV. This involves the following steps:
1. Since HIV is purportedly a retrovirus we need to know (a) what is a virus; (b) what properties distinguish retroviruses from viruses in general.
2. From our knowledge of (1) we must devise a method of proving the existence of a retrovirus in AIDS patients that is congruent with the properties of such a family of viruses.
3. An examination of the published evidence in order to ascertain whether (2) has been achieved for HIV.
What is a virus? The answer is intuitive from common experience. A person in a crowded train is suffering a cold. He or she coughs several times and within hours the former, fellow passengers develop the same symptoms. A child develops hepatitis and a few weeks later his brother and sister complain of anorexia, nausea and soon their skin is also yellow. In turn, these individuals cause others to develop identical symptoms so on. According to the germ theory of disease, the process occurring is that a particle, having a separate existence from the person with the disease, is transferred to another person, invades the cells forming the lining of the upper respiratory passages or liver cells and, in the process of multiplying inside and at the expense of these cells, causes the illnesses. Thus we affirm a virus as a microscopic object (a particle), transmitted from one individual to another and which is able to multiply only at the behest of living cells. The latter property differentiates viruses from bacteria which may multiply on an inanimate source of materials and energy. Not surprisingly, since viruses are obligatory intracellular parasites, they are much smaller than cells or bacteria and do not crowd their limited space with the food and machinery necessary to generate the energy to turn chemicals into copies of themselves. In practice virus particles are a stretch of nucleic acid (DNA or RNA) "instructions" for making proteins (the stretch is called the viral genome), packaged inside a protein core which in turn is surrounded by an envelope containing yet more proteins protecting the viral genome from the rigors of extracellular life. However, the viral envelope is not just packaging. Its chemical nature determines its interactional proclivities and thus for example, to what kinds of cells the particle is capable of attaching and entering, that is, which particular cells the virus can infect. A last but vitally important point is that from an electron microscope (EM) picture it is impossible to claim that a particle is a virus, even if it looks like one. From our definition, being a virus is entirely contingent upon a demonstrating that the particles of interest possess the ability to make more of the same particles. This is in fact what is meant by the term infectious and to demonstrate this property experiments are required. All the electron microscope can tell the experimenter is that particles are viral-like (and that the preparation of such particles is pure or impure).
What properties make up retroviruses? For the technically minded, these are taxonomical, physical and biochemical. The family Retroviridae is divided in three subfamilies, Oncovirinae, Lentivirinae and Spumavirinae.(23) Oncovirinae are in turn divided into genus type -A,-B,-C and -D particles. These subdivisions are based on EM descriptive properties (morphology), principally a restricted range of diameters, that is, 100-120nM and containing "condensed inner bodies (cores)" and surfaces "studded with projections (spikes, knobs)".(24) According to accepted wisdom, HIV is now classified as a Lentivirus but this was not always the case. Past descriptions of the particles found in cultures of tissues from AIDS patients but nonetheless all claimed to be the HIV particle include type -A, -C and -D as well as the current appellation.(13) (This is analogous to describing a new species of mammal first as human, then a gorilla and finally an orang-utan). The principal physical property is a density of 1.16 gm/ml which forms the basis for the method of their purification, that is, separation from everything else that is not retroviral particles. Biochemically, retroviruses are packaged with an RNA (not a DNA) genome and a small number of proteins, one of which is an enzyme which copies RNA into DNA (reverse transcription). Having listed these properties, it is important not to make the common mistake that what is different about retroviruses is unique to retroviruses. Especially their ability to reverse transcribe. Reverse transcription is carried out by hepatitis B virus and indeed by all cells including bacteria.(25) Significantly, particles with the morphology of retroviruses, even those containing a reverse transcribing enzyme, are not proof that a particle is a retrovirus. Gallo himself confirmed this in his writings as far back as 1976.(26) What is said to be "special" about retroviruses is that they insert a DNA copy of their RNA genome into the cellular DNA as a prelude to their reproduction. It is this act, and not the means, that is regarded as the most important distinguishing feature of retroviruses.
What method of proving the existence of a virus is congruent with its definition? This is quite easy to conceptualise although its realisation may prove difficult, tedious and relatively expensive in practice. This unfortunate reality may tempt scientists to adopt shortcuts (see below) and the dangers implicit in the failure to utilise a scientifically authentic method is perhaps no better illustrated than in the caveat issued by JW Beard (27) in 1957 (ironically when the technological craze was electron microscopy coupled with the inconsistent use of pure materials). Beard warned that "identification, characterisation, and analysis [of viruses] are subject to well-known disciplines established by intensive investigations, and the possibilities have by no means been exhausted. Strangely enough, it is in this field that the most frequent shortcomings are seen. These are related at times to evasion of disciplines or to their application to unsuitable materials. As was foreseen, much of the interest in the more tedious aspects of particle isolation and analysis has been diverted by the simpler and undoubtedly informative processes of electron microscopy. While much can be learned quickly with the instrument, it is nevertheless clear that the results obtained with it can never replace, and all too often may obscure, the need for the critical fundamental analyses that are dependent on access to homogenous materials" (italics mine).
The steps to prove the existence of a retrovirus flow logically from an appreciation of their nature:
1. Culture the cells that are considered infected by the retrovirus particle.
2. Purify putative retroviral-like particles by application of a method that is capable of extracting them from everything else that is not retroviral-like particles (banding in sucrose density gradients).
3. Proof obtained by use of electron microscopy that (a) there are such particles. (It is frankly misleading to proceed as if there are particles when in fact there are none). (b) the particles are pure; (c) the morphology of such particles is consistent with this family of viruses. The procedure to judge the morphology and purity of particles is to focus one’s eye on one particle, decide it has the appropriate size, shape and other distinguishing characteristics, then satisfy oneself that each particle surrounding the first particle is identical, and then repeat this process for all particles. Retroviral particles need to have a dense core, a diameter of 100-120 nM, to be almost spherical and to have their surface studded with knobs approximately 10nM in length.
4. Disrupt a preparation of pure particles and analyse the constituents (RNA and proteins). The latter must include an enzyme able to catalyse the synthesis of DNA from a piece of RNA.
5. Take a preparation of pure particles and prove that such particles, when introduced into fresh, uninfected cells, produce exactly the same particles, that is, the particles are infectious. This necessitates repeating steps (1) to (4). Thus proving the existence of a retrovirus involves isolating the particles twice. (And although it may seem trite to need even mention the fact, viral proteins and RNA are those and only those proteins and RNA that appear following disruption of purified viral particles).
Indeed, (1) to (5), with the addition of experiments involving control cultures of cells obtained from sick, non-AIDS affected individuals with AIDS-like diseases, are the challenge underlying the Continuum prize. (This £1000 reward is for a scientific paper proving that HIV exists and is still on offer). For those scientists who fail to use suitable controls (and that is the vast majority of HIV experts), "Nature will soon make a complete fool out of you" if the "assemblage of such properties" is also observed under circumstances where there are no retroviruses. Here it is not necessary to go into details since the views of the Perth group have been published in the scientific literature since 1988. Suffice it to repeat categorically that to date no HIV/AIDS researcher has published such evidence for HIV. Indeed, the interview with Professor Montagnier revealed that (a) despite a "Roman effort", he was unable to find any viral-like particles in his "purified" specimens. (Whatever the other "assemblage of such properties", no particles, no virus but these are the very specimens from which all HIV/AIDS researchers and biotechnology companies obtain "HIV" proteins and RNA by the ton for use in diagnosis and treatment); (b) despite not having any evidence for the existence of retroviral-like particles in his 1.16 gm/ml sucrose density gradient this material was used in other experiments to pronounce certain proteins in this culture "soup" as the "viral" proteins; (c) in his opinion neither did Gallo purify his HIV. Thus, according to the disparity between the definition of a virus and the evidence provided by Montagnier in 1983 and Gallo in 1984 (and everyone else since), there is no scientific proof for the existence of HIV. This leaves us with the uncomfortable question as to why, despite this lack of evidence, does nearly the rest of the world appear to believe otherwise and boldly act on the consequences of this belief?
Perhaps the first thing necessary to discuss is the notion of "the rest of the world". Given the population of Earth, only a tiny proportion of the "rest of the world" consists of physicians. However, physicians as an example, are far more likely than most to possess knowledge and understanding of the laboratory experiments that are said to support the existence of HIV and the HIV theory of AIDS. But in practice and of necessity, physicians, even specialist physicians, need to accept in good faith the vast majority of claims that form the basis of their practice. Medical training including postgraduate and continuing education consists of so much data that it is impossible to treat every statement as a scientific investigation. For example, as far as HIV/AIDS is concerned, the average, busy, practising doctor accepts that HIV has been isolated and that a positive HIV antibody test signifies HIV infection. However, the same doctor has little or no idea that seropositivity is defined by use of a discriminatory test called the Western blot, how a Western blot is manufactured, constructed and read, and that Western blots positive under the interpretive rules of one country or institution are not positive under the rules of another. The position with the properties of retroviruses or the rules of isolation is far worse. In my experience even HIV/AIDS experts are not aware that reverse transcription is non-specific for retroviruses, for example, that normal lymphocytes, grown under the influence of the same chemicals obligatory to produce "HIV" from co-cultures of tissues from AIDS patients (28,29), as well as normal spermatazoa,(30) reverse transcribe RNA including the same synthetic RNA used to "prove" the existence of HIV reverse transcriptase. Or that retroviral particles are purified taking advantage of their density by banding at 1.16 gm/ml in sucrose density gradient solutions. In my view, the clinician is excused for failing to appreciate the implications such knowledge poses against the HIV theory of AIDS. But not the experts. Thus, the oft heard statement that "99.99% of the world’s scientists can’t be wrong that HIV exists and is the cause of AIDS" needs to be reworked. The reality is that nearly all the world’s scientists, along with the remainder of humanity including virtually all the remaining non-scientists including physicians, accept the HIV theory of AIDS because they are wedded to the word of a relatively tiny number of specialists whose positions assert their claim on the basis of being experts. In the religion of science, these few are sacrosanct. This view is not meant to trivialise in a political sense the power of experts or the effect of that power magnified by public opinion. After all, for aeons 99.99% of the world’s authority figures asserted to an accepting populace that the sun circled the earth and flying machines an impossibility. Indeed, there is little doubt that the experts feel their views are scientifically justified. But, and here is the rub, according to the rules of proof determined by the properties of retroviruses, no expert can claim there are experiments which prove the existence of HIV according to the schema detailed above. There are no such experiments. Notwithstanding, even though it is firmly entrenched in the public record that both in May 1983 and July 1998 Montagnier had no evidence of viral-like particles in his "purified" specimens, the status quo staunchly remains. This represents the most pernicious kind of folly because, although there are no scientific impediments to a debate, the experts, the institutions and the journals steadfastly refuse to engage. One is led to wonder how far our civilisation has progressed since the murder of Giordio Bruno and the trial of Galileo? And who is paying the ultimate price?
The 1983 Montagnier paper (31) and the four, 1984 Gallo papers,(32-35) all published in Science, the journal founded by the philanthropy of Alexander Graham Bell, purportedly prove the existence of HIV and that HIV causes AIDS. Unfortunately, to the chagrin of "the rest of the world", these papers contain a plethora of unfamiliar data and detail none of which make for light reading. Nonetheless, it is possible to take a few steps back from the data presented in these crucial publications and begin to understand why their conclusions are so unreservedly unwarranted. (It is also important to note that these papers remain the very best published on the existence of HIV. None more modern is even remotely nearer the mark and to this day these are the papers cited as proof of HIV and causation). What soon becomes obvious, and as Montagnier has recently affirmed is, that in place of the logic and rigor demanded by the steps discussed above, a series of nonspecific phenomena has been accepted as proof for the existence of HIV. From papers he published in the 1970s we know Gallo at least realised that particles and reverse transcription are not sufficient to prove the existence of retrovirus. In other words Gallo realised the need to demonstrate replication to prove that particles bearing the expected morphological and biochemical properties of retroviruses are not exanimate and are in fact retroviruses. For example, in 1976 he wrote, "Release of virus-like particles morphologically and biochemically resembling type-C virus but apparently lacking the ability to replicate have been frequently observed from leukaemic tissue".(26) Whether he appreciated it or not, this concession by Gallo is in fact no more than an acknowledgment of the "particle problem", the same problem that exercised the minds and pens of researchers such as JW Beard two decades earlier. The "particle problem" is that cell cultures have the propensity to produce a myriad of particles of many morphologies and thus strict rules must apply to make sense of this menagerie, that is, which if any particles are viruses and which are not. Beard’s own words (27), again no more than common sense, preempt by two decades the Pasteur rules for the isolation of retroviruses. "…the scheme of approach, as well illustrated by that devised and rigorously tested in investigations of viral agents, is relatively simple. This consists in (1) isolation of the particles of interest; (2) recovery (purification) of the particles in a given preparation that are homogeneous with respect to particle kind; (3) identification of the particles, and (4) analysis and characterisation of the particles for the physical, chemical, or biological properties desired". To confirm retrovirus-like particles as a retrovirus the quintessential biological property required is proof of their ability to replicate. However, given there are no published data that retroviral-like particles have been isolated, analysed, reintroduced into fresh culture and subsequently reanalysed, we must conclude that HIV researchers regard other data as proof of replication. What are these data?
For HIV/AIDS researchers the crux of their proof is the fact that some antibodies in AIDS patients react with some proteins that exist in the chemically stimulated cultures of lymphocytes derived from the same patients. (So what, we may wonder and even if significant, where is there evidence of a nexus between reverse transcription and antibody/antigen reactions in a test-tube, and the scant particles seen only in unpurified material?) If we adopt the premise that there do exist unique, exogenously acquired retroviral particles, HIV, which cause thirty different diseases (AIDS), certainly we would expect proteins from unpurified cultures or from a 1.16 gm/ml sucrose density gradient (the latter regarded by all experts as the "purified virus") from such individuals to interact with antibodies in the sera of AIDS patients. This is because such particles will be expected to replicate in humans (as well as in their cell cultures), and induce antibodies in vivo because they are foreign. However, in the HIV expert scheme, "proof of replication" relies not only on assuming the existence of such antibodies but also on the specificity of protein/antibody reactions, that is, given the existence of an agent HIV, this agent and this agent alone is capable of stimulating the clones of B lymphocytes that produce particular antibodies which are the only antibodies capable of reacting with particular culture proteins which are constituents of HIV. Apart from adopting the very premise they are setting out to prove, the mistake made by all HIV researchers is the overvalued idea that antibody/antigen reactions a priori are specific. (The argument is also circular since antibodies are used to "prove" which proteins in the cultures are "HIV" and then these proteins are used to "prove" the antibodies are "HIV"). Antibody/antigen reactions do not possess such specificity properties, a fact well publicised and discussed in most Immunology text books and by many research scientists such as Stratis Avrameaus from the Pasteur Institute. Antibody molecules, even monoclonal antibodies, may not interact only with the inducing antigen but also with other antigens, that is, antibodies "cross-react".(36-42) Indeed, there are instances where "cross-reactive antigen binds with higher affinity than the homologous antigen itself...The most obvious fact about cross-reactions of monoclonal antibodies is that they are characteristic of all molecules and cannot be removed by absorption without removing all reactivity...Even antigens that differ for most of their structure can share one determinant, and a monoclonal antibody recognizing this site would then give a 100% cross-reaction. An example is the reaction of autoantibodies in lupus with both DNA and cardiolipin" (italics mine). However, "It should be emphasised that sharing a "determinant" does not mean that the antigens contain identical chemical structures, but rather that they bear a chemical resemblance that may not be well understood, for example, a distribution of surface charges"43 (italics mine). Since polyclonal [mixtures of] antibodies are no more than a miscellany of monoclonal [single] antibodies these facts apply equally, if not more so, to polyclonal antibodies. Thus HIV/AIDS experts, in ignoring the "particle problem", have come hard up against the "antibody problem" and, in apparent ignorance of this fundamental problem, have fallen foul of Nature and been misled into thinking something that is not actually known. However, the bitter consequence of this logical slip is the contrivance of a retrovirus and a retrovirus theory of AIDS. Indeed, given (a) the experimental methods employed by HIV/AIDS researchers; (b) that retroviral-like particles are virtually ubiquitous in biological material; (c) that reverse transcription is likewise a commonplace and trivial cellular function; (d) the many and varied pathological processes associated with antibodies each with propensities to cross-react with an array of antigens; a jocose sceptic might logically argue that sets of the "assemblage of such properties" await future generations of robustly funded virologists and the discovery of a host of new retroviruses as causative agents of perhaps all diseases.
This also leads to yet another great AIDS mystery. To prove HIV isolation, both Montagnier and Gallo and their colleagues also employed sera from rabbits which they claimed contained "specific reagents".(44) However, rabbits do not develop HIV infection or AIDS and if such specific antibodies were to exist they could only be produced by immunisation of rabbits with pure HIV or, as the first Gallo group paper reported, "from rabbits infected repeatedly with disrupted HTLV-III [HIV]". If rabbits were immunised with pure virus, why should it be necessary to produce specific reagents to define the isolation of virus that had already been isolated? That an antibody/antigen reaction cannot be use to prove the existence of a new virus is accepted by Donald Francis, a researcher who with Gallo, played a significant role in developing the theory that AIDS is caused by a retrovirus.(45) In 1983, Francis, then the chief collaborator of the AIDS Laboratory Activities, US Center for Disease Control (CDC) and former chief of the WHO smallpox program, speculated on a viral cause for AIDS: "One must rely on more elaborate detection methods through which, by some specific tool, one can "see" a virus. Some specific substances, such as antibody or nucleic acids, will identify viruses even if the cells remain alive. The problem here is that such methods can be developed only if we know what we are looking for. That is, if we are looking for a known virus we can vaccinate a guinea pig, for example, with pure virus...Obviously, though, if we don't know what virus we are searching for and we are thus unable to raise antibodies in guinea pigs, it is difficult to use these methods...we would be looking for something that might or might not be there using techniques that might or might not work"(46) (italics mine).
Significantly, at the time when gay men were first developing the diseases which now constitute the clinical AID syndrome, scientists should have well and truly been aware of the humiliating caveat consequent upon the sudden, 1980 "disappearance" of the world’s "first human retrovirus", Gallo’s HL23V.(15) Even though the laboratory evidence for the existence of HL23V surpasses that of HIV, HL23V fell ignominiously from its proud place because "its" antibodies were found to be antibodies that form in response to a large range of non-viral, non-infectious agents which are common in human populations. In the view of the scientists who made this critical discovery, these antibodies follow "exposure to many natural substances possessing widely cross-reacting antigens and are not a result of widespread infection of man with replication-competent oncoviruses [retroviruses]".(47) The intriguing part of this murky episode of virology is that although Gallo conceded the nonspecificity of the antibody reactions for the purposes of defining certain culture proteins as "HL23V" proteins (exactly the same method is used to define the "HIV" proteins and thus "HIV"), the common belief remains that HL23V was a contaminant mixture of monkey retroviruses. Reading to learn the history of this episode one cannot help be impressed by Gallo’s detailed account as to how difficult (if not impossible) it would have been for such contamination to occur in his laboratory. However, from the point of view of retrovirology, contamination is a far more propitious explanation because it at least is congruent with the existence of a retrovirus (or retroviruses) albeit nonhuman, rather than no retrovirus(es). Given the latter, the use of antibody/culture protein reactivity to "prove" the existence of retroviruses would long have been seen to have much to do with sophistry and nothing whatsoever to do with science. This follows because, in the case of HL23V, antibody reactivity would have predicated the presence of a virus which does not exist. This episode, more than anything else, illustrates just how fragile is the notion of HIV. When dispassionate scientists and others realise what is actually the basis for the characterisation of proteins deemed to be HIV, and accept the already abundant evidence that, like antibodies to HL23V, "HIV" antibodies arise where there is no HIV, HIV will likewise fall. (It is worth adding that as far as AIDS is concerned, it is sufficient to argue that HIV has not been shown to exist. There is no need to postulate that no retroviruses exist. To present such data and argument, while of scientific interest would represent a gargantuan effort both diversionary and irrelevant to the current problem).
In summary, what can be said is this: In their attempts to prove the existence of HIV, HIV/AIDS researchers have made two fundamental mistakes. They have ignored the particle problem and have either ignored or misunderstood the antibody problem. Rather, in seeking their goal, the few scientists involved have adopted the premises that (i) a retrovirus does exist; (ii) it is present in AIDS patients; (iii) it induces specific antibodies in vivo; (iv) it can be successfully cultured in vitro from tissues derived from AIDS patients; (v) the antibodies interact specifically with particular proteins in such cultures. Although these postulates may ultimately prove correct, since none can be verified without recourse to the virus ("virological habeas corpus"), they cannot be used as a platform from which to interpret experimental data as proof of the existence of HIV. In virology as in life, one cannot put the cart before the horse. The reality is this: when it is pared down to the essentials, what masquerades as proof of the existence of HIV is sets of antibody/antigen reactions between two sets of unknowns (culture proteins and antibodies). And for those unlucky enough to possess the cells or antibodies capable of producing similar reactions, the enormous weight of the HIV theory of AIDS becomes their lifelong yoke. This, the HIV theory of AIDS, is par excellence an example of Robert Pirsig’s warning, "One false deduction about the machine and you can get hung up indefinitely". However, from the scientific point of view, it is still possible that experiments, properly constituted (with controls) as enumerated by JW Beard and the Pasteur Institute, could be performed to prove there is a , so called HIV. This would represent an admission of the pressing need to start out all over again but even if successful, would not overcome the otbona fideher multitudinous difficulties accepting that such an HIV is the cause of AIDS. Thus, in the absence of scientific evidence that it even exists, thorough investigations of alternative hypotheses should be urgently pursued, especially those that offer hope of control or even cure for the many affected.
The final matter to consider is how long humanity must endure the scientific misdemeanors of the HIV/AIDS experts. Or to be unreservedly blunt, since gay men with AIDS far out number all others, when will gay men wake up? Consider for a moment the strange but true story of the current "technological craze", the use of AZT and protease inhibitor (PI) "cocktails" to treat both AIDS patients and healthy seropositive individuals. Both classes of drugs are stated to prevent viral replication, that is, they are claimed to interfere in the cycle of newly hatched HIV particles infecting fresh T4 cells and generating more HIV particles to infect more cells and so on. According to HIV "science", AZT does this "on the way in", PIs "on the way out". Thus AZT prevents HIV copying its RNA into the nuclear, DNA proviral form while PIs produce defective, incompetent HIV. Either way, no "new" HIVs arise capable of perpetuating the replication cycle. According to Ho, "virus producing" infected T4 cells die after only a few days. Thus, after a short time (weeks) on these drugs, T4 cells already infected should die (thus eliminating their contribution to the viral DNA equation), and no new cells should become infected (no new viral DNA can enter the equation). Thus the level of viral DNA, (referred to as the "viral burden", not to be confused with "viral load" which is RNA measured in plasma) should decrease. However, neither class of drugs has any effect on viral burden.(48-50) The levels are unmoved by administration of these drugs. The failure to decrease viral burden means the drugs cannot work in the manner stated and/or that "HIV DNA" (and thus HIV) has nothing to do with the beneficial effects (if any) of these agents. If the latter then what does HIV have to do with causing AIDS? (And to pour salt into the wounds, any increase in T4 cells observed in individuals taking AZT is claimed to be caused by decreased HIV despite the fact that AZT raises the number of T4 cells (sometimes dramatically) in humans who take it following a needlestick injury but who never seroconvert.(51,52)) Notwithstanding, various HIV/AIDS experts are now proclaiming that PIs, like AZT from the earlier days, are doomed to failure. Researchers at the University of California at San Francisco, who first reported a failure rate of more than 50%, say the "honeymoon" is over. A recent paper in the journal AIDS reported that three PIs failed in 30-64% of patients. Given all the hope (and hype) made over these drugs at various times, perhaps there may at last be a catalyst to a denouement. The more one reads, and the more one studies the vast HIV/AIDS literature, the more it becomes apparent that the data are far better explained without recourse to an HIV. I reiterate our group’s earlier position: HIV is the greatest single obstacle to overcoming the problem of AIDS14. In the sixties Bob Dylan put it all in a song: "How many deaths will it take till he knows that too many people have died?". Reprehensibly, the answer is still the song.*
Dr. Valendar F. Turner is a member of the Perth Group of HIV/AIDS 'dissident' scientists. He graduated from the University of Sydney in 1996, is a fellow of the Royal Australiasan College of Surgeons and Fellow of the Australasian College of Emergency Medicine. He practises at the Royal Perh Hospital in Western Australia.
Refrerences
1. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Hedland-Thomas B, Causer D, Page B. (1995). A critical analysis of the HIV-T4-cell-AIDS hypothesis. Genetica 95:5-24.
2. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Causer D. (1995). Factor VIII, HIV and AIDS in haemophiliacs: an analysis of their relationship. Genetica 95:25-50.
3. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Bialy H. (1995). AIDS in Africa: Distinguishing fact and fiction. World J. Microbiol. Biotechnol. 11:135-143.
4. Papadopulos-Eleopulos E. (1982). A Mitotic Theory. J. Theor. Biol. 96:741-758.
5. Papadopulos-Eleopulos E. (1988). Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Med. Hypotheses 25:151-162.
6. Papadopulos-Eleopulos E, Hedland-Thomas B, Causer DA, Dufty AP. (1989). An alternative explanation for the radiosensitization of AIDS patients. Int. J. Radiat. Oncol. Biol. Phys. 17:695-697.
7. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1992). Kaposi's sarcoma and HIV. Med. Hypotheses 39:22-9.
8. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1992). Oxidative stress, HIV and AIDS. Res. Immunol. 143:145-8.
9. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1993). Is a positive Western blot proof of HIV infection? Bio/Technology 11:696-707.
10. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1993). Has Gallo proven the role of HIV in AIDS? Emerg. Med. [Australia] 5:113-123.
11. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. (1995). A reply to Wei and Ho. Unpublished letter to Nature.
12. Papadopulos-Eleopulos E, Turner VF, Causer DS, Papadimitriou JM. (1996). HIV transmission by donor semen. Lancet 347:190-1.
13. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1996). Virus Challenge. Continuum 4:24-27.
14. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. (1996). The Isolation of HIV: Has it really been achieved? Continuum 4:1s-24s.
15. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. (1997). HIV antibodies: Further questions and a plea for clarification. Curr. Med. Res. Opinion 13:627-634.
16. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. (1997). A critical analysis of the evidence for the isolation of HIV. At Website http://www.virusmyth.com/aids/data/epappraisal.htm
17. Tahi D. (1998). Did Luc Montagnier discover HIV? Text of video interview with Professor Luc Montagnier Pasteur Institute July 18th 1997. Continuum 5:30-34.
18. Todaro GJ, Benveniste RE, Sherr CJ. Interspecies Transfer of RNA Tumour Virus Genes: Implications for the search for "Human" Type C Viruses. (1976). p. 369-384 In: Animal Virology Baltimore D, Huang AS, Fox CS, eds Academic Press Inc., New York.
19. Gallo RC, Fauci AS. The human retroviruses. (1994). p. 808-814 In: Harrison's Principles of Internal Medicine Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL, eds 13 ed McGraw-Hill Inc., New York.
20. Kurth R, Teich NM, Weiss R, Oliver RTD. (1977). Natural human antibodies reactive with primate type-C antigens. Proc. Natl. Acad. Sci. U S A 74:1237-1241.
21. Sinoussi F, Mendiola L, Chermann JC. (1973). Purification and partial differentiation of the particles of murine sarcoma virus (M. MSV) according to their sedimentation rates in sucrose density gradients. Spectra 4:237-243.
22. Toplin I. (1973). Tumor Virus Purification using Zonal Rotors. Spectra No. 4:225-235.
23. Frank H. Retroviridae. (1987). p. 253-256 In: Animal Virus and Structure Nermut MV, Steven AC, eds Elsevier, Oxford.
24. Gelderblom HR, Özel M, Hausmann EHS, Winkel T, Pauli G, Koch MA. (1988). Fine Structure of Human Immunodeficiency Virus (HIV), Immunolocalization of Structural Proteins and Virus-Cell Relation. Micron Microscopica 19:41-60.
25. Varmus HE. (1989). Reverse transcription in bacteria. Cell 56:721-724.
26. Gallo RC, Wong-Staal F, Reitz M, Gallagher RE, Miller N, Gillepsie DH. Some evidence for infectious type-C virus in humans. (1976). p. 385-405 In: Animal Virology Balimore D, Huang AS, Fox CF, eds Academic Press Inc., New York.
27. Beard JW. (1957). Physical methods for the analysis of cells. Ann. N. Y. Acad. Sci. 69:530-544.
28. Gallo RC, Sarin PS, Wu AM. On the nature of the Nucleic Acids and RNA Dependent DNA Polymerase from RNA Tumor Viruses and Human Cells. (1973). p. 13-34 In: Possible Episomes in Eukaryotes Silvestri LG, ed North-Holland Publishing Company, Amsterdam.
29. Tomley FM, Armstrong SJ, Mahy BWJ, Owen LN. (1983). Reverse transcriptase activity and particles of retroviral density in cultured canine lymphosarcoma supernatants. Br. J. Cancer 47:277-284.
30. Whitkin SS, Higgins PJ, Bendich A. (1978). Inhibition of reverse transcriptase and human sperm DNA polymerase by anti-sperm antibodies. Clin Exp Immunol 33:244-251.
31. Barré-Sinoussi F, Chermann JC, Rey F. (1983). Isolation of a T-Lymphotrophic Retrovirus from a patient at Risk for Acquired Immune Deficiency Syndrome (AIDS). Science 220:868-871.
32. Gallo RC, Salahuddin SZ, Popovic M, 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.
33. Popovic M, Sarngadharan MG, Read E, Gallo RC. (1984). Detection, Isolation,and Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science 224:497-500.
34. Sarngadharan M, G., Popovic M, Bruch L. (1984). Antibodies Reactive to Human T-Lymphotrophic Retroviruses (HTLV-III) in the Serum of Patients with AIDS. Science 224:506-508.
35. Schupbach J, Popovic M, Gilden RV, Gonda MA, Sarngadharan MG, Gallo RC. (1984). Serological analysis of a Subgroup of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS. Science 224:503-505.
36. Guilbert B, Fellous M, Avrameas S. (1986). HLA-DR-specific monoclonal antibodies cross-react with several self and nonself non-MHC molecules. Immunogenetics 24:118-121.
37. Gonzalez-Quintial R, Baccala R, Alzari PM, et al. (1990). Poly(Glu60Ala30Tyr10) (GAT)-induced IgG monclonal antibodies cross-react with various self and non-self antigens through the complentarity determining regions. Comparison with IgM monoclonal polyreactive natural antibodies. Europ. J. Immunol. 20:2383-2387.
38. Fauci AS. (1988). The Human Immunodeficiency Virus: Infectivity and Mechanisms of Pathogenesis. Science 239:617-622.
39. Ternynck T, Avrameas S. (1986). Murine natural monoclonal antibodies: a study of thier polyspecificities and their affinities. Immunol. Rev. 94:99-112.
40. Owen M, Steward M. Antigen recognition. (1996). p. 7.1-7.12 In: Immunology Roitt I, Brostoff J, Male D, eds 4th ed Mosby, London.
41. Parravicini CL, Klatzmann D, Jaffray P, Costanzi G, Gluckman JC. (1988). Monoclonal antibodies to the human immunodeficiency virus p18 protein cross-react with normal human tissues. AIDS 2:171-177.
42. Pontes de Carvalho LC. (1986). The faithfullness of the immunoglobulin molecule: can monoclonal antibodies ever be monospecific. Immunol. Today 7:33.
43. Berzofsky JA, Berkower IJ, Epstein SL. Antigen-Antibody Interactions and Monoclonal Antibodies. (1993). p. 421-465 In: Fundamental Immunology Paul WE, ed 3rd ed Raven, New York.
44. Gallo RC, Sarin PS, Kramarsky B, Salahuddin Z, Markham P, Popovic M. (1986). First isolation of HTLV-III. Nature 321:119.
45. Caton H. (1994). The AIDS Mirage. Sydney: The University of New South Wales Press Ltd., 1994.
46. Francis DP. The search for the cause. (1983). p. 137-150 In: The AIDS epidemic Cahill KM, ed 1st ed Hutchinson Publishing Group, Melbourne.
47. Snyder HW, Fleissner E. (1980). Specificity of human antibodies to oncovirus glycoproteins: Recognition of antigen by natural antibodies directed against carbohydrate structures. Proc. Natl. Acad. Sci. U S A 77:1622-1626.
48. Lee TH, Sheppard HW, Reis M, Dondero D, Osmond D, Busch MP. (1994). Circulating HIV-1-infected cell burden from seroconversion to AIDS: importance of posseroconversion viral load on disease course. J. Acquir. Immun. Defic. Syndr. 7:381-388.
49. Holodniy M, Mole L, Winters M, Merigan TC. (1994). Diurnal and short-term stability of HIV virus load as measured by gene amplification. J. Acquir. Immun. Defic. Syndr. 7:363-8.
50. O. Brien W, Grovit-Ferbas K, Namazi A, et al. (1995). Human immunodeficiency virus-type 1 replication can be increased in peripheral blood of seropositive patients after influenza vaccination. Blood 86:1082-9.
51. Levy JA. (1996). Surrogate markers in AIDS research. Is there truth in numbers? JAMA 276:161-2.
52. Milazzo LM, Cremoni V, Cremoni L. (1996). CD4+ lymphocyte count variations in HIV-negative subjects treated with zidovudine. AIDS 10:1444-1445.