Damned Heretics

Condemned by the established, but very often right

I am Nicolaus Copernicus, and I approve of this blog

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Qualified outsiders and maverick insiders are often right about the need to replace received wisdom in science and society, as the history of the Nobel prize shows. This blog exists to back the best of them in their uphill assault on the massively entrenched edifice of resistance to and prejudice against reviewing, let alone revising, ruling ideas. In support of such qualified dissenters and courageous heretics we search for scientific paradigms and other established beliefs which may be maintained only by the power and politics of the status quo, comparing them with academic research and the published experimental and investigative record.

We especially defend and support the funding of honest, accomplished, independent minded and often heroic scientists, inventors and other original thinkers and their right to free speech and publication against the censorship, mudslinging, false arguments, ad hominem propaganda, overwhelming crowd prejudice and internal science politics of the paradigm wars of cancer, AIDS, evolution, global warming, cosmology, particle physics, macroeconomics, health and medicine, diet and nutrition.

HONOR ROLL OF SCIENTIFIC TRUTHSEEKERS

Henry Bauer, Peter Breggin , Harvey Bialy, Giordano Bruno, Erwin Chargaff, Nicolaus Copernicus, Francis Crick, Paul Crutzen, Marie Curie, Rebecca Culshaw, Freeman Dyson, Peter Duesberg, Albert Einstein, Richard Feynman, John Fewster, Galileo Galilei, Alec Gordon, James Hansen, Edward Jenner, Benjamin Jesty, Michio Kaku, Adrian Kent, Ernst Krebs, Thomas Kuhn, Serge Lang, John Lauritsen, Mark Leggett, Richard Lindzen, Lynn Margulis, Barbara McClintock, George Miklos, Marco Mamone Capria, Peter Medawar, Kary Mullis, Linus Pauling, Eric Penrose, Max Planck, Rainer Plaga, David Rasnick, Sherwood Rowland, Carl Sagan, Otto Rossler, Fred Singer, Thomas Szasz, Alfred Wegener, Edward O. Wilson, James Watson.
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Many people would die rather than think – in fact, they do so. – Bertrand Russell.

Skepticism is dangerous. That’s exactly its function, in my view. It is the business of skepticism to be dangerous. And that’s why there is a great reluctance to teach it in schools. That’s why you don’t find a general fluency in skepticism in the media. On the other hand, how will we negotiate a very perilous future if we don’t have the elementary intellectual tools to ask searching questions of those nominally in charge, especially in a democracy? – Carl Sagan (The Burden of Skepticism, keynote address to CSICOP Annual Conference, Pasadena, April 3/4, 1982).

It is really important to underscore that everything we’re talking about tonight could be utter nonsense. – Brian Greene (NYU panel on Hidden Dimensions June 5 2010, World Science Festival)

I am Albert Einstein, and I heartily approve of this blog, insofar as it seems to believe both in science and the importance of intellectual imagination, uncompromised by out of date emotions such as the impulse toward conventional religious beliefs, national aggression as a part of patriotism, and so on.   As I once remarked, the further the spiritual evolution of mankind advances, the more certain it seems to me that the path to genuine religiosity does not lie through the fear of life, and the fear of death, and blind faith, but through striving after rational knowledge.   Certainly the application of the impulse toward blind faith in science whereby authority is treated as some kind of church is to be deplored.  As I have also said, the only thing ever interfered with my learning was my education. My name as you already perceive without a doubt is George Bernard Shaw, and I certainly approve of this blog, in that its guiding spirit appears to be blasphemous in regard to the High Church doctrines of science, and it flouts the censorship of the powers that be, and as I have famously remarked, all great truths begin as blasphemy, and the first duty of the truthteller is to fight censorship, and while I notice that its seriousness of purpose is often alleviated by a satirical irony which sometimes borders on the facetious, this is all to the good, for as I have also famously remarked, if you wish to be a dissenter, make certain that you frame your ideas in jest, otherwise they will seek to kill you.  My own method was always to take the utmost trouble to find the right thing to say, and then to say it with the utmost levity. (Photo by Alfred Eisenstaedt for Life magazine) One should as a rule respect public opinion in so far as is necessary to avoid starvation and to keep out of prison, but anything that goes beyond this is voluntary submission to an unnecessary tyranny, and is likely to interfere with happiness in all kinds of ways. – Bertrand Russell, Conquest of Happiness (1930) ch. 9

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Duesberg’s papers are neglected science classics

Elegance in argument

One of the few beautiful things about AIDS and its science that will strike anyone new to this debate, if they actually go and look over the five classic papers Duesberg has written on AIDS and its scientific discontents, is how well written they are. To some discerning minds, this might in itself indicate truth.

One can, frankly, say they are quite superb as literary artefacts. Small wonder one of them (the first one) was chosen by Walter Gilbert as a specimen of excellence for his graduate biology students to study at Harvard. Gilbert felt it would teach them just how a claim might be professionally reviewed in an exemplary way. (One wonders what those students now think of the Duesberg arguments. It seems impossible that they cannot still respect them, but if so, where are they hiding? A naive question, perhaps….)

One does not even need to be fully persuaded by the arguments of thse papers to rate them highly, though it is questionable whether anyone intelligent and educated who reads them thoroughly will find anything lasting to quibble with.

After all, the battalions of hostile peer reviewers who were marshaled by the editors of the respective journals, no doubt out of a healthy sense of editorial self-preservation and caution, could find no permanent flaws or make any objections that that Duesberg could not meet.

In fact, one can notice that Duesberg’s papers put the articles which purport to rebut them to shame in terms of logical precision and academic clarity.

That’s why even before assessing the balance of argument, it is difficult to have much respect for the responses that Duesberg has met with in the pages of Science, Nature and other science journals, simply because of the obviously lower quality of their reasoning and style, lacking in literary poise, order and clean logic of the first class academic kind that Duesberg typically produces.

Ptolemaic goalposts

But what is most striking is the consistent tendency, time and again, to try and escape the force of Duesberg’s critique by embroidering the paradigm (ruling theory) with endless speculative additions and complications. As a historian of science might say, it’s positively Ptolemaic (the theory recorded by Ptolemy that the sun orbits the earth was defended against Copernicus with ever more subtle adjustments in like manner). Since this strategy removes the requirement to meet the objections originally raised, HIV skeptics, borrowing a metaphor from football, like to call the manoever “moving the goalposts”.

All of the papers in his remarkable series are listed on this page of Duesberg’s papers. But it seems to us that Duesberg’s greatest works among equals are these:

1. The Cancer Research paper

The initial Cancer Research paper (Duesberg, P.H. (1987) Retroviruses as Carcinogens and Pathogens: Expectations and Reality (Cancer Research 47: 1199-1220), which is first of all a rejection of retroviruses as cancer causing, and ultimately, of the whole theory of cancer genes, a field Duesberg helped trigger and now in this paper repudiates; the sting for HIV careerists was in the tail, however, as Duesberg reviewed the new theory and decisively rejected it as lacking any laboratory or epidemiological proof, and contrary to all known science and common sense. Far more likely, he concluded, was that the radical immune deficit syndrome that had suddenly appeared among highly active gays was due to the surge in novel drug taking that enabled their newly escalated activities in the expanded club and baths infrastructure.

Here is the full paper, Part II. The first part on cancer is too technical for lay readers, but this second half on whether HIV makes any sense as a cause of AIDS, is surprisingly accessible and convincing.


II. Retroviruses and AIDS
The isolation in 1983 of a retrovirus from a human patient with lymphadenopathy, a typical symptom of AIDS, led to the proposal that the virus, now termed lymphadenopathy-associated virus, is the cause of AIDS (26). Related viruses, termed HTLV-III, ARV, or HIV (209), have since been isolated from about one-half of the AIDS patients that have been sampled (210-214). In the United States about 26,000 AIDS cases and 15,000 AIDS fatalities have been reported between 1981, when the disease was first identified (215), and October 1986 (216). Women represent only 7% of the AIDS cases in the United States (216). The number of AIDS cases reported in the United States has increased from about 100 per 6-month period in 1981 to about 5,000 during the last three 6-month periods from January 1985 (216). At the same time the case-fatality rate has declined from a high of 88% in 1981 to 32% in 1986 (216). In absolute numbers the known deaths have declined from a high of 2,600 in the first 6 months of 1985 to 1,800 in the first 6 months of 1986. This suggests either that the virulence of the disease is dropping or that other diseases were diagnosed as AIDS. Recently the virus was also suggested to cause disease of the brain and of the nervous system (230, 255, 268, 274) and lymphoid interstitial pneumonia (275).
Antibody to the virus is found in about 90% of AIDS patients and correlates with chronic latent infection by the virus (217-221). Because of the nearly complete correlation between AIDS and immunity against the virus, the virus is generally assumed to be the cause of AIDS (13, 27). Accordingly, detection of antiviral antibody, rather than virus, is now most frequently used to diagnose AIDS and those at risk for AIDS (27, 217-224). This is paradoxical, since serum antibody from AIDS patients neutralizes AIDS virus (225-227) and since antiviral immunity or vaccination typically protects against viral disease. It is even more paradoxical that a low antibody titer is equated with a low risk for AIDS (228, 229).
Unlike all other retroviruses, AIDS viruses are thought to be direct pathogens that kill their host cells, namely T-lymphocytes (13, 27), and possibly cells of the brain (230, 255). This view is compatible with the phenotype of AIDS, the hallmark of which is a defect in T-cells (13, 27, 215), and with experimental evidence that many but not all viral isolates induce cytopathic fusion of T-lymphocytes under certain conditions in vitro (Section D). Further it is compatible with neurological disease (231, 232, 255). However, cell killing is incompatible with the obligatory requirement of mitosis for retrovirus replication (16, 25) and with the complete absence of cytocidal effects in all asymptomatic infections in vivo (Section D).

A. Infections with No Risk and Low Risk for AIDS Indicate That the Virus Is Not Sufficient to Cause AIDS

Since their original discoveries in AIDS patients, the virus and more frequently antibody to the virus have also been demonstrated in a large group of asymptomatic persons (212, 214). The virus has been estimated to occur in about 1 to 2 x 106 or about 0.5 to 1% of all Americans (223, 224). In the United States persons at high risk for infection include promiscuous homosexual and bisexual men, of whom 17 to 67% are antibody positive; intravenous drug users, of whom 50 to 87% are positive; and hemophiliacs, of whom 72 to 85% are positive according to some studies (13, 218, 223). On the basis of this particular epidemiology, it was concluded that the virus is not transmitted as a cell-free agent like pathogenic viruses but only by contacts that involve exchange of cells (13, 27).

In these virus-infected groups the annual incidence of AIDS was found to average 0.3% (224) and to reach peak values of 2 to 5% (218, 223, 233). However even in these groups there are many more asymptomatic than symptomatic virus carriers. Other infected groups appear to be at no risk for AIDS. In Haiti and in certain countries in Africa antibody-positive individuals range from 4 to 20% of the population, whereas the incidence of AIDS is estimated at less than 0.01% (223, 229, 234). Several reports describe large samples of children from Africa who were 20 (228) to 60% (221) antibody positive and of female prostitutes who were 66 to 80% antibody positive (221,235), yet none of these had AIDS. Among male homosexuals and hemophiliacs of Hungary about 5% are AIDS virus positive, yet no symptoms of AIDS were recorded (161). Among native male and female Indians of Venezuela 3.3 to 13.3% have antiviral immunity, but none have symptoms of AIDS (236). Since these Indians are totally isolated from the rest of the country, in which only one hemophiliac was reported to be virus positive (236), the asymptomatic nature of their infections is not likely to be a consequence of a recent introduction of the virus into their population. Thus it is not probable that these infections will produce AIDS after the average latent period of 5 years (Section B).
Since the percentage of virus carriers with symptoms of AIDS is low and in particular since it varies between 0 and 5% depending on the AIDS risk group of the carrier, it is concluded that the virus is not sufficient to cause AIDS and that it does not encode an AIDS-specific function. The virus is also not sufficient to cause neurological disease, since it has been detected in the brains of persons without neurological disease and of healthy persons who had survived transient meningitis (230-232).
Thus the virus appears only rarely compatible with Koch’s third postulate as an etiological agent of AIDS. It may be argued that the asymptomatic infections reflect latent infections or infections of only a small percentage of susceptible cells, compared to presumably acute infections with symptoms of AIDS. However, it is shown in Section C that infections of neither symptomatic nor asymptomatic carriers are acute; instead both are equally latent and limited to a small percentage of susceptible cells.
Further, the observations that some virus carriers are at high and others at essentially no risk for AIDS directly argue for a cofactor (218, 237) or else for a different cause for AIDS. The strong bias against women, because only 2.5% (479 of 17,000 cases) of the sexually transmitted AIDS cases in the United States are women (216), is a case in point. The virus-positive but AIDS-negative children and prostitutes of Africa (221) or Indians from Venezuela (236) are other examples.

B. Long Latent Period of AIDS Incompatible with Short Latent Period of Virus Replication

The eclipse period of AIDS virus replication in cell culture is on the order of several days, very much like that of other retroviruses (238). In humans virus infection of a sufficient number of cells to elicit an antibody response appears to take less than 4 to 7 weeks. This estimate is based on an accidental needle-stick infection of a nurse, who developed antibody 7 weeks later (239), and on reports describing 12 (240) and 1 (232) cases of male homosexuals who developed antibody 1 to 8 weeks after infection. During this period a mononucleosis-like illness associated with transient lymphadenopathy was observed. In contrast to AIDS (see below), this illness appeared 1 to 8 weeks after infection and lasted only 1 to 2 weeks until antiviral immunity was established. The same early mononucleosis-like disease, associated with lymphocyte hyperplasia, was observed by others in primary AIDS virus infections (234). This is reminiscent of the direct, early pathogenic effects observed in animals infected with retroviruses prior to the onset of antiviral immunity (Part I, Section B).
By contrast the lag between infection and the appearance of AIDS is estimated from transfusion-associated AIDS to be 2 to 7 years in adults (220, 223, 241, 242) and 1 to 2 years in children from infected mothers (220, 223). The most likely mean latent period was estimated to be 5 years in adults (220, 223). Unexpectedly, most of the AIDS virus-positive blood donors identified in transfusion-associated AIDS transmission did not have AIDS when they donated blood and were reported to be in good health 6 years after the donation (220). Likewise there is evidence that individuals shown to be antibody positive since 1972 have not developed AIDS (228). Further, 16 mothers of babies with AIDS did not have AIDS at the time of delivery but three of them developed AIDS years later (276). This indicates that the latent period may be longer than 5 years or that AIDS is not an obligatory consequence of infection.
In view of the claim that the virus directly kills T-cells and requires 5 years to cause disease, we are faced with two bizarre options: Either 5 year old T-cells die 5 years after infection or the offspring of originally infected T-cells die in their 50th generation, assuming a generation time of one month for an average T-cell (176). It may be argued that the virus is biochemically inactive during the first five years of infection and then activated by an unknown cause. However, AIDS virus is biochemically inactive even during the acute phase of the disease (Section C). Moreover it would be difficult for the retrovirus to become acute five years after it had induced chronic antiviral immunity.
Because of the 5 year latency between infection and AIDS, the virus has been likened to the lentiviruses (277), a group of animal retroviruses that is thought to cause debilitating diseases only after long latent periods (13) (Part I, Section B). However, recently an ovine lentivirus, the visna or maedi virus of sheep, was shown to cause lymphoid interstitial pneumonia in 2 to 4 weeks if expressed at high titer (269). [The same disease is believed to be caused by AIDS virus in humans (see below)]. Therefore lentiviruses are not models for retroviruses that are only pathogenic after long latency (Part I, Section B).
Based on the 5-year latent period of the disease and on the assumption that virus infection is sufficient to cause AIDS, one would expect the number of AIDS cases to increase to 1 to 2 x 106 in the United States in the next 5 years. The virus has reportedly reached its present endemic level of 1 to 2 x 106 in the United States (223, 224) since it was introduced there, presumably, less than 10 years ago (27). Yet the spread of AIDS from 1981 to 1986 has not followed the spread of virus with a latent period of 5 years. Instead, recent statistics (see above) indicate no further increases in the number of AIDS cases and a significant decline in the number of AIDS fatalities in the United States (216, 244).
Clearly, the long lag between infection and AIDS and the large number of virus-positive cases in which as yet no AIDS is observed, even after long latent periods, lead to the conclusion that the virus is not sufficient to induce AIDS and does not encode an AIDS-specific function. Indeed, this conclusion is directly supported by genetic evidence against a viral AIDS gene. Deletion analysis has proved that all viral genes are essential for replication (28, 245), which requires not more than 1 or 2 days, yet AIDS follows infection only with an average lag of 5 years and even then only very rarely.

C. Levels of AIDS Virus Expression and Infiltration Appear Too Low to Account for AIDS or Other Diseases

If AIDS viruses were pathogenic by killing susceptible lymphocytes, one would expect AIDS to correlate with high levels of virus infiltration and expression, because uninfected cells would not be killed by viruses nor would unexpressed or latent viruses kill cells. As yet no report on virus titers of AIDS patients has appeared, despite the record interest in the epidemiology and nucleic acid structure of this virus (13, 27, 223). In view of the consistent antiviral immunity of AIDS patients and the difficulties in isolating virus from them (213), the virus titers are probably low. Titers have been said to range between only 0 and 102 per ml blood (213).8
Proviral DNA has been detected in only 15% (9 of 65) AIDS patients; in the remaining 85% the concentration of provirus, if present, was apparently too low for biochemical detection (246). Moreover, among positive samples less than 1 in 102 to 103 lymphocytes contained the provirus (246). Viral RNA was detected in 50 to 80% of AIDS blood samples. However, among the positive samples, RNA was found in only less than 1 of 104 to 105 presumably susceptible lymphocytes (247). The relatively high ratios of provirus-positive (10-2 to 10-3) to viral RNA positive cells (10-4 to 10-5) of AIDS patients indicate latent infections. Further there is no evidence that the virus titer or the level of virus infiltration increases during the acute phase of the disease. It is probably for this reason that cells from AIDS patients must be propagated several weeks in culture, apart from the host’s immune system, before either spontaneous (210-214) or chemically induced (248) virus expression may occur. Further, the AIDS virus is completely absent from the Kaposi sarcoma (27, 246), which is associated with 15% (216) to 30% (249) of AIDS cases and is one of the most characteristic symptoms of the disease.
Similar extremely low levels of virus infiltration and expression were also recorded in AIDS virus-associated brain disease (274). Likewise, in interstitial lymphoid pneumonia less that 0.1% of lung cells expressed viral RNA (275).
Indeed there is evidence that even latent virus may not be necessary for AIDS, since 85% of AIDS patients lack proviral DNA (246) and since over 10% of AIDS patients have been observed to lack antiviral immunity (214, 221, 222, 234). Further, in a study from Germany 3 of 91 AIDS patients were found to be virus free, based on repeated negative efforts to detect antibody or to rescue virus.9
It is concluded then that the AIDS virus infects less than 1%, and is expressed in less than 0.01%, of susceptible cells both in carriers with or without AIDS. This raises the question of how the virus could possibly be pathogenic and responsible for immunodeficiency or other diseases. For instance even if the virus were to claim its 10-4 or 10-5 share of T-cells that express viral RNA every 24 to 48 h, the known eclipse period of retroviruses, it would hardly ever match or beat the natural rate of T-cell regeneration (176).
All other viruses function as direct pathogens only if they are biochemically active and expressed at high levels. For instance, the titers that correlate with direct pathogenicity for avian retroviruses are 105-12 (31, 35, 250)4 and they are 104-7 for murine retroviruses (12, 38, 40, 42, 251) (Section B). Hepatitis viruses reach titers of 1012-13 when they cause hepatitis (15), and latent infections are not pathogenic (83). Further, the very low levels of AIDS virus expression in vivo are difficult to reconcile with reports based on in vitro studies with synthetic indicator genes that the AIDS virus encodes a potent transcription-stimulating protein (28, 153, 245). Clearly such activators are not at work in vivo.
The extremely low virus titers of symptomatic and asymptomatic carriers also explain why infection by the virus in the United States is essentially limited to contacts that involve transmission of cells (244) rather than being transmitted as a cell-free, infectious agent like pathogenic viruses. For instance, among 1750 health care workers with exposure to AIDS, only 1 or 2 were found to be antibody positive (252). Another study failed to find a single antibody-positive person among 101 family contacts of 39 AIDS patients, all of whom had lived in the same household with an AIDS patient for at least 3 months (253).

D. AIDS Viruses Not Directly Cytocidal

The AIDS viruses are reported to display in culture a fast cytocidal effect on primary T-cells within 1 to 2 months after infection (13, 27, 254). The cytocidal effect was shown to involve cell fusion (27, 238, 254). The effect is thought to reflect the mechanism of how the virus generates AIDS after a latent period of 5 years (27, 254).
This is debatable on several grounds: (a) above all, the in vitro assay cannot account for the large discrepancy between the short latent period of cell death in vitro and the 5-year latent period of the disease; (b) Tcell fusion is not observed in vivo in chronic, asymptomatic virus carriers and not in prospective AIDS patients during the long latent period of the disease (255), although virus expression is not lower than during the acute phase of AIDS; (c) T-cell killing is also not observed in T-cell lines in vitro (27) and not in primary lymphocytes under appropriate conditions (238). Further primary lymphocytes infected by AIDS virus were shown to double every 5 days in cell culture for three weeks; at the same time the previously latent AIDS virus was activated to high levels of expression (278); (d) virus strains that do not cause cytopathic fusion in vitro have been isolated from 7 of 150 AIDS patients.9 This demonstrates that the fusion-inducing function of the virus can be dissociated from a putative AIDS function.
Thus T-cell killing by fusion is apparently a cell culture artifact that depends on the virus strain and the cell used, as has been shown for many other retroviruses including HTLV-I (Part I, Section B), and not an obligatory feature of virus infection. As with other retroviruses, fusion involves binding of viral envelope antigens on the surface of infected cells with receptors of uninfected cells. Accordingly, fusion is inhibited by AIDS virus-neutralizing antibody (256). It apparently depends on high local virus titers that in particular in the case of AIDS are not observed in vivo. This view of the cell-killing effect also resolves the apparent contradiction between the postulated cytocidal effects of AIDS viruses and the obligatory requirement of all retroviruses for mitosis in order to replicate (16, 25). Indeed AIDS viruses have been reported to replicate without cytocidal effects not only in T-cells but also in human monocytes and macrophages (257, 278), which share the same virus-specific receptors (258), and in B-cell lines (259), in fibroblasts (261) in human brain and the lung (213, 230, 232, 257, 261).

E. No Simian Models for AIDS

Since retroviruses have been isolated from monkeys in captivity with immunodeficiencies and since experimental viremia can depress immune functions in monkeys, such systems are considered to be animal models of human AIDS. For example, 42 of 68 newborn monkeys died with a broad spectrum of diseases that included runting and lymphadenopathy 4 to 6 weeks after inoculation with Mason-Pfizer monkey virus (91). However, this virus has since been found in healthy macaques (262). More recently a retrovirus termed simian AIDS or SAIDS virus was isolated from monkeys with immunodeficiency (92, 262). Inoculation of three juvenile rhesus monkeys by one isolate was reported to cause splenomegaly and lymphadenopathy within 2 to 5 weeks. One animal became moribund and two others were alive with simian AIDS at the time of publication (92). However, in another study only transient lymphadenopathy but no lasting AIDS-like disease was observed in macaques inoculated with this virus (263). Another simian virus that is serologically related to AIDS virus, termed STLV-III, was isolated from immunodeficient macaques and from one macaque with a lymphoma. Macaques inoculated with blood or tissue samples of the viral lymphoma died 50 to 60 days later with various diseases (93). However, asymptomatic infections by the same virus have since been identified in no less than 50% of wild green monkeys that did not show any symptoms of a disease (264).
Eight chimpanzees infected with human AIDS virus had not developed symptoms of AIDS 1.5 years past inoculation (265). However, each animal developed antiviral immunity about 1 month after infection, followed by persistent latent infection, as in the human cases (265). A follow-up of champanzees inoculated with sera from AIDS patients in 1983 reports no evidence for AIDS in 1986 although the animals had developed antibodies to the virus (243).
Several reasons suggest that these experimental infections of monkeys are not suitable models for human AIDS. Above all, the human virus is not pathogenic in animals. The diseases induced in monkeys by experimental infections with simian viruses all occur fast compared to the 5-year latency for AIDS. Moreover the simian viruses are never associated with a disease in wild animals. Therefore these diseases appear to be exactly analogous to the direct, early pathogenic effects caused by other retroviruses in animals prior to antiviral immunity (see Part I, Section B), and thus are probably models for the early mononucleosis-like diseases which occur in humans infected with AIDS virus prior to antiviral immunity (232, 234, 240) (Section B). Indeed the persistent asymptomatic infections of wild monkeys with simian retroviruses appear to be models for the many asymptomatic infections of humans with AIDS virus or HTLV-I.

F. AIDS Virus As an Indicator of a Low Risk for AIDS

The only support for the hypothesis that the AIDS virus causes AIDS is that 90% of the AIDS patients have antibody to the virus. Thus it would appear that the virus, at least as an immunogen, meets the first of Koch’s postulates for an etiological agent. This conclusion assumes that all AIDS patients from whom virus cannot be isolated (about 50%) (278) or in whom provirus cannot be demonstrated (85%) and the antibody-negative cases (about 10%) and the virus-free cases reported in one study (3%) (Section C) are false negatives. Indeed, the diagnosis of AIDS virus by antibody has recently been questioned on the basis of false positives (234).
At this time the hypothesis that the virus causes AIDS faces several direct challenges. (a) First it fails to explain why active antiviral immunity, which includes neutralizing antibody (225-227) and which effectively prevents virus spread and expression, would not prevent the virus from causing a fatal disease. This is particularly paradoxical since antiviral immunity or “vaccination” typically protects against viral pathogenicity. It is also unexpected that AIDS patients are capable of mounting an apparently highly effective, antiviral immunity, although immunodeficiency is the hallmark of the disease. (b) The hypothesis is also challenged by direct evidence that the virus is not sufficient to cause AIDS. This includes (i) the low percentage of symptomatic infections, (ii) the fact that some infected groups are at a relatively high and others at no risk for AIDS, (iii) the long latent period of the disease (Section B), and (iv) the genetic evidence that the virus lacks a late AIDS function. Since all viral genes are essential for virus replication (28, 245), the virus should kill T-cells and hence cause AIDS at the time of infection rather than 5 years later. (c) The hypothesis also fails to resolve the contradiction that the AIDS virus, like all retroviruses, depends on mitosis for replication yet is postulated to be directly cytocidal (Section D). (d) The hypothesis offers no convincing explanation for the paradox that a fatal disease would be caused by a virus that is latent and biochemically inactive and that infects less than 1% and is expressed in less than 0.01% of susceptible lymphocytes (Section D). In addition the hypothesis cannot explain why the virus is not pathogenic in asymptomatic infections, since there is no evidence that the virus is more active or further spread in carriers with than in carriers without AIDS.
In view of this it seems likely that AIDS virus is just the most common among the occupational viral infections of AIDS patients and those at risk for AIDS, rather than the cause of AIDS. The disease would then be caused by an as yet unidentified agent which may not even be a virus, since cell-free contacts are not sufficient to transmit the disease.
Other viral infections of AIDS patients and those at risk for AIDS include Epstein-Barr and cytomegalovirus in 80 to 90% (222, 268), and herpes virus in 75 to 100%.10
In addition hepatitis B virus is found in 90% of drug addicts positive for antibody to AIDS virus (267). Among these different viruses, retroviruses are the most likely to be detectable long after infection and hence are the most probable passenger viruses of those exposed to multiple infectious agents. This is because retroviruses are not cytocidal and are unsurpassed in establishing persistent, nonpathogenic infections even in the face of antiviral immunity. Therefore AIDS virus is a useful indicator of contaminated sera that may cause AIDS (13, 27) and that may contain other cell-free and cell-associated infectious agents. It is also for these reasons that latent retroviruses are the most common nonpathogenic passenger viruses of healthy animals and humans. For the same reasons, they are also frequently passenger viruses of slow diseases other than AIDS like the feline, bovine and human leukemias (see Part I) or multiple sclerosis (268) in which latent or defective “leukemia viruses” are occasionally found.
It is concluded that AIDS virus is not sufficient to cause AIDS and that there is no evidence, besides its presence in a latent form, that it is necessary for AIDS. However, the virus may be directly responsible for the early, mononucleosis-like disease observed in several infections prior to antiviral immunity (Section B). In a person who belongs to the high risk group for AIDS, antibody against the AIDS virus serves as an indicator of an annual risk for AIDS that averages 0.3% and may reach 5%, but in a person that does not belong to this group antibody to the virus signals no apparent risk for AIDS. Since nearly all virus carriers have antiviral immunity including neutralizing antibody (225-227), vaccination is not likely to benefit virus carriers with or without AIDS.

2. The 1989 Proceedings Paper

The paper in the Proceeedings of the National Academy of February 1989, Duesberg, P. H. (1989) Human immunodeficiency virus and acquired immunodeficiency syndrome: Correlation but not causation (Proc Natl Acad Sci USA 86: 755-764) is the real classic, produced when, after the Cancer Research paper was studiously ignored by everybody, including the White House after initial interest (a meeting on the issue was scotched when NIH (ie Anthony Fauci and Robert Gallo), Duesberg returned to the attack with a full blown analysis of 9000 words backed by 196 references.

The optimistic last paragraph of the definitive piece was a recounting of the “benefits” of the analysis, primarily that HIV had no longer to be feared and that AZT could be studied to see what its contribution to AIDS decline might be, as well as other drugs and risks.

(Here it is – the entire paper, with the paragraph at the end)

Human Immunodeficiency Virus and Acquired Immunodeficiency
Syndrome: Correlation But Not Causation1,2
By Peter H. Duesberg

Proc. Natl. Acad. Sci. USA, Vol. 86, pp. 755-764, February 1989
Contributed June 14, 1988; revision received October 21, 1988

Abstract

AIDS is an acquired immunodeficiency syndrome defined by a severe depletion of T cells and over 20 conventional degenerative and neoplastic diseases. In the U.S. and Europe, AIDS correlates to 95% with risk factors, such as about 8 years of promiscuous male homosexuality, intravenous drug use, or hemophilia. Since AIDS also correlates with antibody to a retrovirus, confirmed in about 40% of American cases, it has been hypothesized that this virus causes AIDS by killing T cells. Consequently, the virus was termed human immunodeficiency virus (HIV), and antibody to HIV became part of the definition of AIDS. The hypothesis that HIV causes AIDS is examined in terms of Koch’s postulates and epidemiological, biochemical, genetic, and evolutionary conditions of viral pathology. HIV does not fulfill Koch’s postulates: (i) free virus is not detectable in most cases of AIDS; (ii) virus can only be isolated by reactivating virus in vitro from a few latently infected lymphocytes among millions of uninfected ones; (iii) pure HIV does not cause AIDS upon experimental infection of chimpanzees or accidental infection of healthy humans. Further, HIV violates classical conditions of viral pathology. (i) Epidemiological surveys indicate that the annual incidence of AIDS among antibody-positive persons varies from nearly 0 to over 10%, depending critically on nonviral risk factors. (ii) HIV is expressed in �1 of every 104 T cells it supposedly kills in AIDS, whereas about 5% of all T cells are regenerated during the 2 days it takes the virus to infect a cell. (iii) If HIV were the cause of AIDS, it would be the first virus to cause a disease only after the onset of antiviral immunity, as detected by a positive “AIDS test.” (iv) AIDS follows the onset of antiviral immunity only after long and unpredictable asymptomatic intervals averaging 8 years, although HIV replicates within 1 to 2 days and induces immunity within 1 to 2 months. (v) HIV supposedly causes AIDS by killing T cells, although retroviruses can only replicate in viable cells. In fact, infected T cells grown in culture continue to divide. (vi) HIV is isogenic with all other retroviruses and does not express a late, AIDS-specific gene. (vii) If HIV were to cause AIDS, it would have a paradoxical, country-specific pathology, causing over 90% Pneumocystis pneumonia and Kaposi sarcoma in the U.S. but over 90% slim disease, fever, and diarrhea in Africa. (viii) It is highly improbable that within the last few years two viruses (HIV-I and HIV-2) that are only 40% sequence-related would have evolved that could both cause the newly defined syndrome AIDS. Also, viruses are improbable that kill their only natural host with efficiencies of 50-100%, as is claimed for HIVs. It is concluded that HIV is not sufficient for AIDS and that it may not even be necessary for AIDS because its activity is just as low in symptomatic carriers as in asymptomatic carriers. The correlation between antibody to HIV and AIDS does not prove causation, because otherwise indistinguishable diseases are now set apart only on the basis of this antibody. I propose that AIDS is not a contagious syndrome caused by one conventional virus or microbe. No such virus or microbe would require almost a decade to cause primary disease, nor could it cause the diverse collection of AIDS diseases. Neither would its host range be as selective as that of AIDS, nor could it survive if it were as inefficiently transmitted as AIDS. Since AIDS is defined by new combinations of conventional diseases, it may be caused by new combinations of conventional pathogens, including acute viral or microbial infections and chronic drug use and malnutrition. The long and unpredictable intervals between infection with HIV and AIDS would then reflect the thresholds for these pathogenic factors to cause AIDS diseases, instead of an unlikely mechanism of HIV pathogenesis.
Introduction

The important thing is to not stop questioning.

-Albert Einstein

In 1981, acquired immunodeficiency was proposed to be the common denominator of a newly defined syndrome (AIDS) of diseases that were on the rise in promiscuous male homosexuals and intravenous drug users, referred to as “AIDS risk groups” (1, 2). Since then, about 70,000 persons have developed AIDS in the U.S., of whom over 90% are still from these same risk groups (3, 4). The hallmark of AIDS is a severe depletion of T cells (3, 5-7). By definition, this immunodeficiency manifests itself in over 20 previously known degenerative and neoplastic diseases, including Kaposi sarcoma, Burkitt and other lymphomas, Pneumocystis pneumonia, diarrhea, dementia, candidiasis, tuberculosis, lymphadenopathy, slim disease, fever, herpes, and many others (5, 7-11). The frequent reference to AIDS as a new disease (12-14), instead of a new syndrome composed of old diseases, has inspired a search for a single new pathogen (12). However, it is debatable whether a single pathogen can explain over 20 diseases, whether a clustering of old diseases in risk groups that only recently became visible signals a new pathogen, and whether an AIDS pathogen must be infectious. Indeed, compared to conventional infectious diseases, AIDS is very difficult to acquire and has a very selective host range, usually manifesting only in individuals who have taken AIDS risks for an average of 8 years (see below).

The Virus-AIDS Hypothesis. About 40% of the AIDS patients in the U.S. (5), and many of those who are at risk for AIDS, have been confirmed to have neutralizing antibodies to a retrovirus (3, 7) that was discovered in 1983 (15). These antibodies are detected by the “AIDS test” (3). Less than a year later, in 1984, this virus was adopted as the cause of AIDS by the U.S. Department of Health and Human Services and the AIDS test was registered as a patent, even before the first American study on the virus was published (16). The epidemiological correlation between these antibodies and AIDS is the primary basis for the hypothesis that AIDS is caused by this virus (3, 7, 12, 14, 17, 18). AIDS is also believed to be caused by this virus because AIDS diseases appear in a small percentage (see below) of recipients of blood transfusions that have antibodies to this virus (3, 12, 19-22). In view of this the virus has been named human immunodeficiency virus (HIV) by an international committee of retrovirologists (18) and antibody to HIV became part of the definition of AIDS (3, 5, 7). “… Patients are excluded as AIDS cases if they have a negative result(s) on testing for serum antibody to HIV, do not have a positive culture for HIV” (3). If confirmed, HIV would be the first clinically relevant retrovirus since the Virus-Cancer Program called for viral carcinogens in 1971 (23, 24).

The virus-AIDS hypothesis holds that the retrovirus HIV causes AIDS by killing T cells in the manner of a cytocidal virus (3, 6, 7, 12, 18) and is transmitted by sex and parenteral exposure (3, 7, 12, 19, 22). Early evidence for a T cell-specific HIV receptor lent support to this hypothesis (25). Recently, however, the presumed T cell specificity of HIV has lost ground, as HIV is only barely detectable in T cells and often is detectable only in monocytes (26-28) and other body cells (23, 29-32), displaying the same lack of virulence and broad host range toward differentiated cells as all other human and animal retroviruses (17, 23). In about 50% of those who habitually practice risk behavior or regularly receive transfusions, AIDS is estimated to occur after an average asymptomatic period of about 8 years from the onset of antiviral immunity, and in up to 100% after about 15 years (5-7, 20-22, 33-38). Therefore, HIV is called a “slow” virus, or lentivirus (40). It is on the basis of the relatively high conversion rates of these risk groups that every asymptomatic infection by HIV is now being called “HIV disease” (7), and that some are subjected to chemotherapy (39). Nevertheless, individual asymptomatic periods are unpredictable, ranging from <1 to >15 years (22, 33-38). Once AIDS is diagnosed, the mean life expectancy is about 1 year (35).

The early adoption of the virus-AIDS hypothesis by the U.S. Department of Health and Human Services (16) and by retrovirologists (17, 18) is the probable reason that the hypothesis was generally accepted without scrutiny. For instance, the virus is typically referred to as deadly by the popular press (41, 42) and public enemy number 1 by the U.S. Department of Health and Human Services (43). In view of this, it is surprising that the virus has yet to cause the first AIDS case among hundreds of unvaccinated scientists who have propagated it for the past 5 years at titers that exceed those in AIDS patients by up to 6 orders of magnitude (see below) with no more containment than is required for marginally pathogenic animal viruses (44). It is also surprising that despite 2000 recorded (and probably many more unrecorded) parenteral exposures to HIV-infected materials, unvaccinated health care workers have exactly the same incidence of AIDS as the rest of the U.S. labor force (19, 22, 45, 186). Further, it is difficult to believe that a sexually transmitted virus (7, 12) would not have caused more than 1649 sex-linked AIDS cases among the 125 million American women in 8 years (4)-and this number is not even corrected for the antibody-negative women who might have developed such diseases over an 8-year period. Moreover, it is paradoxical for a supposedly new viral epidemic (12-14) that the estimates of infected persons in the U.S. have remained constant at 0.5 to 1.5 million (46, 47) or even declined to <1 million (7, 38) since the “AIDS test” became available in 1985.

About 2 years ago I proposed that HIV is not likely to be the cause of AIDS (23, 48-50, 180). This proposal has since been fiercely challenged or defended at meetings and in publications (14, 32, 51-65, 180). Here I respond to these challenges.
HIV Does Not Meet Koch’s Postulates

HIV Cannot Account for the Loss of T Cells and the Clinical Course of AIDS. The causative agent of an infectious disease is classically defined by the postulates of Robert Koch and Jacob Henle (66, 67). They were originally formulated a priori by Henle about 50 years before bacteria and viruses were discovered to be pathogens (67). However, their definitive text was formulated by Koch to distinguish causative from other bacteria at a time when bacteriologists applying newly developed tools in the search for pathogenic microbes found all sorts of bacteria in humans. This situation was quite similar to our current increasing proficiency in demonstrating viruses (68). The first of these postulates states that “the parasite must be present in every single case of the disease, under conditions that can account for the pathological lesions and the clinical course of the disease” (67). However, there is no free virus in most-and very little in some-persons with AIDS, or in asymptomatic carriers (69, 70). Virus titers range from 0 to 10 infectious units per milliliter of blood (69, 70). Viral RNA is found in a very low percentage (see below) of blood cells of 50-80% of antibody-positive persons (71-74, 187). Further, no provirus is detectable in blood cells of 70-100% of symptomatic or asymptomatic antibody-positive persons, if tested by direct hybridization of cellular DNA with cloned proviral DNA (73, 75, 187) at the limit of detection by this method (76). Antibody to HIV is confirmed in only about 40% of the U.S. cases and in only 7% of the AIDS cases from New York and San Francisco, which represent one-third of all U.S. cases (5). In some cases, even the antibody to HIV disappears, due to chronic dormancy or loss of the HIV provirus (77, 78)-analogous to the loss of antibody to other viruses long after infection. Indeed, the Centers for Disease Control publishes specific guidelines for AIDS cases in which laboratory evidence for HIV is totally negative (5). Thus, although viral elements can be traced in many AIDS patients, and antibody to HIV is, at least by definition, present in all of them, HIV violates Koch’s first postulate in terms of a tangible presence, of being “under conditions that can account for” the loss of T cells, and of the “clinical course of the disease” that lags 8 years behind infection.

The absence of free virus in most AIDS cases and in antibody-positive asymptomatic carriers explains why HIV is not casually transmitted (19, 22, 23, 35). For example, the probability of transmission of the virus from an antibody-positive to an antibody-negative person by heterosexual intercourse is estimated to be 1 in 500 (79, 80).

Due to Extremely Low Titers, HIV Can Be Isolated Only with Great Difficulty from AIDS Patients. Koch further postulated that it must be possible to isolate and propagate the etiological agent from all cases of the disease. However, virus isolation, although possible in up to 80% of AIDS cases, is technically very difficult and is perhaps best described as maieutic (23, 69, 70, 81-84). It depends on reactivation of dormant proviruses from one or a few latently infected lymphocytes among millions of uninfected lymphocytes from AIDS patients. This is only possible by culturing these cells for several weeks in vitro, away from the suppressive, virus-neutralizing immune system of the host (23, 48-50). Even then success sometimes comes only after 15 (!) trials (85). These difficulties and the often over 20% failure rate (84) in isolation of HIV from AIDS patients are consistent with the extremely low titers of HIV in such patients. Thus, HIV does not meet Koch’s second postulate.

In vitro reactivation of latent HIV from antibody-positive persons is exactly analogous to the in vitro reactivation of latent Epstein-Barr virus (EBV) from healthy persons with antibody to EBV (86). As in the case of HIV (see below), acute EBV infections occasionally cause mononucleosis (86-88). Subsequent antiviral immunity restricts EBV to chronic latency (86). Since latent EBV, again like latent HIV, is present in only 1 of 107 lymphocytes, millions of these cells must be cultivated in vitro to reactivate the virus (86).

HIV Does Not Reproduce AIDS When Inoculated into Animals or Humans. Animal infections. Koch’s third postulate calls for inducing the disease by experimental infection of a suitable host with pure pathogen. Chimpanzees infected with pure HIV develop antibodies, indicating that they are susceptible to HIV. However, all attempts to cause AIDS in chimpanzees have been unsuccessful, even after they have been antibody-positive for 4 to 5 years (23). Thus, Koch’s third postulate has not been fulfilled in animals.

Accidental human infections. Due to the extremely low titers of HIV in all antibody-positive materials, very few infections have occurred. Four women who received infected donor semen in 1984 developed antibody to HIV. Yet none of them developed AIDS or transmitted the virus to their husbands, although insufficient time has elapsed for the average latent period that the virus is thought to require to cause AIDS (see below). Moreover, three of these women subsequently became pregnant and gave birth to healthy infants (89). Further, 15 to 20 accidental infections of health care workers and scientists propagating HIV were identified during the last 4 years on the basis of antiviral antibodies, and none of these people have developed AIDS (19, 22, 23, 45, 85, 90, 186).

Recently, a single conversion to AIDS of such an antibody-positive health care worker was reported anonymously without data on gender, latent period, or AIDS symptoms (45). This case was claimed to prove Koch’s third postulate (14). However, 2586 health care workers got AIDS without occupational infection. About 95% of these fall into the conventional risk groups and 5% are without verifiable AIDS risks (4, 45)-which are notoriously difficult to verify (91, 92). From the 135 (5% of 2586) health care workers who developed AIDS without verifiable risks, the one who contracted an occupational infection was selected to prove that such infections, rather than other risks, caused AIDS. It is arbitrary to base a hypothesis on 1 case when 134 cases do not support the hypothesis. To prove the hypothesis, it is necessary to show that the percentage of health care workers with AIDS who do not belong to the known risk groups exceeds that of the rest of the population and reflects their sexual distribution. However, the incidence and even the sexual distribution of AIDS cases among health care workers are exactly the same as that of AIDS in the general population (4), namely 92% males, although 75% of the health care workers are female (45). Moreover, a subsequent study (186) that included this case described only transient, mononucleosis-like symptoms but not one AIDS case among occupationally infected health care workers.

Blood transfusions are another source of iatrogenic infections. The best-documented cases are the 10,000 to 14,000 U.S. hemophiliacs with antibody to HIV (19, 38, 47, 93, 94), of whom only 646 developed symptoms of AIDS between 1981 and August 1988 (4). During the year that ended in August 1988, 290 developed AIDS, whereas 178 developed AIDS in the previous year (4). This corresponds to annual conversion rates of about 1-3%. Higher rates, of up to 25%, have been observed in certain groups of hemophiliacs (20, 21, 35, 36, 38). However, the view that AIDS in recipients of transfusions is due to HIV transmission is presumptive on several grounds. (i) Blood transfusion does not distinguish between HIV and other undetected viruses, microbes, and blood-borne toxins. This is particularly true since HIV-positive blood was never knowingly transfused. (ii) It is presumed that the recipients had no AIDS risks other than HIV during the average of 8 years between HIV infection and AIDS symptoms (20, 21). The transfusion evidence would be more convincing if AIDS appeared in step with virus replication (see below) soon after a singular transfusion. (iii) Transfusion-related AIDS cases occur primarily in persons with other health risks, such as hemophilia, that are not representative of healthy individuals. (iv) Above all, the transfusion cases are all anecdotal (95, 96). There are no controlled studies to show that recipients of transfusions with antibody to HIV have more of the diseases now called AIDS than those without antibody to HIV.

The assertion that HIV causes AIDS is also contained in the erroneous claims that new cases of transfusion AIDS have virtually ceased appearing since the AIDS test became available in 1985 (12, 14), due to a factor-of-40 reduction of transfusions with antibody-positive blood (95). In fact, adult transfusion AIDS cases have doubled and pediatric cases have tripled in the year ending August 8, compared to the previous year (4, 49). The increase in adult cases could be expected if one were to accept the assumptions that HIV requires 8 years to cause AIDS (see below) and that there was a rapid increase in unconfirmed HIV transfusions 8 years ago, which stopped 3 years ago. However, the increase in pediatric cases in the face of a 40-fold reduction of antibody-positive transfusions argues directly against HIV as the cause of AIDS, because the average latent period in children is only 2 years (21, 36).

HIV Does Not Meet Established Epidemiological, Biochemical, Genetic, and Evolutionary Criteria
of a Viral Pathogen

Epidemiologies of AIDS and HIV Are Not Consistent. Epidemiology has been proposed as adequate to identify causative agents, particularly in human diseases where Koch’s postulates are difficult to meet (67), as in the case of HIV (12, 14, 32). Nevertheless, even a consistent correlation with virus-not with antibody-would fulfill only the first postulate. However, the epidemiologies of AIDS and HIV are not consistent in different risk groups and countries.

About 10% of the 30 million people in Zaire have been reported since 1985 to be antibody-positive (46, 98, 184). However, only 335 AIDS cases have been reported in Zaire as of 1988 (97, 99). This corresponds to an annual conversion rate of 0.004%. Also, since 1985, 6% of the 6 million Haitians have been reported to be antibody-positive (46,100), but only 912 had developed AIDS by 1988 (97). This corresponds to an annual conversion rate of 0.1%. of 0.5 to 1.5 million antibody-positive Americans, about 29,000 [including 9000 who meet only the 1987 definition for AIDS (5)] developed AIDS in the year ending August 1988, and, according to earlier definitions, 16,000 to 17,000 developed AIDS in each of the previous 2 years (4). This corresponds to an annual conversion rate of about 1.5% for the average antibody-positive American. Thus, the AIDS risk of an antibody-positive person varies with the country of residence. These calculations all assume that the pools of short- and long-term HIV carriers in each of these countries are comparable. This assumption is based on the claims that HIV was newly introduced into all countries with AIDS about 10 to 20 years ago (3, 7, 12-14).

Moreover, the AIDS risk of an antibody-positive American varies a great deal with his or her risk group. For example, 3-25% of antibody-positive Americans who habitually practice risk behavior or are hemophiliacs develop AIDS annually (7, 21, 22, 33-38). Thus, the 1.5% annual conversion rate of antibody-positive Americans is an average of minorities with high conversion rates of 3-25% and a majority with a conversion rate close to 0%.

Since the incidence of AIDS among antibody-positive persons varies from 0 to over 10% depending on factors defined by lifestyle, health, and country of residence (35), it follows that HIV is not sufficient to cause AIDS.

AIDS Occurs Despite Minimal Viral Activity. During replication, viruses are biochemically very active in the host cell. If they replicate in more cells than the host can spare or regenerate, they typically cause a disease (48, 86).

Paradoxically, HIV is very inactive even when it is said to cause fatal immunodeficiency. Viral RNA synthesis is detectable in only 1 of 104 to 106 mononuclear lymphocytes, including T cells (71-74). Frequently, virus can only be found in monocytes, and not in T cells (26-28). Virus expression recorded in monocyte-macrophages is at the same low levels as in other lymphocytes (72). Thus, there is as yet no experimental proof for the suggestion, based on experiments in cell culture, that monocyte-macrophages may be the reservoirs of the virus in vivo (6, 12, 28). Also, very few lung and brain cells ever express HIV (101, 102, 187). At this level of infiltration HIV cannot account by any known mechanism for the loss of T cells that is the hallmark of AIDS (3, 5, 6, 12), even if all actively infected T cells died. During the 2 days it takes for a retrovirus to replicate, the body regenerates about 5% of T cells (23, 103), more than enough to compensate for presumptive losses due to the virus. Hence, HIV cannot be sufficient to cause AIDS.

Although there is virtually no free virus, and HIV RNA synthesis is extremely low, both in AIDS patients and in asymptomatic carriers (71-74), it has been argued that the viral core protein p24 is produced at higher levels in AIDS patients than in asymptomatic carriers (83, 84, 104-108, 183). However, all studies on p24 report AIDS cases that occur without p24 antigenemia, indicating that p24 is not necessary for AIDS (83, 84, 104-108, 183). They also report antigenemia without AIDS, indicating that p24 is not sufficient for AIDS (72, 84, 104-108, 183). Moreover, antigenemic carriers are not viremic because they always maintain an excess of virus-neutralizing antibodies directed against the viral envelope, a positive AIDS test (72, 83, 84, 104-108, 183). In addition, the colorimetric antibody test used to measure p24 protein raises unresolved questions. Reportedly, the assay’s detection limit is 50 pg/ml, and up to 100 times more p24 than that is found in some HIV carriers (83, 84, 104-109). Five hundred picograms of p24 is the protein equivalent of 106 HIV particles, given 10-3 pg per retrovirus, half of which is core protein (110). Yet such high concentrations of p24 cannot be reconciled with the extremely low numbers of cells in AIDS patients that are engaged in viral RNA synthesis (6, 71-74, 101, 102), nor can the failure to isolate virus from 20-50% of p24-antigenemic patients (83, 84). Based on my 24-year experience with retroviruses, only large numbers of infected cells growing in the absence of antiviral immunity in vivo or in vitro produce such high titers of virus or viral protein. Thus, the assertions that HIV becomes activated during AIDS or that p24 antigenemia is necessary for the syndrome (6, 7, 12, 31, 35) are without experimental support.

AIDS Occurs Despite Antiviral Immunity. Viruses typically cause disease before virus-neutralizing antibodies and cellular immunity appear. Antiviral antibodies signal a successful rejection of the virus and a lasting protection (vaccination) against diseases by the same or related viruses. Immunity is the only weapon against viral disease.

Paradoxically, HIV is said to cause AIDS, by definition, only years after inducing very active antiviral immunity (3, 5). If this assertion were correct, HIV would be the first virus to cause a disease only after antiviral immunity. Yet the effectiveness of this immunity is the reason that provirus remains dormant and that free HIV cannot be found in AIDS patients (69). In view of this, vaccination of antibody-positive persons would appear to be completely superfluous, even if HIV were the cause of AIDS (3, 7, 12, 111-113). The claims of some scientists that antiviral antibodies fail to neutralize HIV (3, 32, 55, 56, 59, 113-115) are incompatible with the efficient immunity in vivo and with experimental evidence for virus-neutralizing activity in vitro (23, 115-119).

Although most viruses are eliminated by immunity, some, such as the retroviruses and the herpes viruses, may persist-severely restricted by antiviral immunity-as latent infections (23, 86, 87). Such viruses can again become pathogenic, but only when they are reactivated. For example, upon reactivation, the herpes viruses cause fever blisters or zoster even in the presence of serum antibody (120). Reactivation may follow a decline of cellular immunity in response to other parasitic infections, radiation, or immunosuppressive therapy (23, 86). Further, it has been claimed that 8 years after primary infection and immunity, latent measles virus may cause subacute sclerosing panencephalitis (121) in about 1 case per million (86) and that another latent paramyxovirus may cause multiple sclerosis (121). However, these viruses could be isolated from each system in only 2 of 8 cases after cultivating millions of patient cells in vitro (121). Moreover, multiple sclerosis has since been suggested to be caused by a latent retrovirus closely related to HIV (122) and subacute encephalitis by HIV (28, 187). Thus, there is no proven precedent for the hypothesis that HIV causes AIDS only years after the onset of antiviral immunity and yet remains as inactive as it is in asymptomatic infections.

It has been proposed that pathogenic HIV mutants arise during the long intervals between infection and AIDS and that these mutants might escape antiviral immunity by losing specific epitopes (28, 31, 82, 90, 112, 113, 123, 124) or even by changing their host range from T cells to macrophages (44). However, there is no report of a mutant HIV present at high titer in AIDS. Further, it is very unlikely that a mutant could escape an existing immunity, because it would share most variable and, of necessity, all constant determinants with the parent virus. Even though all retroviruses, including HIV (125-128), mutate at a frequency of 1 in 104 nucleotides per replicative cycle, they have never been observed to escape an existing antiviral immunity. It has also been proposed that HIV escapes immunity by spreading via cell-to-cell transmission (28, 32, 115, 117, 129). However, consistent with the syncytium-blocking function of natural antibodies (23, 115, 119), there is no spread of HIV in vivo.

Intervals of 2 to 15 Years Between Infection and AIDS Are Incompatible with HIV Replication. If cytocidal viruses or retroviruses cause disease, they do so within 1 to 2 months of infection (23, 86). By that time, the host’s immune system either eliminates the virus or restricts it to latency, or the virus overcomes the immune system and kills the host. Indeed, clinicians have reported that, in rare cases, HIV causes a disease like mononucleosis prior to immunity, presumably due to an acute infection (23, 69, 130, 186). Since this disease correlates with viral activity (69) and disappears within weeks as the body develops antiviral immunity, it may reflect the true pathogenic potential of HIV.

Considering that HIV replicates within 2 days in tissue culture and induces antiviral immunity within 1 to 2 months (19, 23, 69, 130), the inevitably long and seemingly unpredictable intervals, ranging from 1 to 15 years (20, 35, 37), between the onset of antiviral immunity and AIDS are bizarre. The average latent period is reported to be 8 years in adults (21, 33-38) and 2 years in children (21, 36). Indeed, at least 2 years of immunity is required before AIDS appears in adults (7, 38). If one accepts that 50-100% of antibody-positive Americans eventually develop AIDS (7, 20-22, 33-37), the average 1.5% annual conversion corresponds to grotesque viral latent periods of 30 to 65 years. These intervals between HIV infection and AIDS clearly indicate that HIV by itself is not sufficient to initiate AIDS. Because all genes of HIV are expressed during the early immunogenic phase of the infection, AIDS should occur at that time, rather than years later when it is latent (23).

In an effort to rationalize the long intervals between infection and AIDS, HIV has been classified as a slow virus, or lentivirus (40), a type of retrovirus that is thought to cause disease only after long incubation periods (129). Yet there are no “slow” viruses. Since viral nucleic acids and proteins are synthesized by the cell, viruses must replicate as fast or faster than cells (i.e., within hours or days) to survive (86, 87).

Nevertheless, as pathogens, viruses may be (i) fast in acute infections that involve many actively infected cells, (ii) slow in subacute infections that involve moderate numbers of actively infected cells, or (iii) asymptomatic and latent. Retroviruses provide examples of each different pathogenic role. Acute infections with the “slow” Visna/Maedi retrovirus of sheep, a lentivirus, rapidly cause pneumonia (131), and those with equine anemia lentivirus cause fever and anemia within days or weeks of infection (132). Such infections typically generate titers of 104 to 105 infectious units per milliliter or gram of tissue (132, 133). The caprine arthritis-encephalitis lentivirus is also pathogenic within 2 months of inoculation (134). Acute infections with other retroviruses also rapidly cause debilitating diseases or cancers (23). This includes retrovirus infections that are now considered to be animal models of AIDS, termed simian or feline AIDS (12, 23, 30, 111, 135). Unlike HIV in AIDS, these viruses are all very active when they cause diseases, and the respective diseases appear shortly after infection (23). In rare cases, when antiviral immunity fails to restrict Visna/Maedi or other retroviruses, they persist as subacute symptomatic infections (3, 86, 129, 133). Under these conditions, Visna/Maedi virus causes a slow, progressive pulmonary disease (129, 133, 136) by chronically infecting a moderate number of cells that produce moderate titers of 102 to 105 virus particles per gram of tissue (136). However, in over 99% of all Visna/Maedi or caprine arthritis-encephalitis virus infections, and in most equine anemia virus infections, the retrovirus is either eliminated or restricted to latency by immunity, and hence asymptomatic, exactly like almost all other retroviruses in mice, chickens, cats, and other animals (23). For instance, 30-50% of all healthy sheep in the U.S., Holland, and Germany have asymptomatic Visna/Maedi virus infections (129, 137, 138), and 80% of healthy goats in the U.S. have asymptomatic caprine arthritis-encephalitis virus infections (133) in the presence of antiviral immunity.

Thus, the progressive diseases induced by active retroviruses depend on relative tolerance to the virus due to rare native or acquired immunodeficiency or congenital infection prior to immune competence. Since tolerance to HIV that would result in active chronic infection has never been observed and is certainly not to be expected for 50-100% of infections [the percentage of infections said to develop into AIDS (ref. 7 and above)], the rare retrovirus infections of animals that cause slow, progressive diseases are not models for how HIV might cause AIDS. Indeed, not one acute retrovirus infection has ever been described in humans (23).

The Paradox of How HIV, a Noncytocidal Retrovirus, Is to Cause the Degenerative Disease AIDS. Unlike cytocidal viruses, which replicate by killing cells, retroviruses need viable cells for replication (139). During retroviral infection, proviral DNA becomes a cellular gene as it is integrated into the DNA of the cell. Such a mechanism is superfluous for a cytocidal virus. Virus reproduction from then on is essentially gene expression in viable cells, often stimulating hyperplastic growth (17, 23). Alternatively, retroviruses survive as latent proviruses, like latent cellular genes. The very distinction of not killing the host cell is the reason that scientists have for so long considered retroviruses to be the most plausible viral carcinogens (17, 23, 140).

Yet HIV, a retrovirus, is said to behave like a cytocidal virus, causing AIDS by killing billions of T cells (3, 5, 6, 12, 31). This is said even though some infected T-cell lines remain immortal (12, 23), and primary umbilical-cord blood cells may continue to divide in culture while propagating up to 106 infectious units per milliliter (82), much more than in AIDS patients. Also, there are no cytopathic changes or cell death in cultures of HIV-infected monocytes and macrophages (28, 141-146) and B cells (17, 23, 147). As is typical of retroviruses, HIV does not kill its host cells.

The cytocidal effects that are occasionally observed in HIV-infected cultures (but as yet, never in humans) soon after infection do not break this rule (23). These early effects result from fusions of HIV-infected and uninfected cells that depend on virus isolates and cell culture conditions (23, 82, 146, 147), and are completely inhibited by antiviral antibody (23, 115, 119). They are not HIV-specific, because many animal and human retroviruses show conditional, but never absolute, cytocidal effects in cell culture (23). Thus, the fusion effect in culture might be relevant for the mononucleosis observed in some patients soon after infection, when free virus (but no fusion-inhibitory antibody) is present. However, the effect cannot be relevant to AIDS because there is plenty of fusion-inhibitory antibody and because the virus isolates from some patients fuse, and those from others don’t (23, 82, 146, 147). Thus, HIV is not sufficient to kill even the few T cells it infects in AIDS.
HIV Is a Conventional Retrovirus, Without an AIDS Gene. The virus-AIDS hypothesis proposes that HIV is an unorthodox retrovirus (6, 12, 14, 31, 32) containing specific suppressor and activator genes that control the 2- to 15-year intervals between infection and AIDS (12, 37,188). However, the two known HIVs (see below) are profoundly conventional retroviruses. They have the same genetic complexity of about 9150 nucleotides, the same genetic structure, including the three major essential retrovirus genes linked in the order gag-pol-env, the same mechanism of replication, and the same mutation frequency (3, 7, 17, 90, 125, 126, 148) as all other retroviruses (17, 127, 128, 149, 150). Humans carry between 50 and 100 such retroviruses in their germ line, mostly as latent proviruses (151). The presumably specific genes of the HIVs (12, 188) are alternative reading frames of essential genes shared by all retroviruses (3, 7, 12, 23, 90, 148). Their apparent novelty is more likely to reflect new techniques of gene analysis than to represent HIV-specific retroviral functions. Indeed, analogous genes have recently been found in other retroviruses, including one bovine and at least three other human retroviruses that do not cause AIDS (23, 152, 188). Because HIV and all other retroviruses are isogenic, the newly discovered genes cannot be AIDS-specific. Moreover, it is unlikely that these genes even control virus replication. In vivo, HIV lies chronically dormant, although the presumed suppressor genes are not expressed. In vitro, HIV is propagated at titers of about 106 per ml in the same human cells in which it is dormant in vivo, although the presumed suppressor genes are highly expressed (23, 188). Therefore, I propose that antiviral immunity rather than viral genes suppress HIV in vivo, as is the case with essentially all retroviruses in wild animals (23). Further, I propose that the multiplicity of AIDS diseases are caused by a multiplicity of risk factors (see below), rather than by one or a few viral activator genes, since viral gene expression in AIDS is just as low as in asymptomatic carriers. Also, the extremely low genetic complexity of HIV can hardly be sufficient to control the inevitably long times between infection and AIDS, and the great diversity of AIDS diseases. Thus, there is neither biochemical nor genetic evidence that HIV genes initiate or maintain AIDS.

The Paradoxes of an AIDS Virus with Country- and Risk-Specific Pathologies and Host Ranges. It is yet another paradox of the virus-AIDS hypothesis that HIV is said to cause very different diseases in different risk groups and countries. For example, in the U.S. over 90% of AIDS patients have Pneumocystis pneumonia or Kaposi sarcoma. However, Kaposi sarcoma is found almost exclusively in homosexuals (8, 191). By contrast, in Africa over 90% of the AIDS cases are manifested by slim disease, fever, and diarrhea (9, 10, 64). Moreover, it is paradoxical that the prevalence of Kaposi sarcoma among U.S. AIDS cases has shifted down from 35% in 1983 (156) to 6% in 1988 (4) (see below and refs. 190 and 191), and Pneumocystis pneumonia has shifted up from 42% to 64% (8), while the alleged cause, HIV, has remained the same.

One explanation of these facts is that HIV is not sufficient to cause AIDS but depends critically on country- and risk-specific cofactors. However, the simplest explanation proposes that HIV is a harmless, idle retrovirus that is not the cause of AIDS.

In view of the claims that AIDS is a sexually transmitted viral syndrome (3, 7, 12), it is surprising (47, 64, 65, 91, 92, 154, 155) that, in the U.S., about 90% of all HIV carriers and AIDS patients are male (4, 7, 22, 38, 47). Even if one assumes that the virus was originally introduced into the U.S. through homosexual men (7), this epidemiology is hard to reconcile with the spread of a sexually transmitted virus 8 years later. In order to survive, a virus must infect new hosts, which it does most readily when it is at the highest titer (153). In the case of HIV, this would be before antiviral immunity, or 1 to 2 months after infection (69). Thus, the 8 years of AIDS in the U.S. represent about 50 to 100 human passages of HIV, enough time for the virus to equilibrate between the sexes. By contrast, the uniform sexual distribution of HIV in Africa appears consistent with a sexually transmissible virus, underscoring the paradox of the U.S. epidemiology, particularly since the viruses (12) and the epidemics (12-14, 90, 113) of both countries are thought to be equally new.

A solution of the paradox is that HIV is not new but is endemic in Africa and, like most retroviruses (23), is transmitted perinatally rather than sexually. Accordingly, 10% of healthy Zairians are antibody-positive (46, 98,184), and not more than 30% of the Kaposi sarcoma patients in Africa are infected with HIV (157, 158). Indeed, perinatal transmission between mother and child occurs with an efficiency of 30-50% (7, 22, 39), while sexual transmission is extremely inefficient (65, 79, 80, 154, 155). Since the virus is not endemic in the U.S., it is transmitted more often by parenteral exposures associated with risk behavior (see below) than perinatally.

Evolutionary Arguments Against AIDS Viruses. It is now claimed that there are at least two new retroviruses capable of causing AIDS, HIV-1 and HIV-2 (3, 7, 12-14), which differ about 60% in their nucleic acid sequences (148). Both allegedly evolved only 20 to <100 years ago (12). Since viruses, like cells, are the products of gradual evolution, the proposition that, within a very short evolutionary time, two different viruses capable of causing AIDS would have evolved or crossed over from another species is highly improbable (56, 64, 159). It is also improbable that viruses evolved that kill their only natural host with efficiencies of 50-100% as is claimed for the HIVs (7, 33-38).
Conclusions and Perspectives

It is concluded that HIV is not sufficient to cause AIDS because HIV meets neither Koch’s postulates nor established epidemiological, biochemical, genetic, and evolutionary criteria of a viral pathogen. Further, it is concluded that HIV may not even be necessary for AIDS because there is neither biochemical nor genetic evidence that it initiates or maintains AIDS. HIV infiltration and activity are just as low in symptomatic carriers as in asymptomatic carriers, and HIV lacks an AIDS gene. The association between AIDS and antibody to HIV-now part of the definition of AIDS-does not prove causation because otherwise indistinguishable diseases are now set apart only on the basis of this antibody. According to this view, HIV is an ordinary harmless retrovirus that, in rare acute infections, may cause a mononucleosis-like disease before immunity.

Antibody to HIV Is a Surrogate Marker for Risk of AIDS. Although HIV does not appear to cause AIDS, it may serve in the U.S. and Europe as a surrogate marker for the risk of AIDS for the following reasons. (i) In these countries, HIV is not widespread but is one of the most specific occupational infections of persons at risk for AIDS (3, 7, 38, 47, 61, 94, 160). (ii) Since HIV is extremely difficult to transmit, like all latent viruses, it would specifically identify those who habitually receive transfusions or intravenous drugs or are promiscuous. Indeed, the probability of being antibody-positive correlates directly with the frequency of drug use (38, 47, 160), transfusions (94, 161), and male homosexual activity (38, 160). (iii) Since HIV is not cytocidal, it persists as a minimally active virus in a small number of cells, which will chronically boost antiviral immunity to produce a positive AIDS test. Latent EBV, cytomegalovirus, or other herpes virus infections will likewise maintain a chronic immunity (86, 120), although less specific for AIDS risk. By contrast, antibodies against viruses and microbes, which cannot persist at subclinical levels, tend to disappear after primary infection.

Epidemiology Is Not Sufficient to Prove Etiology. It has been argued that Koch’s postulates can be abandoned as proof for etiology in favor of epidemiological correlations (67, 68, 162), most recently in the case of HIV (14, 32). However, adherence to this epidemiological concept (68, 162) as a substitute for biochemical and genetic proof of etiology has resulted in some of the most spectacular misdiagnoses in virology. (a) Based on epidemiological correlations, EBV was thought to be the cause of Burkitt lymphoma-until Burkitt lymphomas free of the virus were discovered (163). [It is ironic that HIV is currently a proposed cause of Burkitt lymphoma (5).] (b) Also on the basis of seroepidemiological evidence, retroviruses were thought to cause human and bovine leukemias after bizarre latent periods of up to 40 years in humans (164), until the discovery of these viruses in billions of normal cells of millions of asymptomatic carriers cast doubt on this hypothesis (23). It is scarcely surprising that the particular T cell from which a rare clonal leukemia originated was also infected. It is consistent with this view that these tumors are clonal and not contagious, like virus-negative leukemias, and that the presumably causative viruses are biochemically inactive in the human and bovine leukemias (23). Instead of viruses, the only specific markers of such tumors are clonal chromosomal abnormalities (23). (c) Likewise, slow viruses have gained acceptance as causes for such diseases as kuru, Creutzfeld-Jacob disease, and Alzheimer disease on the basis of epidemiological evidence (165), although these viruses have never been detected.

Proof of Etiology Depends on Evidence for Activity. Regrettably, the hasty acceptance of the virus as the cause of AIDS (16), signaled by naming it HIV (18), has created an orthodoxy whose adherents prefer to discuss “how” rather than “whether” HIV causes AIDS. They argue that it is not necessary to understand HIV pathology, or how a latent virus kills, in order to claim etiology (7, 14, 32, 51). Therefore, many different mechanisms, including ones in which HIV is said to depend on cofactors to cause AIDS, have been discussed (6, 12, 31, 32, 35, 61, 91) to explain how the virus supposedly kills at least 104 times more T cells than it actively infects (26-28, 71-74). Yet all speculations that HIV causes AIDS through cofactors cast doubt on HIV as a cause of AIDS, until such factors are proven to depend on HIV.

In contrast to what is claimed for HIV, there is unambiguous genetic evidence that biochemical activity in or on more cells than the body can spare or regenerate is absolutely necessary for viral or microbial pathogenicity. Examples are transformation-defective mutants of Rous sarcoma virus (166) and replication-defective mutants of cytocidal viruses (87). If latent viruses or microbes were pathogenic at the level of activity of HIV, most of us would have Pneumocystis pneumonia (80-100%) (167), cytomegalovirus disease (50%) (88), mononucleosis from EBV (50-100%) (see above; ref. 88), and herpes (25-50%) (88) all at once, and 5-10% also would have tuberculosis (168), because the respective pathogens are latent, immunosuppressed passengers in the U.S. population at the percentages indicated. Since we can now, through molecularly cloned radioactive probes, detect latent viruses or microbes at concentrations that are far below those required for clinical detectability and relevance, it is necessary to reexamine the claims that HIV is the cause of AIDS.

In response to this, it has been argued that a biochemically inactive HIV may cause AIDS indirectly by a mechanism(s) involving new biological phenomena (12, 14, 31, 32). This is argued even though HIV is like numerous other retroviruses studied under the Virus-Cancer Program during the last 20 years (17, 140), which are only pathogenic when they are biochemically active (23). Nevertheless, some retroviruses (23) and DNA viruses [e.g., hepatitis virus in hepatomas (169)] are thought to cause tumors indirectly by converting, by means of site-specific integration, a specific gene of a rare infected cell to a cancer gene. Such a cell would then grow autonomously to form a monoclonal tumor, in which the virus may be inactive and often defective (17, 23, 140, 169). However, such highly specific, and hence rare, virus-cell interactions cannot explain the loss of billions of cells during a degenerative disease like AIDS. It is also hard to accept that HIV could cause AIDS through a T cell autoimmunity (12, 31, 32, 170), because it reaches far too few cells to function as a direct immunogen and because it is unlikely to function as an indirect immunogen since it is not homologous with human cells (73, 75, 77). Further, it is extremely unlikely that any virus could induce autoimmunity, which is a rare consequence of viral infection, as efficiently as HIV is thought to cause AIDS, namely in 50-100% of all infections.

Not All AIDS Diseases Can Be Explained by Immunodeficiency. Clearly, immunodeficiency is a plausible explanation for the microbial and viral AIDS diseases (5) and Pneumocystis pneumonia. However, the effective immunity against HIV, which defines AIDS, together with those against cytomegalovirus, herpes simplex virus, hepatitis virus, and other viruses (3, 23, 61, 94), is hard to reconcile with acquired immunodeficiency. One would have to argue that T cell depletion in AIDS is highly selective in order to allow Pneumocystis but not HIV or other viruses to become active. If HIV were able to induce T cell immunodeficiency against itself, its titer during AIDS should be as high as it is in cultures of infected human monocytes-namely, up to 106 infectious units per milliliter (see above), just as high as the titers of all other retroviruses when they are pathogenic in animals (23).

Moreover, immunodeficiency does not explain AIDS neoplasias such as lymphomas or Kaposi sarcoma, which may be a hyperplasia (175, 178). The hypothesis that cancers reflect a defective immune system, the immune-surveillance hypothesis (176), has been disproven through athymic (nude) mice, which develop no more cancers than other laboratory mice (177). In fact, no immunodeficiency was observed in HIV-infected African patients who had Kaposi sarcomas (157, 158). In addition, Kaposi sarcoma tissue does not contain any HIV (23, 178, 179). Immunodeficiency also cannot explain dementia; nor can dementia be explained by HIV infection of neurons, because retroviruses are dependent on mitosis for infection (17, 23, 139, 140) and neurons do not divide (169). HIV would indeed be a mysterious virus (31) to kill T cells and neurons that are not infected and, at the same time, to induce hyperplastic or neoplastic growth of other cells that are also not infected.

HIV Is Not a Rational Basis for AIDS Therapy. Since there is no proven mechanism of HIV pathogenesis, HIV is not a rational basis for the control of AIDS. Thus the treatment of symptomatic and even asymptomatic HIV carriers with azidothymidine (AZT) (7, 39) cannot be justified in terms of its original design, which is to inhibit HIV DNA synthesis by chain termination (171). Even if HIV were to cause AIDS, it would hardly be a legitimate target for AZT therapy, because in 70-100% of antibody-positive persons proviral DNA is not detectable (73, 75, 187) without amplification (77), and its biosynthesis has never been observed.

Nevertheless, AZT has been claimed to have beneficial effects for AIDS patients on the basis of a 16- to 24-week double-blind trial (194). However, AZT, originally developed for chemotherapy by terminating cellular DNA synthesis, efficiently kills dividing blood cells and other cells (39, 84, 172-174, 189, 193, 195) and is thus directly immunosuppressive. Moreover, the immediate toxicity of AZT (174, 189, 193, 195) suggests that this trial could hardly have been double-blind and hence unbiased.

What Are the Causes of AIDS? I propose that AIDS is not a contagious syndrome caused by one conventional virus or microbe, because no such virus or microbe would average 8 years to cause a primary disease, or would selectively affect only those who habitually practice risk behavior, or would be able to cause the diverse collection of over 20 degenerative and neoplastic AIDS diseases. Neither could a conventional virus or microbe survive if it were as inefficiently transmitted as AIDS, and killed its host in the process. Conventional viruses either are highly pathogenic and easy to transmit or are nonpathogenic and latent and hence very difficult to transmit (153). Conventional viruses or microbes also exist that cause secondary-or even primary-diseases long after infection, but only when they are activated from dormancy by rare acquired deficiencies of the immune system (86). Such opportunistic infections are the consequence rather than the cause of immunodeficiency.

Since AIDS is defined by new combinations of conventional diseases, it may be caused by new combinations of conventional pathogenic factors. The habitual administration of factor VIII or blood transfusions (94, 161) or of drugs (47, 64, 160, 190-192), chronic promiscuous male homosexual activity that is associated with drugs (64, 160, 191), numerous acute parasitic infections, and chronic malnutrition (159, 160)-each for an average of 8 years-are factors that appear to provide biochemically more tangible and plausible bases for AIDS than an idle retrovirus. Indeed, the correlation between AIDS and such factors is 95% (4, 5). Among these factors, EBV, cytomegalovirus, herpes simplex virus, and administration of blood components and factor VIII have all been identified as causes of immunodeficiency not only in HIV-positive, but also in HIV-negative, hemophiliacs (11, 61, 94, 161). In fact, the dose of factor VIII received was found to be directly proportional to subsequent immunodeficiencies (94, 161). The habitual admission of narcotic toxins appears to play a major immunosuppressive role in the U.S. and Europe (11, 64). About 30% of the American AIDS patients are confirmed users of injected drugs (4, 47). Because of the difficulties in assessing drug data (47, 91, 92), it is probable that the percentage who use injected and/or noninjected drugs is even higher (64, 155, 185, 190-192). For example, nine different drugs were used in combination by a cohort of antibody-positive homosexuals in San Francisco (160). Again there are quantitative drug-AIDS correlations. For example, the decreased use of nitrite inhalants was shown to correlate with the decreased incidence of Kaposi sarcoma in homosexuals (190, 191). Moreover, that the Kaposi sarcoma cases decreased exactly with the use of nitrites, rather than lagging behind it by 8 years as would be expected from the presumed 8-year latent period of HIV, argues directly against a role of HIV in Kaposi sarcoma. Further, it has been documented that protein malnutrition and parasitic infections are the most common causes of T cell immunodeficiency worldwide, particularly in developing countries (181). Unlike HIV, the specifics of these risk factors provide a plausible explanation for the risk specificity of AIDS diseases. The long and unpredictable intervals between the appearance of antibody to HIV and the onset of AIDS would then reflect the thresholds for these factors to cause AIDS diseases, rather than an unlikely mechanism of HIV pathogenesis.

In response to this view it is often pointed out that AIDS risks have existed for a long time (55, 59), whereas AIDS is said to be a new syndrome (3, 7, 12-14). However, this argument fails to consider that the major risk groups-male homosexuals and intravenous drug users-have only become visible and acceptable in the U.S. and in Europe during the last 10 to 15 years, about the same time that AIDS became visible. Acceptability facilitated and probably enhanced risk behavior, and thus the incidence of the many diseases now called AIDS. Increased consumption of drugs was reported to have increased the number of drug-related deaths, although unconfirmed HIV infections were the prefered interpretation (190, 192). Moreover, the particular permissiveness toward these risk groups in metropolitan centers encouraged the clustering of cases that was necessary to detect AIDS. Further, it has been pointed out that slim disease, fever, and diarrhea in Africa are not a new epidemic, but old diseases under a new name, caused by previously known infectious agents and malnutrition (11, 64, 98, 182).

This analysis offers several benefits. It ends the fear of infection by HIV, and particularly of immunity to HIV, because it proves that HIV alone is not sufficient to cause AIDS. To determine whether HIV is necessary for AIDS, controlled, randomized analyses (196) either of risk takers who differ only by the presence of antibody to HIV or of antibody-positive individuals who differ only in taking AIDS risks must be carried out. Moreover, assessment of a pathogenic potential of HIV would depend on evidence that the life-span of antibody-positive risk takers is shorter than that of antibody-free controls. In addition, it should be determined whether, prior to 1981, AIDS-risk takers ever developed what are now called AIDS diseases. This analysis also suggests studies on how the nature, frequency, and duration of AIDS risks generate risk-specific diseases. Such studies should include persons treated with AZT before or after AIDS symptoms to assess the AIDS risks of AZT. To this end, diseases should be reported by their original names (8-10), rather than as AIDS (4) because of their association with antibody to HIV. Finally, this analysis suggests that AIDS prevention efforts be concentrated on AIDS risks rather than on transmission of HIV (43).

There is something charming about the naivete of this last paragraph, and the already anachronistic faith it shows in the traditional standards of science, and the underlying purpose of benefiting society and advancing medicine.

This analysis offers several benefits. It ends the fear of infection by HIV, and particularly of immunity to HIV, because it proves that HIV alone is not sufficient to cause AIDS. To determine whether HIV is necessary for AIDS, controlled, randomized analyses (196) either of risk takers who differ only by the presence of antibody to HIV or of antibody-positive individuals who differ only in taking AIDS risks must be carried out. Moreover, assessment of a pathogenic potential of HIV would depend on evidence that the life-span of antibody-positive risk takers is shorter than that of antibody-free controls. In addition, it should be determined whether, prior to 1981, AIDS-risk takers ever developed what are now called AIDS diseases. This analysis also suggests studies on how the nature, frequency, and duration of AIDS risks generate risk-specific diseases. Such studies should include persons treated with AZT before or after AIDS symptoms to assess the AIDS risks of AZT. To this end, diseases should be reported by their original names (8-10), rather than as AIDS (4) because of their association with antibody to HIV. Finally, this analysis suggests that AIDS prevention efforts be concentrated on AIDS risks rather than on transmission of HIV (43).

None of these suggestions were undertaken since, presumably because they are hardly welcome to those already heavily invested in the paradigm, Federally funded since 1984 and climbing rapidly to a total now estimated at more than $140 billion).

3. The 2003 paper in the Journal of Biosciences.

This is a paper which is the final one, up-to-date, completely loaded and fired broadside against the HIV-AIDS fantasy, a word which it is difficult not to use about the current AIDS theory once one has gone through this paper.

Here is an abstract, with a link on the page to the pdf, which is unfortunately not available in html.

This is the text of the abstract:

The chemical bases of the various AIDS epidemics: recreational
drugs, anti-viral chemotherapy and malnutrition

Peter Duesberg�, Claus Koehnlein* and David Rasnick

Donner Laboratory, University of California Berkeley, Berkeley, CA 94720, USA

*Internistische Praxis, Koenigsweg 14, 24103 Kiel, Germany

�Corresponding author (Fax, 510-643-6455; Email: duesberg@uclink4.berkeley.edu)

In 1981 a new epidemic of about two-dozen heterogeneous diseases began to strike non-randomly growing numbers of male homosexuals and mostly male intravenous drug users in the US and Europe. Assuming immunodeficiency as the common denominator the US Centers for Disease Control (CDC) termed the epidemic, AIDS, for acquired immunodeficiency syndrome. From 1981�1984 leading researchers including those from the CDC proposed that recreational drug use was the cause of AIDS, because of exact correlations and of drug-specific diseases. However, in 1984 US government researchers proposed that a virus, now termed human immunodeficiency virus (HIV), is the cause of the non-random epidemics of the US and Europe but also of a new, sexually random epidemic in Africa. The virus-AIDS hypothesis was instantly accepted, but it is burdened with numerous paradoxes, none of which could be resolved by 2003: Why is there no HIV in most AIDS patients, only antibodies against it? Why would HIV take 10 years from infection to AIDS? Why is AIDS not self-limiting via antiviral immunity? Why is there no vaccine against AIDS? Why is AIDS in the US and Europe not random like other viral epidemics? Why did AIDS not rise and then decline exponentially owing to antiviral immunity like all other viral epidemics? Why is AIDS not contagious? Why would only HIV carriers get AIDS who use either recreational or anti-HIV drugs or are subject to malnutrition? Why is the mortality of HIV-antibody-positives treated with anti-HIV drugs 7�9%, but that of all (mostly untreated) HIV-positives globally is only 1.4%? Here we propose that AIDS is a collection of chemical epidemics, caused by recreational drugs, anti-HIV drugs, and malnutrition. According to this hypothesis AIDS is not contagious, not immuno�genic, not treatable by vaccines or antiviral drugs, and HIV is just a passenger virus. The hypothesis explains why AIDS epidemics strike non-randomly if caused by drugs and randomly if caused by malnutrition, why they manifest in drug- and malnutrition-specific diseases, and why they are not self-limiting via anti-viral immunity. The hypothesis predicts AIDS prevention by adequate nutrition and abstaining from drugs, and even cures by treating AIDS diseases with proven medications.

[Duesberg P, Koehnlein C and Rasnick D 2003 The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy and malnutrition; J. Biosci.28 383�412]

None of these impeccably phrased, rigorously argued and completely referenced pieces received any reply but silence in the same journals, to our knowledge, even though the always ebullient Robert Gallo, for one, read a galley of the Proceedings paper and promised the editors a response.

It never happened, a non-event which was very much in line with Gallo’s subsequent evasion of any personal confrontation with Duesberg. Time and again, when both were scheduled to appear on the same stage Gallo would suddenly find an urgent reason not to be able to attend, sometimes when he was no more than an hour away.

Since journal pages are the platform on which the reliable ie peer-reviewed scientific debate is conducted, one really has to conclude that Duesberg won the HIV debate a long time ago in the venue where it counted. Simply put, if he was wrong and they could show it, his opponents would naturally have replied on the same level, in the same place.

Why scientists won’t read them

Unfortunately, that mountain plateau battleground doesn’t actually count for much these days, since few scientists visit it to read papers of this kind for several reasons.

One, they know in advance the paper attacks ideas they hold dear. Unfortunately, one of the traits we humans are heir to that we all have a strange distaste for reading material that disagrees with us, especially if it is well done and persuasive. As Lady Bracknell avers in Oscar Wilde’s “The Importance of Being Ernest”, “I dislike arguments of any kind. They are always vulgar, and often convincing.”

Two, they don’t have time to “waste” reading such attacks, which would change their world view if accepted.

In fact, asking them to read such material with an open mind is rather like asking an Indonesian to stand firmly on the beach and keep an eye on the approaching tsunami instead of fleeing. Th only sensible thing for them to do is to run in the opposite direction as fast as they can.

Three, they know in advance they can’t accept the reasoning and conclusions even if those seem to be true, since they are already wedded to the notion that may be disproved. A man who is already married to a loyal and beautiful wife will not easily entertain the idea of marrying another, at least in a society which is as monogamous as science.

The sad irony is that it is all too easy for those who agree with a paper of this kind not to read it, since they may well assume they know what it says already. This makes sense. After all, it is written as an argument to persuade those who don’t agree with it, not those friends of the author who do agree with it.

Other scientists, even those in the field, may not have the time to read it and make up their own minds. So they don’t read it either. They wait for those colleagues they assume will read it to tell them what they think. Then they simply go by what their friend says.

With all these time-saving strategies in place to help the world of science turn, it seems quite possible that many if not most of the papers Duesberg has written have actually only been closely studied by a tiny handful of other scientists�the peer reviewers who acted at gatekeepers, the journal editors or at least the copyeditors, the friends of Duesberg who helped to armorplate them, Duesberg himself and his co-authors.

That these masterpieces should be so neglected is a shame, for they deserve to be admired for their literary and artistic quality as well as for their scientific reasoning. This quality arises because they were forged in the white-hot crucible of idealism, truth seeking, political threat and intense antagonism from their reviewers, and they are papers for which the penalty of being wrong and unclear was the equivalent of professional death.

On a purely practical basis, also, they are worth reading by outsiders for two reasons:

One, they are classics of argument and exposition.

Two, they present the meat of the matter more clearly and more concisely than any of the popular books on the topic all of which are derived from Duesberg’s arguments in these papers.

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