Reprinted from the proceedings of the conference Actes du Colloque, 5th International Colloquium on ‘THS’ held in Grasse, France September 14, 2001, this is a translation of a lecture by Professor Etienne de Harven, Emeritus Professor of Pathology, University of Toronto
AIDS: Open Debate is Long Overdue
By Dr. Etienne de Harven
 
"All the catastrophic predictions for AIDS epidemics have, with the passage of time, been proven wrong. Unbiased analysis of epidemiological data demonstrates that an actual AIDS epidemic has never been observed. Virtual epidemics have, however, been reported. But they have all been ‘invented’ with several redefinitions of AIDS..."
 
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I wish, at the outset, to thank the organizers of this conference for the invitation to participate in this important conference, and for t
heir courageous initiative in opening the debate on controversial issues.         
 
AIDS being a major problem of public health, one must recognize the existence of a considerable controversy regarding the causes of this syndrome.   
 
However, before getting to the center of our topic, I wish to introduce myself briefly to help you understand why I feel authorized to speak on retroviruses. I spent almost all my professional career in the US, at the Sloan Kettering Cancer Institute in New York, the main area of my research being the isolation, purification and ultrastructural characterization of retroviruses associated with certain types of leukemia in mice, using the electron microscope.   
 
We shall start with two points of history.          
 
The first one concerns the publication by Gottlieb (1), in 1981, at the CDC of Atlanta, in which the first 5 cases of AIDS were reported in five male homosexual patients. All five were drug addicts. All five used amyl nitrite ("Poppers"). They did not know each other and could not, therefore, have contaminated one another. Nonetheless, Gottlieb immediately suggested the contagious nature of the disease and its transmission by sexual contacts, a hypothesis that was, instantly, favorably received by the CDC. Still, there was absolutely no justification, based on these first 5 cases, for considering the possibility that AIDS could be a sexually transmitted contagious disease.
 
Let me clarify this with a parable:
 
Imagine you are medically in charge of about 100 workers, all working in a poorly ventilated factory where lead salts are profusely used. You soon diagnose 10 cases of lead poisoning. Are you going to conclude that lead poisoning is a contagious disease transmitted sexually? This is exactly what Gottlieb did!
 
How is it possible that such a highly unlikely hypothesis was received with so much credibility? The answer is simple and tragic. Remember, we were in the late 70s early 80s: morale was rather low at the CDC where very few epidemics were detected since the days of polio, and morale was also very low at the National Cancer Institute (NCI), Bethesda, where gigantic efforts, developed over the past 20 years and funded on monumental budgets primarily aimed at demonstrating the hypothetical role of retroviruses in human cancer, were ending in total failure. The CDC as well as the NCI therefore jumped with considerable precipitation on this retrovirus related, hypothetical AIDS epidemic, their precipitation resulting from considerations of scientific policy, not from any rigorous analysis of virological data.
 
A second point of history is of a bibliographical nature. When one states "AIDS is caused by HIV", such a statement should be supported by at least one bibliographical reference. You will be surprised to learn that such a reference has never existed, even in the early 1980s. Karry Mullis, who won the Nobel prize in 1993 for the discovery of the PCR method, searched extensively for such a reference without any success (2). All you will find is a reference to a most celebrated press conference which took place in Washington, DC, on April 23, 1984 and during which Margaret Heckler, Secretary of Health and Human Services, proudly announced, in presence of Robert Gallo, that a retrovirus had just been discovered that was "the probable" cause of AIDS. The next morning, all newspapers in the US and worldwide, flashed big headlines in which they omitted only one word: "probable". The media carries an enormous responsibility in misinforming the public in regards to AIDS causation.
 
As you can see from these two historic events, the hypothesis according to which "HIV causes AIDS" began with a very shaky start.
 
In medical research, when an hypothesis is formulated suggesting the possible viral etiology of a disease, and when 20 years later, all the research based exclusively on that hypothesis still fails to establish a curative therapeutic protocol, fails to lead to an efficient vaccine, and alsofails to lead to verifiable epidemiological predictions, don’t you think it is time to courageously ask ourselves if the hypothesis was correct? I amconvinced that this is an absolute necessity.
 
Please, don’t think that this radical opinion is that of an isolated "dissident". The group of AIDS dissidents initially led by Peter Duesberg in 1987 (3) counts thousands of members, including two Nobel laureates. They can be found worldwide, in the US, in Europe, in Australia, in South Africa, in India, etc. All of them worry about the same fundamental questions (4), the most significant of which can be summarized as follows:
 
1) HIV purification.
 
Nobody has ever succeeded in purifying HIV (5). Centrifugation in sucrose gradients at the 1.16 gm/ml density is a classical approach to the purification of all the well-known animal retroviruses. Unfortunately, numerous cell debris settle at that very same density gradient. Consequently, without a rigorous control by transmission electron microscopy, identifying material sedimenting at that density as "purified" retroviruses is a very dangerous scientific mystification. The very same criticism must be addressed to Temin (6) and Baltimore (7) who, independently, recognized reverse transcriptase (RT) activity in "retroviral" samples, the purity of which had not been verified, therefore making it impossible to exclude RT activity originating from cell debris or from mycoplasma fragments.
 
2) Identification of HIV molecular "markers".
 
In absence of any HIV purification, numerous molecules are currently used as surrogate "markers" supposedly demonstrating the presence of HIV: protein (p24), enzyme (RT), or short sequences of nucleic acid. But HIV should have been purified first in order to demonstrate convincingly that these molecules, considered HIV markers, were indeed specifically of retroviral origin. This purification having never been achieved, it remains impossible to demonstrate the retroviral specificity of these molecular markers because similar molecules are abundantly present in cell debris which contaminate all the samples falsely regarded as "purified" retroviruses, simply because they originate from sucrosegradients at the 1.16 gm/ml density.
 
All "markers" being non-specific, it was no big surprise to learn that tests for so-called seropositivity (Elisa and Western Blot), based on the very same markers were not specific either. The was clearly and originally demonstrated by Eleni Papadopulos, Val Turner and the Australian group of researchers in Perth (8), Australia, as early as 1993, in a paper published in Nature/Bio-Technology, a paper which has been (most conveniently) ignored by the AIDS establishment.
 
3) The Elisa test being non-specific, it was no surprise to learn that many medical conditions, without any connection with HIV/AIDS, often give "HIV +" responses (9). This may occur, for example, in cases of tuberculosis (10), malaria, leprosy (11), multiple vaccinations, anti-flu vaccination, multiple blood transfusions, various hepatitis, and pregnancy. Percentages are not negligible. For example, more than 43 % of cases of systemic lupus erythematosus (SLE) are seropositive. Obviously, the Elisa test is positive in individuals who have a high level of circulating antibodies, but these antibodies have probably nothing to do with HIV.
 
Even more confusing is the fact that in the Elisa test, a blood sample has to be diluted 400 times. And, as demonstrated recently in a New York laboratory (12), if samples are not diluted 400 times, everybody tests sero-positive. This Elisa test is being sold at great profit worldwide and the results continue to terrorize an entire generation.
 
Testing for p24 is apparently not any more informative. In a study of 77 cases of biliary cirrhosis, 35 % were found p24 +(13). Still, p24 is currently regarded as highly HIV specific, so specific as to be frequently used as evidence for successful HIV "isolation". Are we prepared to accept that biliary cirrhosis is HIV induced? Moreover, the discussion on cross-reactivity is made more complex by the fact that 43 % of dogs have been found positive for p 24 (14).
 
4) For patients with a positive reaction to the Elisa test, a Western Blot (WB) test is usually performed for "confirmation". However, the WB uses the same antigens as Elisa, therefore a better specificity could hardly be expected (15). Moreover, an international agreement on the interpretation of WB results has never been reached, and the same blood sample may give a positive result in Europe and a negative one in the US! Incidentally, the WB test is not accepted in England for reasons of inadequate specificity, but accepted in Scotland and throughout Europe!
 
5) Viral load.
 
Measuring so-called "viral load" by Polymerase Chain Reaction (PCR) technology represents a third test, extensively used in the clinical follow-up of AIDS patients. The reliability of "viral load" PCR results is raising many questions, however.
 
a) Karry Mullis, who invented the PCR method, strongly disagrees on its use to measure the number of HIV particles in the peripheral blood.
 
b) Moreover, measuring the so-called viral load implies a quantitative estimation of the number of HIV particles in the peripheral blood. To transmit the alleged HIV infection, intact HIV particles must be present in the blood. The presence of alleged HIV molecular "markers" (genomicor proteinic in nature) is unable to explain infectivity, unless intact viral envelopes protect these retroviral molecules.
 
c) Intact enveloped retroviral particles can readily be identified with the transmission electron microscope (TEM). Unfortunately, nobody has ever succeeded in demonstrating one single HIV particle, by TEM, in the blood of an AIDS patient, even when patients are selected for having an alleged high viral load "measured" by PCR (16).
 
d) Finally, using molecular probes allegedly hybridizing specifically with an exogenous HIV provirus does not take into consideration the presence of a sizable amount of endogenous retroviral sequences in the human genome. Sequencing the human genome has indeed demonstrated that an appreciable percentage of our genome consists of DNA sequences having very close homology with the alleged HIV genome (17).
 
6) Many HIV pictures, taken with the electron microscope, are found in magazines, newspapers, and scientific literature. All these pictures originated from complex, laboratory cell cultures. They never originated directly from one single AIDS patient. These mixed co-cultures included frequently human lymphocytes isolated from umbilical cord blood. And still, it is known since the early observations by Sandra Panem in 1978 that human placenta (19), as well as some embryonic cells (18) contain large numbers of endogenous retrovirus. It would be most surprising if lymphocytes from umbilical cord blood were not, similarly, carriers of endogenous retrovirus. This would provide an explanation for the presence of retroviral particles, resembling the alleged HIV, in some co-cultures highly stimulated by various factors (PHA, IL2, etc) and observed with the electron microscope.
 
7) Alleged heterosexual transmission of AIDS.
 
In a prospective study started in California in 1990, Padian et al. studied 175 serodiscordant couples (one partner seropositive, the other negative) during a 6-year period (20). They did not observe one single case of seroconversion of the negative partner. I am not aware of a single publication that would contradict Padian’s work.
 
Moreover, the hypothetical heterosexual transmission of AIDS had been predicted as the likely cause of a dramatic AIDS epidemic in North America as well as in Europe. All these catastrophic predictions have, with the passage of time, been proven wrong. Gordon Stewart, from the University of Glasgow, initially analyzed epidemiological data and demonstrated that an actual AIDS epidemic has never been observed (21, 22). Virtual epidemics have, however, been reported. But they have all been "invented" with several redefinitions of AIDS; redefinitions imposed by the US Centers for Disease Control, as well as by the World Health Organization.
 
The fact that there is no heterosexual transmission of AIDS should not, however, be interpreted as justifying any tolerant attitude about unprotected sex practices. On the contrary, safe sex remains essential for the prevention of classic venereal diseases (STDs) as well as for the avoidance of unwanted pregnancies.
 
8) Mortality of seropositive hemophiliacs in the UK.
 
The key reference is the paper by Darby et al., which appeared in Nature in 1995 (23). The study covered more than 6.000 hemophiliacs, between 1977 and 1991. The annual mortality rate was remarkably stable until 1985, around 8/1000. However, starting in 1986, the death toll rose sharply (x10), reaching 81/1000 in 91-92. Most importantly, it is precisely in 86-87 that AZT started to be given to seropositive patients at the extremely toxic dosage of 1.5, even 1.8 gm/day. Surprisingly, the authors interpreted their observations solely on the basis of deadly HIV infections, without ever alluding to an alternative interpretation based on the extreme toxicity of AZT (24).
 
9) The effects of triple therapy.
 
Two recent papers published in the Journal of Infectious Diseases demonstrate remarkable effects of the protease inhibitors used in HAART. The protease inhibitors are apparently highly active against Candida albicans (25) as well as against Pneumocystis carinii (26), two micro-organisms responsible for severe opportunistic infections in the majority of progressing AIDS cases. Consequently, the sometimes striking, transient clinical improvement observed in AIDS patients treated with HAART could possibly have an alternative interpretation, the improvements resulting from the effects of the drugs on Candida and/or on Pneumocystis, and having nothing to do with possible anti-retroviral effects against the alleged HIV.
 
In conclusion, it appears that the public at large, the patients, and the practicing physicians are not well informed. When it comes to HIV/AIDS, their information is neither complete nor objective. Efforts towards better information, independent from any dogma, independent from any unproven hypothesis, and independent from the interference of profit-motivated pharmaceutical industries, should receive the highest priority. This will imply opening up a large international debate which is long overdue. This debate, based on scientific facts and not on "consensus", should receive the most objective media coverage, exempt from hysterical passion and totally protected against any dogmatic censorship.
 
Engaging in such a debate will not require much money; it will require a lot of courage.
 
This debate will offer a considerable opportunity to improve prevention and treatment of AIDS worldwide. Its effectiveness will be far greater than that offered by the accumulation of billions of dollars, wasted in the purchase of highly toxic antiretroviral drugs, drugs prescribed on the basis of a 20 year old hypothesis which has still never been proven, and on the basis of serological tests which totally lack specificity.
 
ERRARE HUMANUM EST, SED DIABOLICUM PERSEVERARE
 
References:
 
1) Gottlieb MS. Pneumocystis pneumonia – Los Angeles. MMWR Morb Mortal Wkly Rep 1981;30:250-2.
 
2) Mullis K. Foreword in "Inventing the AIDS Virus », by P. Duesberg. Regnery Publishing, Inc. Washington, D.C., 1966
 
3) Duesberg P. Retrovirus as carcinogens and pathogens: expectations 351:1620-1634.
 
4) Strandstrom HV, Higgins JR, Mossie K, et al. Studies with canine sera that contain antibodies which recognize human immunodeficiency virus structural proteins. Cancer Res 1990; 50: 5628s-5630s.
 
5) Midthum K et al. Frequency on indeterminate Western Blot tests in healthy adults at low risk for HIV infection. J. Infectious Dis 1990; 162:1379-1382.
 
6) de Harven E. Summary statement. Interim Report of the AIDS advisory panel, Pretoria, May 2000. Published by the SA Government, on April 4, 2001.
 
7) Löwer, R et al. The viruses in all of us: characteristics and biological significance of human endogenous retrovirus sequences. Proc. Natl. Acad. Sci. USA 1996; 93 :5177-5184.
 
8) Panem S. C type virus expression in the placenta. Curr Top Pathol 1979; 66 :175-189.
 
9) Bronson DL et al. Morphological evidence for retrovirus production by epithelial cells derived from a human testicular tumor metastasis: brief communication. J. Natl Cancer Inst 1978 ; 60 : 1305-1307.
 
10) Padian NS et al. Heterosexual transmission of human immunodeficiency virus (HIV) in Nothern California. Am J Epidemiology 1997 ;146 :350-357.
 
11) Stewart GT. Changing the case definition of AIDS. Lancet 340 ;1414, 1992.
 
12) Stewart GT. Errors in predictions of the incidence and distribution of AIDS. Lancet 341 ;898, 1993.
 
13) Darby SC et al., Mortality before and after HIV infection in the complete UK population of haemophiliacs. Nature 377 ;79-82,
 
1995.
 
14) Concorde : MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Concorde Coordinating Committee. Lancet 1994; 343(8902) :871-881.
 
15) Cassone A et al. In vitro and in vivo anticandidal activity of human immunodeficiency virus protease inhibitors. Jour Infect Diseases 1999; 180 :448-453.
 
16) Atzori C et al. In vitro activity of human immunodeficiency virus inhibitors against Pneumocystis carinii. Jour Infect Diseases 2000;
 
181: 1629-1634.
 
17) and reality. Cancer Res. 47: 930-937, 1987.
 
18) Stewart GT, Mhlongo S, de Harven E, et al. The Durban Declaration is not accepted by all. Nature 2000; 407:286.
 
19) Djamel Tahi. Did Montagnier discover HIV? "I repeat, we did not purify!" Continuum vol. 5, N° 2, 1997, page 30-34.
 
20) Temin HM, Mizutani S. RNA-dependent DNA polymerase in virions of Rous sarcoma virus. Nature 1970; 226: 1211-1213.
 
21) Baltimore D. RNA-dependent DNA polymerase. Nature 1970; 226: 1209-1211.
 
22) Papadopulos-Eleopulos E, Turner VF, Padimitriou JM. Is a positive Western Blot proof of HIV infection? Bio/Technology 1993; 11:696-707.
 
23) Johnson C. Whose antibodies are they anyway? Factors known to cause false positive HIV antibody test results. Continuum Sept/Oct 1996.
 
24) Mann J et al. Association between HTLV-III/LAV infection and tuberculosis in Zaïre. JAMA 1986; 256:346.
 
25) Kashala O et al. Infection with human immunodeficiency virus type-1 HIV-and human lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 crossreactivity and antibodies to lipoarabinomannan. J. Infectious Diseases1994; 169:296-304.
 
26) Giraldo R. The HIV testing scandal. Internat. J. Alternative and Complementary Medicine 1999; 17: 24-26.
 
Mason A et al. Detection of retroviral antibodies in primary biliary cirrhosis and other idiopathic biliary disorders. Lancet 1998; EdH
 
Correspondence: Prof. Etienne de Harven, « Le Mas Pitou », 2879 Route de Grasse, 06530 Saint Cézaire sur Siagne, France
 
E-mail <pitou.deharven@wanadoo.fr

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