I am now Dead at Last free from being left all alone with the All Dead the Living Dead the Undead for the Living have all Left and aborted Abeings are All about.

Michael James Guy Verney-Elliott (1938-2007), State Scholarship to Magdalen College, Oxford; student actor, Hamlet; tour of Germany; diverse career included: vision mixer, Sir Winston Churchill State Funeral, 1965 (ITV); senior vision mixer: Upstairs, Down Stairs, Helen - A Woman of Today; television producer and writer, The Gentle Touch, writer and producer Channel 4/Meditel AIDS The Unheard Voices, AZT: Cause for Concern; also thinker, theorist, carpenter, dress maker, and the founder of the AIDS dissident movement in the UK being the first person to prove that 'HIV' does not exist.

Alex Verney-Elliott  July 1st 2007

                                                                                                 Michael Verney-Elliott (far left) acting in the late 1950s

'SIV' AND POLIOVACCINATION - A SHOT IN THE FOOT?

By Michael Verney-Elliott 

Introduction.                                    

I propose there are no human retroviruses.  What are being called 'human' retroviruses are more likely to be simian (monkey) viruses which infected humans as contaminants in poliovaccines since 1961 when live poliovirus vaccines began to be made utilising the kidney cells of African green monkeys.  What are being called 'HIV'-1 and 'HTLV'-1 are in fact both simian viruses known as SIVAGM and STLVAGM when they are found in wild-caught African green monkeys.  As a result, millions of men, women and particularly children have been exposed to these simian viruses wherever the polio vaccines have been tested and used for some 40 years.  Where infection has occurred, the viruses are harmless, usually dormant, classic passenger viruses.  'HIV' is in fact merely SIVAGM partially speciated to a human host. 

SIVAGM  infected humans in exactly the same way as Simian Virus 40 (SV40), a previous poliovaccine contaminant, is known to have done from the mid 1950's until c.1962.  SV40 has been a largely latent virus for some 40 years until its recent reactivation in certain human cancers in the late 1990's.  SIVAGM  also remains dormant until reactivated years later and is probably no more capable of disease causation, or perhaps even horizontal transmission, than SV40.  The contaminant SIVAGM infected male and female infants alike, and will only be detectable by an antibody response when subsequently reactivated in adulthood, usually in people with an already compromised immune system, principally caused by mainly avoidable risk behaviours in the West, and mainly unavoidable risks imposed by poverty and environmental conditions prevailing in the 3rd World.  SIVAGM/'HIV' is not the cause of AIDS but an epiphenomenal surrogate marker for immune suppression and AIDS risk.

On April 23rd 1984, the world was told that the 'probable' cause of AIDS had been found - a novel 'human' retrovirus called variously LAV, ARV, and HTLV-111.  Subsequently, despite a complete lack of convincing scientific evidence, which persists to this day, that this virus actually causes immunosuppression by direct or indirect killing of T4 cells, in a pre-emptive move the novel retrovirus was named 'HIV' (Human Immunodeficiency Virus) by an international committee (1986).  From the outset, no-one seems to have realised, or will not admit, that 'HIV' is not 'human'; that like all other retroviruses, it is difficult to transmit horizontally, especially sexually; and perhaps most importantly, that the two human diseases alleged to be caused by 'human retroviruses' are as novel as those viruses.  The most fearful acronym of our time is wrong at all points: 'HIV' is not Human; it has never been proven to be the cause of Immunodeficiency; and may not even be a Virus at all, but a misinterpreted artefact of human and simian cell cultures. 

Why vaccines?

The probability that a virus, 'HIV', has recently infected the human population (see below) inevitably raises the question of where it came from.  All sorts of theories abound, from spontaneous zoonosis (accidental cross-over from another animal species - monkey bites man etc.) to risibly sinister conspiracy theories about a doom-bug created at the behest of Pentagon red-necks for use in germ warfare. A strong possibility was the accidental introduction of an animal retrovirus into the human bloodstream as a contaminant in a widely used vaccine.  This is still the most logical and scientifically plausible explanation of how an animal retrovirus could infect humans on such a world-wide scale in such a short space of time, approximately 40 years. 

Disasters resulting from the use of vaccines are legion.  Viera Scheibner 1 and Leon Chaitow 2 in their books on the dangers of vaccination give extensive, fully referenced details of such tragedies.  Having learnt of these and many other vaccine disasters by the mid-1980's, when I still believed 'HIV' was the cause of AIDS, I wondered if an animal virus, a precursor of 'HIV', had got into the human bloodstream by mistake, and if AIDS was a man-made disaster.

Prof. Cedric Mims in his standard work The Pathogenesis of Infectious Disease 3 states:   "Many vaccines contain large numbers of irrelevant antigens, derived either from the micro-organism itself or from the culture system used to produce it.  It would be better to replace these crude soups with cocktails of defined polypeptides."  Intrigued by the phrase 'crude soups', I went to see Prof. Mims at Guys Hospital in 1988.  He explained that it was difficult, if not impossible, at that time to make a vaccine which does not contain contaminants, despite the most stringent precautions taken in the manufacturing process.  These contaminants might be other viruses, infectious stretches of DNA/RNA, bacteria (unlikely), alloantigenic cell debris etc.

The SV40 precedent.

By 1960, the '50's US polio epidemic had begun to abate, and the polio vaccine devisers - Salk, Sabin and Koprowski - were being congratulated, when two virologists called Sweet and Hilleman dropped a bombshell.  They had recently isolated a new monkey virus from the kidney cells of rhesus monkeys, until then the species most commonly used in the manufacture of polio vaccines. The fortieth simian virus to be isolated, it was named Simian Virus 40 (SV40).  Subsequent experiments with human cell cultures soon showed that infection with this virus caused cell transformation, and tumours in laboratory animals: SV40 was therefore deemed carcinogenic.  By the time the virus was first isolated, millions of contaminated doses of both live and killed poliovirus vaccine had been administered world-wide, especially in Central Africa.  The formaldehyde treatment used to kill the polio virus did not kill all the SV40 particles, so Salk's killed poliovirus vaccine contained live, ostensibly cancer-causing SV40.  Worse still, Salk's poliovirus seed stock, later used by Sabin in an attenuated form in his live poliovaccine, was contaminated with SV40.  Crucially, although not a retrovirus, the SV40 genome, which consists of circular, double-stranded DNA, is known to integrate into the human genome, making the infection permanent. 

The principal species of monkey used to make polio vaccines were originally rhesus macaques, cynomolgus and African greens, the last species being almost universally adopted from 1961 onwards (Research in Virology, Vol 144, p177).  Ironically, in seeking to replace the Asian rhesus monkey, a natural reservoir of SV40, with a 'safer' species, the major world poliovaccine manufacturers adopted African greens, a species which would be found in the 1980's to be natural carriers of several retroviruses, potential contaminants of their vaccines.  At the suggestion of Maurice Hilleman, co-discoverer of SV40, who in turn was acting on the advice of William Mann, Director of the Washington DC Zoological Park, (Nature Medicine, Vaccine Supplement, May 1998, pp 509-510) and starting in the early '60's, more than 10,000 wild-caught African greens were eventually being exported annually from sub-Saharan Africa to meet the needs of poliovaccine manufacturers worldwide.4  By 1988, it was found that up to 70% of wild-caught African greens were infected with SIV (Simian Immunodeficiency Virus), >50% homologous with 'HIV', designated SIVAGM;  and up to 40% with an STLV (Simian T-cell Leukaemia Virus) 95-100% homologous with HTLV1, the alleged cause of adult T-cell leukaemia in humans. (Essex and Kanki, Scientific American, October 1988 pp.44-51).

For several anxious years post 1960, the polio vaccine developers waited to see if there would be an increase in the incidence of human infantile cancers, based on the grim in vitro evidence against SV40, but by November 1967 they were confident enough to announce to an international conference that SV40 infections had not caused a significant increase in cancer.  Their findings were published in Monograph No.29, issued by the US National Institutes of Health (NIH) in December 1968.  However, everyone concerned had received a salutary shock.  In 1967 no-one mentioned a 'long incubation period', 'slow' viruses or any of the specious mechanisms used later to explain the 'delayed' pathogenicity of 'HTLV1' and 'HIV', the first two 'human' retroviruses later considered to cause disease.  By the same token, in April 1984 no-one was prepared to admit that the 'probable cause of AIDS' they were so keen to promote was also most probably a vaccine contaminant, and that, as I hope to show, we were merely seeing a re-run of the SV40 fiasco, with infinitely wider implications. 

By 1998, SV40, the carcinogenic monkey virus known to have infected millions of humans via dirty vaccines, had come back to haunt us nearly forty years later.  Phyllida Brown reported in New Scientist (24.8.96, p.16) that a mechanism had recently been demonstrated whereby reactivated SV40 might be responsible for a lung cancer, mesothelioma, more frequently associated with asbestosis.  Other researchers linked rare bone cancers and brain tumours with SV40.  However, Ms. Brown's report wisely cautions that SV40 may merely be an "innocent bystander".  In a later update (New Scientist, 1.2.97) Prof. Robin Weiss, a leading British AIDS expert, predicted that further tests will confirm the presence of SV40 in samples from mesothelioma patients: "...But whether it causes cancer we just don't know."  What is beyond doubt is that simian viruses could and did contaminate poliovaccines, and could and did infect human cells - permanently. 

Much debate now centres on whether SV40 is causing or contributing to the cancers after many years of latency, or is merely a reactivated harmless passenger virus.  I take the latter view, and that SIVAGM  contaminated subsequent batches of poliovaccine in exactly the same way, only to emerge years later as a harmless passenger active in people who are immune suppressed for other reasons.  Indeed, SV40 can be exonerated from causing human cancers for some of the same reasons given by Peter Duesberg for HTLV 1 not being the cause of leukaemia in his ground-breaking paper in Cancer Research (1.3.87). 

In 1994, I attended a lecture by Prof. Weiss in Oxford in which he responded to a question by admitting that the 'HIV'-contaminated vaccine theory was scientifically feasible.  On January 16th 1997, the British Government withheld permission for xenotransplants, the use of animal organs in human replacement surgery, until further research is carried out into the dangers of animal viruses infecting the patient.  Interviewed on TV that evening, Prof. Weiss explained that hitherto unknown animal viruses could be transmitted in animal organ transplants, as they could not be 'screened out'.   In writing on the dangers inherent in xenotransplants, Frederick Murphy, Dean and Professor of Virology at UC Davis, acknowledges that despite heat and irradiation treatments of animal sera , "...viruses occasionally survive such treatments." 5 

Nature (13.3.97 p.126) gave a more specific warning of the dangers of transmitting "Type C retroviruses" in animal transplants.  The article by Jonathan Stoye explains that animal viruses may be ecotropic, meaning they can only infect animals of the same species; or xenotropic, meaning they can infect the cells of other species.  SV40 was obviously one of the latter category and there is mounting evidence that SIV (Simian Immunodeficiency Virus), another xenotropic monkey virus, infected humans, on a world-wide scale, in poliovaccines from 1961 for some 25 years until at least 1985, and perhaps later.

Why 'retroviruses'?

Historically, by 1984 virology had moved on several notches since the discovery of SV40 in 1960.  A previously studied but incompletely understood group of viruses shot to the forefront with the discovery in 1970 by Howard Temin and his colleagues of the phenomenon of reverse transcription and the enzyme reverse transcriptase, and the name 'retroviruses' was coined to describe RNA viruses which encoded this enzyme and uses it to effect infection, integration and replication.  Throughout the 70's, most 'retrovirologists' were convinced that their pet viruses would prove to be the cause of everything from human cancers to multiple sclerosis, but all to no avail.  'AIDS' was  to be the saviour of the retrovirologists, however many virological, microbiological and epidemiological rules they had to bend or ignore to shoehorn 'HIV' in as the qualifying causative agent. 

From the outset, 'HIV' was claimed to have genetic similarities to previously studied animal retroviruses classified as 'lentiviruses', because they are alleged to cause disease slowly - maedi visna virus in sheep,  encephalitis-arthritis virus in goats and equine infectious anaemia virus in horses.  The whole concept of 'slow' viruses is highly suspect, and as Peter Duesberg has said, "There are no slow viruses, only slow virologists."  However, 'HIV'1 and a virus subsequently found in West Africa, 'HIV'2, were classified as lentiviruses.  This ruse was adopted to explain the variable time lag between infection with 'HIV' and the appearance of AIDS symptoms, currently thought to average some 11 years.  However, again as mentioned by Duesberg in Continuum, an unknown time lag between infection and disease is one of the classic hallmarks of a harmless passenger virus

'HIV'2, the second 'human immunodeficiency virus' found soon after 'HIV'1 and thought to have originated in West Africa, differs genomically sufficiently from 'HIV'1 for it to be considered a separate virus.  'HIV'2 is considered less pathogenic than 'HIV'1, and is mostly found in healthy people, of both sexes.   An SIV found in sooty mangabey monkeys (SIVSM), also common to West Africa, has a very close genetic similarity to 'HIV'2, but I have no evidence of that species having been used to make vaccines.  However, sooty mangabey monkeys exported from West Africa for animal experiments were known to have caused fatal infections in other species in primate research centres in the US since the early '60's.5  It is quite possible that their strain of SIV found its way into vaccines via this accidental spread to other species of primates, including rhesus macaques.  In addition, Charles Gilks mentions in Nature (28.11.91, p.262) that sooty mangabey blood was directly injected into human volunteers during research into primate malarial parasites and may thus have spread SIVSM to humans. Moreover, as I hope to show, all sorts of simian viruses contaminated laboratory cultures in the US and elsewhere with  monotonous regularity, as Robert Gallo found to his embarrassment in 1975.

Why 'SIV's?

Since their isolation in the mid-'80's, Simian Immunodeficiency Viruses (SIV's) have been very closely studied for clues about how 'HIV' causes AIDS.  At least five monkey species carry SIV in the wild (claims of natural infection of chimpanzees are suspect, see below), but none of these naturally SIV-infected lower primates except the African green seems to have been used in the regular production of human poliovaccines.  Intensive study of the various SIV's shows that despite the considerable genetic differences between 'HIV'1 and SIVAGM, all the global subtypes of 'HIV'1 (currently at least ten) have more in common with the SIVAGM than any other SIV.  Research into the SIV's further shows them all to remain harmless, classic passenger viruses in their natural hosts. 

We are assured that although related, SIVAGM differs sufficiently - >50% - in its genetic makeup from 'HIV' to rule it out as the precursor of the 'human' virus.  Many papers have been published minutely detailing the genetic differences in the two viruses, replete with all sorts of arcane jargon, philogenetic trees etc.  However, this comparison is illogical, as 'HIV' is believed to be mutating rapidly, often an indication of a recent change of host species.  Current research shows that 'HIV subtypes' already vary world-wide in their genomic structure by 30% (WHO figures) and 40% (Eleopulos et al, Continuum).   As it is widely supposed that 'HIV' is hypermutant and can readily hybridise and genetically recombine with other viruses as well as with its own quasispecies, this may explain why individuals can have so many different strains of 'HIV' simultaneously, dependent on any other vaccines or infections they have received, as well as their own specific genetic susceptibilities.  So quickly does 'HIV' mutate that it was acknowledged ten years ago that there is no such thing as a typical 'HIV' viral isolate . (Science, 26.8.88, p.1039)  Thus, logically there can be no universal Gold Standard 'HIV' test because there is no universal Gold Standard 'HIV' isolate. 

Instability may be the hallmark of a virus in the process of speciation - adapting to survive in a new host species - but research (Johnson et al, J.Virol. 1990; 64: pp 1086-1092) has shown that SIVAGM  also has a high degree of heterogeneity in the various different isolates found in the four different varieties of African green monkeys from different parts of Africa, plus a high degree of mutability, comparable to 'HIV' in humans.  This leads researchers studying why SIVAGM does not cause disease in African greens to conclude that SIVAGM's mutability per se cannot be the cause of disease in its natural host, although 'HIV''s mutability has been proposed as a cause of AIDS in humans.  Thus, to measure the two 'moving target' genomes of 'HIV' and SIVAGM against each other is as misleading and meaningless in percentage terms as comparing two whisps of smoke.

To complicate matters further, it is now common laboratory practise to co-infect human cell cultures with 'HIV'1 and SIVAGM or  SIVSM, forcing a shotgun wedding between the two allegedly different viruses. The artefact offspring of this union, known as 'chimeric viruses', are named 'Simian-Human Immunodeficiency Viruses', (SHIV's).  Whether there is a 'typical' genome of a SHIV is a moot point, but Jon Cohen's description is worth noting: "SHIV is the monkey virus SIV dressed in the outer, or envelope, proteins of the human AIDS virus." 6, (my italics.)  This is also a pretty accurate description of 'HIV' if my hypothesis is correct, and is consistent with an animal virus adapting to a new human host, because the envelope proteins are most immediately subject to change as the virus mutates to survive in its new host environment.  I propose SHIV is merely the result of adding 'HIV', i.e. partially human speciated SIVAGM, to the original SIVAGM  taken directly from the monkey, and recombining them genetically in human cells.  Thus a 'SHIV' is merely SIVAGM doubly passaged through human cells. 

Research by Ronald Desrosiers et al, published in Science (1.6.90) found that as well as the essential Gag, Pol and Env genes found in all conventional retroviruses, 'HIV' and SIVAGM have very similar non-essential, or supernumerary genes, including Tat, Rev, Vip, Vpr and Nef.  It seems unlikely that two highly mutable viruses, independently evolving over thousands of years, in different species, would have picked up or deleted the same supernumerary genes by chance, as Essex and Kanki acknowledged in their Scientific American article two years earlier in October 1988. 

It has been argued that SIVAGM cannot be the precursor of 'HIV' because the monkey virus has a specific gene, VPX, which is absent from 'HIV', which has instead a gene called VPU, which is genetically quite similar.  On the other hand, 'HIV' 2 and SIV from sootey mangabeys both have a VPX gene.  These genes are supposed to have something to do with aiding the viruses to infect simian and human macrophages.  However, retroviruses are very adept at dropping genes not necessary for their survival, so perhaps 'HIV' 1 can survive better in humans by shedding its VPX gene, or mutating it to VPU.

Linkage of AIDS to vaccines.

Once the WHO decided on the extermination of smallpox, saturation vaccination campaigns were mounted world-wide, and the disease was declared globally eradicated by 1979.  Starting on 11 May 1987, the Times ran a short series of articles raising the possibility that AIDS was a man-made disaster "triggered" by the WHO anti-smallpox campaign.  That story was in part based on a recent report of a US army conscript, from no known 'risk group', who had rapidly developed an AIDS-like illness and died, shortly after being given, among others, a smallpox vaccination on induction.  Even after civilians were no longer considered at risk of smallpox, troops were still routinely vaccinated against it as a precaution against possible use of smallpox as a germ warfare weapon by an enemy.  When a global map of the world's AIDS hotspots, particularly in the Third World, was superimposed over another map of the most intense anti-smallpox vaccination areas, the two tallied very closely.  (The same theory fits the global concentrations of anti-polio vaccination even more closely.)  Significantly, when Robert Gallo, who originally claimed to have discovered  the 'AIDS virus', was asked to comment by the Times on the suggestion that smallpox vaccinations may have triggered AIDS, he gave an enigmatic reply: "...I have been saying for some years that the use of live vaccines such as that used for smallpox can activate a dormant infection such as HIV." (The Times, 11.5.87, my italics)  He makes no mention of live poliovaccines, but they had been widespread since the late '50's.  However, he does acknowledge that 'HIV' infection can remain dormant until activated by other factors.  The key words are 'activate' and 'dormant'.

In 1988, I met Mme. Simone Delarue, an anti-vaccinationist seeking to repeal French compulsory vaccination laws, citing evidence of damage caused to children by vaccines.  When she raised the possibility with the French Health Ministry that 'HIV' had been a contaminant in poliovaccines made using African green monkey cells, a spokeswoman wrote back, reassuring her that the French vaccine producers stopped using African greens in 1982, and switched to the 'patas rouges' species. (Mme. Delarue, personal communication.)  Why the sudden switch from greens to reds?  I suggest that when what was claimed to be the first 'human' retrovirus, HTLV-1, thought at that time to cause leukaemia, proved to be  >90% homologous to a simian retrovirus, STLV, found in 1982 in Japan, the French decided to be cautious and change species.  Negligence suits can be expensive!  The French must have congratulated themselves on their prescience when it was subsequently claimed by Myron Essex et al (Scientific American, October 1988), that whereas both STLV and SIV infect a high percentage of wild caught African greens, neither retrovirus is carried by wild-caught patas rouges.

As a further result of meeting Mme. Delarue, I was contacted by two desperately worried Native American women, Bernadine Aitcheson and Mary Ann Wells, who belong to the Dena Ina tribe in Alaska.   They were seeking international help, because the children in the tribe had been forcibly co-opted into a US Government Hepatitis B (HBV) vaccine trial at school, and many of the previously healthy children had been infected with Respiratory Syncytial Virus (RSV), with many falling ill with acute lung disease, and there were several deaths.  There was a strong probability that the HBV vaccine had been contaminated with RSV.  I remembered that many of the original San Francisco and New York PWA's had earlier volunteered for HBV vaccine trials in the late 1970's.  Could it be that what was being diagnosed as PCP was due not to the PC fungus but RSV contamination of their HBV vaccine?   RSV and PCP pneumonia are so similar that careful differential diagnosis is strongly advised 7.  There is also evidence to suggest that RSV infection can reactivate dormant 'HIV' 8, as can subsequent infections with herpes viruses etc.9, and even SV40 may have a role to play in 'HIV' expression due to a degree of homology between 'HIV''s LTR and SV40's "core transcriptional enhancer elements." 10

The Kyle article.

By 1992, I was no longer interested where 'HIV' came from - Peter Duesberg's arguments had totally convinced me that 'HIV' was harmless.  Moreover, no animal retrovirus is known to be characteristically sexually transmitted.11  My interest in the vaccine origin of 'HIV' was reawakened when that most orthodox journal The Lancet (7.3.1992, pp 600-601) published an article by Walter S. Kyle, in their Viewpoint feature, called "Simian Retroviruses, poliovaccine, and the origin of AIDS." 12.

Kyle describes how an analysis of three samples of Sabin live virus poliovaccine, manufactured by Lederle, and carried out by the US Bureau of Biologics (BOB) in 1976, had revealed viral contaminants visible under electronmicroscopy, subsequently confirmed as ''Type C RNA viruses'' - virologyspeak for retroviruses.  Action was taken at the highest level.  After an "unprecedented" deliberation of twenty months, a specially appointed US Government committee, with the full co-operation of the National Institutes of Health, the Food and Drugs Administration, and BOB, gave the go-ahead to use the vaccine, providing the manufacturers guaranteed to limit the number of contaminant retroviral particles to no more than 100/ml in future lots from a previously estimated level of 1000-100,000/ml.  Everyone concerned, up to governmental level, had seemingly acted in the interests of public safety.  

As for the millions potentially already exposed to such contaminants for some fifteen years...?  At least the US government had made an attempt to lock the stable door, however belatedly.  Those retroviral particles must have been deemed neither carcinogenic nor cytopathic, and harmless to humans in such a small dose, or the vaccine would not have been cleared for take-off.  Lederle, a company of the highest possible reputation, both then and now, openly used African Green monkey cells in the production of their vaccine in 1976.  If any companies manufacturing live poliovaccines subsequent to that enquiry still allowed contaminant retroviruses in their product, it would only have been on the advice of the highest scientific authorities, and subject to very stringent government restrictions, so obviously no blame can be attached to the manufacturers.  Similarly, the late Albert Sabin cannot be 'blamed' for the contamination of the vaccines referred to by Kyle as "Sabin virus vaccines."  Sabin, and Hilary Koprovsky, merely worked on the development of the three live, attenuated poliovirus strains used in the vaccines, and were not responsible for the manufacturers' methods of production.

Kyle mentions that the 'Type C RNA viruses' were not specified in 1976, so it could be argued that SIVAGM, an alleged 'lentivirus', has not been proved to be in the vaccine.  However, the test used to confirm 'Type C' RNA viral infection, a recently (1975) devised 'reverse-transcriptase activity' assay, would not distinguish between Type C, or lentiviruses, or spumaviruses (nor, incidentally, from the hepatitis B virus which also replicates using reverse transcriptase, which was not realised in 1976, when RT activity was wrongly considered the sine qua non of retroviral infection).  Moreover, no-one isolated or characterised African green SIV until 1985. 

By 1994 Robin Weiss stated quite clearly that all the known SIV's infect human lymphocytes, utilising the same CD4 cell receptor as 'HIV' 13, and there is evidence that at least two SIV researchers have been infected by accidental needlestick injuries. (New England Journal of Medicine, 20.1.94, pp209-210)  It is also a certainty that those 'unspecified' viruses would have been subjected to intensive and continuous study long after 1977, if the SV40 precedent was anything to go by.  Kyle states that such contaminant retroviral particles were subsequently found, using PCR, in poliovaccines manufactured as late as 1985, and perhaps later. 

The 1976 US government committee must also have been made fully aware of the outbreaks of disease since the early '60's in primate research centres throughout the country in California, Oregon, New England, Washington etc.  Monkey species imported for research purposes from Africa and Asia which would never have encountered each other in the wild, were being housed together in these centres, and in transit facilities.  Inevitably, they transmitted disease causing agents one to another. 4,5  These diseases had been observed since the '60's, so with the revelation that simian retroviruses may have contaminated poliovaccines in 1976, and by implication for many years before that, memories of the SV40 débacle rang warning bells loud enough for the US government to take action. 

By 1984 and the awareness of AIDS, these simian diseases had been studied in some detail, and were classified as Simian AIDS (SAIDS), and the hunt was on to find a causative agent.  A paper on SAIDS 14 written in 1984 is well worth re-reading in 1999.  The sick animals, rhesus macaques, developed 'AIDS-like' symptoms within months and died  - but, unlike human AIDS, with no long incubation period, and no neutralising antibodies.  Most importantly, there was no evidence of sexual activity between animals of different species sharing the same pens.  Many of the sick macaques were less than one year old and not sexually active, and inter-species sexual activity was not observed.  Moreover, some of the disease symptoms in the macaques correlated with reactivation of SV40, including brain diseases.  In late 1984, the first SIV was found in the blood of the diseased macaques, and later shown not to be natural to the species in the wild.  The macaques were thus infected since their captivity.  At the same time, these macaque SIV's were shown readily to infect human lymphocytes.  By 1985 it was found that the macaques had been infected in captivity with SIVAGM from naturally infected African greens.

Kyle's paper is based on the orthodox assumption that 'HIV' is the ipso facto cause of AIDS.  However, Kyle believes that the preponderance of gay cases resulted from repeated monthly doses of potentially SIVAGM contaminated live Sabin poliovaccine, from 1974 onwards, as a treatment for genital herpes lesions, particularly widespread in gay men in the United States 12.  The late Rock Hudson appears to have used the poliovaccine for this purpose (Root-Bernstein, Rethinking AIDS, page 185).  I never heard of such an unorthodox use of the vaccine being practised in Europe, but the gay preponderance of AIDS was and is just as marked in Europe and Australasia.  Incidentally, in the mid '80's, a US patent was granted for the use of typhoid vaccine to treat PWA's. 

Another important possible reason for the apparent preponderance of male 'HIV' infection in developed countries has been overlooked by Kyle - compulsory male military service.  Countries with military service routinely give a whole battery of vaccinations on induction, including poliovaccine, to young conscripted men (see Times article mentioned above), as well as to enlisted men (and a smaller number of women who enlist).  Thus, in any year in countries with compulsory infantile poliovaccination and conscription, two generations will have received potentially contaminated vaccines simultaneously - newborns of both sexes, and 17-19 young, principally male, adults.

There are two possible reasons why Britain has detected less 'HIV' infection than, for example, France, despite a comparable percentage of people in 'risk groups'.  Firstly, Britain has never had compulsory poliovaccination.   Secondly, Britain abolished conscription in the early '60's at about the same time that African green-generated poliovaccines came into widescale use, so that particular revaccination threat would not have been a problem.  Moreover, Britain's own Burroughs-Wellcome was one of two companies listed in 1994 as using the safer human diploid cell lines in the production of their poliovaccine mentioned by Kyle 12.  However, Britain has also been heavily dependent on imported poliovaccines from countries where African green monkey cells were standard in their manufacture.

In a letter to The Lancet (4.4.92, p.867) Thomas F. Schulz, of the Chester Beatty Cancer Institute, commenting on Kyle's article 12, says with reference to the contaminant particles seen in the electronmicrographs in 1976: "However, it is uncertain whether the viral particles observed by electronmicroscopy and reverse transcriptase assays were indeed SIVAGM.  They may have represented endogenous retroviruses (retroviral genomes carried in the germline for millions of years and activated and packaged into virion particles under the conditions of tissue culture)." (my italics)   It is worth considering that all sightings of similar ambiguous particles in electronmicrographs may merely represent endogenous artefacts specific to the cell culture rather than transmissible, reactivated exogenous viruses.  Purported 'HIV' virions shown in electronmicrographs are invariably obtained from chemically stimulated cell cultures, usually involving cancerous cell lines, and invariably accompanied by miscellaneous debris, as Lanka and Eleopulos et al have established in previous issues of Continuum.  Whether they are exogenous retroviral particles or endogenous cellular epiphenomena resulting from tissue culture techniques is a matter of conjecture, as Schulz's letter suggests.   Indeed, recent research (Science, 19.6.98, p.1883) states that none of the SIV's so far found is endogenous in its original host.  However, the fact remains that whatever the precise biological nature of these 'particles', morphologically similar examples have been seen in human and simian cell cultures, as well as directly in cell-free vaccines produced for human consumption, made using African green monkey cell cultures. 

In a recent issue of Continuum, Val Turner refers to George Todaro's statement that given enough time and ingenuity, any researcher could make retroviruses appear in any uninfected cell culture.  This being the case, it is quite possible that the process of incubating polioviruses in ostensibly unifected simian cells could dislodge, dredge up or reactivate previouly latent retroviruses endemic in that species - and pass them on as exogenous, infectious contaminants in poliovaccines.  After all, exogenous viruses, retro or otherwise, have to start somewhere.  As already stated, so far all the known SIV's readily infect human lymphocytes.

Whilst Kyle's Lancet article was largely ignored by the popular press in Europe, US freelance journalist Tom Curtis wrote a long article for Rolling Stone (19.3.92) with the provocative title "The Origin of AIDS.  A startling new theory attempts to answer the question 'Was it an act of God or an act of man?' ".  Several US papers also took up the story.  This forced the Wistar Institute of Philadelphia, for whom Hilary Koprowsky had developed a live virus vaccine tested in Africa in the late '50's, to take action, and they sponsored a committee to look into the theory.  The result, in October 1992, was predictable - the Wistar vaccines were cleared.  All three main arguments used by the committee to exonerate the vaccines were specious and shown subsequently  to be scientifically dubious or wrong.  However, the Wistar committee did strongly recommend that monkey cells, which SIV expert Ronald Desrosiers compared to a 'ticking time bomb', no longer be used in vaccine manufacture.  Many experts were doubtful about the findings of this enquiry due to the paucity of the early vaccine samples available for analysis.  The same year Myers et al published an article in 'AIDS Research and Human Retroviruses' (1992 8: pp.373-386) suggesting that 'HIV' might simply be "SIV adapting to a human host", albeit with the caveat:  "There is no clear answer to this question at this time; however, the notion is less far-fetched in 1992 than it was merely a few years ago..." (My italics.)

A fascinating editorial by Prof. Raanan Gillon coincidentally appeared in the Journal of Medical Ethics in the same year as Kyle's paper appeared in The Lancet. (JME, Vol.18, 3-4, 1992)  The title was "A startling 19,000 word thesis on the origin of AIDS: should the JME have published it?"  In a very frank and fair article, Prof. Gillon outlines an hypothesis by Louis Pascal, originally written in 1987, and subsequently expanded.  As Gillon states "... it is Louis Pascal's thesis that the monkey kidneys used (in the production of the vaccine) were infected with Simian Immunodeficiency Virus, SIV, a retrovirus very similar to HIV, and that the SIV contaminated the oral polio virus vaccine."  Prof. Gillon rightly points out that The Journal of Medical Ethics is not an appropriate journal for such an article, but felt compelled to bring the paper to public attention.  The address to write to for Pascal's paper is appended to the references.(*)

A British enquiry about retroviruses and poliovaccines.

The Lancet (9.10.93, pp.932-933) published a detailed report by Garrett, Dunham and Wood of the British National Institute of Biological Standards and Control.  Using PCR, they "found no evidence of HIV or simian immunodeficiency (SIV) gene sequences in 15 pools of oral poliovaccine prepared on monkey kidney-cell cultures and released for use by four manufacturers in Europe and North America between 1975 and 1984."  Their negative findings were challenged by Ellswood and Stricker (The Lancet, 1.1.94) who claimed their illustration "...does not support this conclusion."  The British report carefully does not specify either the manufacturers or the species of monkeys used in the making of the vaccines.  However, they mention in passing that the WHO had recommended only as late as 1989 that monkeys positive for SIV antibodies should not be used to make vaccines.   (See Morosov and Lagaye findings below.)

Garrett et al also sought to show "the ability of primary monolayer cultures of monkey kidney cells to support the replication of HIV and the likelihood that SIV would contaminate cell cultures prepared from SIV-infected monkeys under conditions used for the commercial production of poliovaccines."  Unfortunately, their methodology seems completely inappropriate. They prepared monolayer cultures of kidney cells from "uninfected cynomolgus monkeys" - they do not mention that cynomolgus monkeys are never infected in the wild, and thus the species was completely inappropriate for use in this context.  They also used as controls kidney cells taken from cynomolgus monkeys deliberately infected with an SIV taken from rhesus macaques (SIVMAC), another species only ever found to be exogenously infected with SIV in captivity by African greens or sooty mangabeys. (14)   Thus their SIV-infected control cells might be seen as an artefact of a double zoonosis, involving two species of monkey never found to be infected in the wild.  Why they did not use the cells of wild-caught African greens, both uninfected and  infected with SIV they do not explain, despite these being the standard cells used in most poliovaccine manufacture since 1961.  Ellswood and Stricker also point out that although Garrett et al were unable to detect SIV infection in their kidney cultures, other researchers had found SIV in the kidney cells of rhesus and pigtail macaques after deliberate infection.  Garrett et al further state that exposure to trypsin would have killed off any SIV present in the kidney cell cultures.  Again, Ellswood and Stricker question this.  However, what Garret et al do not mention is that trypsinisation and all the other standard precautions taken by vaccine manufacturers had not previously prevented vaccines from being infected with SV40.  Neither do they offer any comment on the "Type C RNA viruses" in the Lederle vaccines.

Predictably, their 'HIV' isolate failed to infect the cynomolgus kidney cell cultures - because 'HIV' never infects lower primates, including African greens, for two possible reasons.  Firstly, if 'HIV' is SIVAGM partially speciated to humans, changes in the surface glycoproteins may prevent infection of lower primate cells.  To date, researchers have never been able to establish systemic 'HIV' infection in vivo in lower primates.  There is also the possibility that mass-produced vaccines may not have been so scrupulously prepared on purified kidney cell monolayers as the Garrett et al experiments, and residual SIV-infected lymphocytes could well have been present in the culture flasks typically used in mass production. 

A better designed experiment would have been to prepare and manufacture a finished poliovaccine, faithfully copying the standard manufacturing procedures, and using all three different attenuated poliovirus strains in proven SIVAGM-infected kidney cells.  This would then perhaps clarify whether SIVAGM might recombine genetically with any of the poliovirus genes, or spontaneously delete its VPX gene (see above) during infection of human cells.  Only then could they be sure of their findings.  As Jay Levy, the third person to isolate 'HIV', has stated in 1993, 'HIV' has been shown to recombine genetically with several other viruses in human cells.

Obviously, many batches of vaccine may very well have been free of such contaminants, depending on their manufacturers' methods as Garret et al's study appears to show, but it is worth remembering that even post-1960, when vaccines were supposedly clear of SV40, there was still no assay alleged to identify activity by retroviruses until 1975 12.   Just how many people have an undetected, systemic, dormant but potentially productive SIVAGM infection as a result of vaccine exposure has still to be ascertained, but the authorities are understandably reluctant to look into the matter, at least publicly.  Logically, the numbers of SIVAGM infectees should be even higher than those infected with SV40, as the African green generated vaccines were in use for at least a quarter of a century - as stated, Kyle suggests that retrovirus-contaminated vaccines were being made as late as 1985 (12). 

It is believed that retroviruses have a very high failure rate - that they generate many non-infectious or replication-defective particles, due to error-prone transcription from RNA to DNA.  Thus only a small percentage of people exposed to SIVAGM will be systemically and/or productively infected, although repeated exposure to contaminated vaccines would have increased that risk.  As David Rasnick has shown (Continuum), > 99% of 'HIV' particles detected in 'viral load tests' are non-infectious, so the chance of horizontal transmission between humans is extremely remote.  Moreover, even the less than 1% of particles which may infect cells have a high failure rate in that they may not be capable of replication. I propose that it is easier for a simian virus to infect humans via a vaccine than for humans to transmit zoonotically-acquired integrating viruses to each other, as typified by SV40.  There is no evidence that SIVAGM/'HIV' has entered human germ-line cells as described by Thomas Schulz (see above), further suggesting its recent simian origin.

Does the distribution pattern of SIVAGM/'HIV' fit the theory?

When I outlined my hypothesis to Peter Duesberg, he cut straight to the chase, as any good scientist should.  "The distribution pattern doesn't fit!", meaning since the introduction of retrovirus-contaminated live poliovirus vaccines, starting in 1961, both sexes would have been exposed to them; however, apparent infection with 'HIV' was and still is predominantly male (90%) in the West, albeit using flawed 'HIV' testing procedures.  A vaccine contaminant should have resulted in as many female as male infections, similar to the profile alleged to be present in Africa and elsewhere.  To this extent Peter is obviously correct.  Moreover, in the West even in males the contaminant particles seem to have been selective of infants who would prove to be gay, or become drug addicts or were born with haemophilia, which is patently ludicrous. 

On reflection, I question Peter's damning objection.  The 'distribution pattern' is judged by detectable, i.e. active infections, those provoking an antibody response.  However, a long, latent infection would not necessarily be detectable by antibody response unless reactivated.  Resting cells do not produce retroviral particles, but activated cells do - at least in cell culture.  Consequently chemicals known as mitogens have to be added to cell cultures, to activate the cells and force them to express virus.  It is known that some recreational drugs, cocaine for instance, are powerful mitogens, and could have the same effect in causing virus expression in vivo as other plant-derived mitogens - PHA, Con A and pokeweed mitogen - in cell cultures. It is my contention that 'HIV' infection is infinitely more widespread than 'HIV' tests reveal.  What 'HIV' antibody positivity tests show, if they are to be trusted at all, is a reactivated as opposed to a dormant infection, leaving the true number of dormant infections unknown.  A distinction must be made between  undetected dormant infections, and apparent reactivated infections.  The difference lies in 'risk' behaviour.

The 'risk' implied in the categorisation of 'high risk' groups has always been supposed to be a risk of infection with 'HIV' via 'unsafe sex', dirty needles, contaminated blood products and transfusions etc.  This supposition may always have been wrong, and no more likely than the horizontal spread of SV40 by the same routes.  I propose that it has never been a question of the 'virus' spreading - that had regularly and efficiently been achieved since 1961 as a contaminant in an as yet unknown percentage of poliovaccines.  What are spreading are reactivating factors, spread by chiefly male risk behaviour (drugs, STD's etc.); and the use of unreliable 'HIV' antibody testing kits.  The vaccination against polio was global in its scope, so the more the 'HIV' test kits spread, the more antibodies, mostly not even 'HIV' specific, will be found in people infected by a retrovirus-contaminated vaccine, and then subsequently exposed to extensive reactivating antigenic exposures, including other vaccinations. (See smallpox vaccination and Gallo's comment above.)  This would seem to be confirmed by an article in AIDS Research and Human Retroviruses, (Vol 14, 9.6.1998, pp 727-734) featuring a paper by Clerici et al which shows that "Vaccination of HIV-infected individuals increases viral load, reduces CD4 cell counts, and might influence disease progression."

Where infection with SIVAGM occurred, it would have been at a very low level, and rapidly restricted to latency by cellular and humoral immune responses.  However, where integration of the retroviral genome occurred, the infection may have become persistent, just as with SV40.  I propose the real 'risk' in the so-called 'risk groups' has always been merely the risk of reactivation of a previously undetected dormant infection, by factors such as STD pathogens (herpes viruses, hepatitis viruses etc.); the mitogenic effects of drug use; alloantigens in blood and blood products, and subsequent vaccinatory antigenic challenge.  Most of these 'risks' are still principally found in males in the West, although drug addiction in females is on the rise.  It is commonly supposed that STD's increase the risk of 'HIV' infection, although no-one has been able to demonstrate a mechanism to support this.  However, perhaps STD's should be seen as reactivating factors of an already present but dormant SIV infection 8,9,10 .

Are the scientists being honest?

The implications of Kyle's article 12 are profound, and reveal the lengths that governments and some scientists will go to in order to mislead or misinform the public in the interests of damage containment.  Prior to the late 1970's, despite the most intense searches carried out by virologists and oncologists, led by Robert Gallo at the US National Cancer Institute, there was no trace of any form of 'human' retrovirus.  Gallo admits that he was originally derided by his colleagues in his hunt for a retroviral cause of human cancer, similar to the retroviruses thought to cause cancers in some laboratory animals.  He was warned that even if such viruses could be found, they would prove to be irrelevant to human disease, as Peter Duesberg so convincingly proved in 1987 (Cancer Research, 1.3.87).  Gallo's first excited discovery of such a virus resulted in bathos in 1975, when it was shown to be a mix of three monkey viruses which had 'somehow' contaminated his lab cultures of human cancer cells.  Moreover, the antibodies raised by this virus, "HL23V", were shown not even to be virus specific.  Note - contamination, monkey viruses and human cells, and a presage of things to come. 

A series of quite amazing coincidences started soon after the US Government gave retrovirus- contaminated vaccines official sanction in 1977.  Within a year, Robert Gallo 'discovered' the first 'human' retrovirus in 1978 in human cancer cells, which he called Human T-cell Lymphoma Virus (HTLV 1).  Almost simultaneously, Japanese researchers also found an HTLV endemic in Japan.  It was later shown the same virus was endemic in humans in Central Equatorial Africa, the USA and the Caribbean.  Subsequently, in 1985 a virus was found in African green monkeys 95-100% homologous with both the American and Japanese HTLV's, and later called  STLVAGM.  The Japanese correlated their discovery of HTLV with a recently found (1977!) rare form of leukaemia in the elderly, and Gallo's HTLV was pragmatically metamorphosed into a 'Human T-cell Leukaemia-Lymphoma' virus.  Thus, starting with HTLV 1, eager retrovirologists, including the usually punctilious Japanese, driven by their desire to find a 'human' retrovirus which 'causes' cancer, ignored the cardinal rule of aetiology - correlation does not prove causation! 

The important question was - how could African green monkey STLV have got into the Japanese human bloodstream to the extent of being heavily endemic in the southern two islands, and oddly, the Ainu people in the far north of Japan?  Gallo's proffered 'explanation' (Scientific American, Dec.1986), must rank as one of the most baroque, bare-faced pieces of obfuscation ever perpetrated by an alleged scientist.  He suggested that Portuguese traders had taken African slaves and monkeys to southern Japan in the 16th century, thereby spreading HTLV/STLV, even illustrating his theory with a contemporary Japanese print depicting Europeans with black servants and pet monkeys.  He must have been well aware of the findings of the 1976 poliovaccine enquiry, being a retrovirologist working at the NIH at that time, but he never once alluded to a possible vaccine origin for HTLV in humans.  It's as if the ludicrous Portuguese traders theory was artfully designed to pre-date the HTLV infection in Japan and elsewhere by several hundred years, safely deflecting attention from an STLVAGM vaccine contamination connection.  In doing this, Gallo set the precedent for demonising black people for spreading 'their' HTLV which was to be repeated with 'HIV', when Africans, Haitians, Afro-Caribbeans, Afro-Americans, gay men, prostitutes and drug addicts were 'blamed' for infecting each other, and everyone else, with 'HIV'. 

Japan mounted massive vaccination campaigns to deal with their severe post-WW2 polio and smallpox epidemics; and some of the largest tests of live poliovaccine ever mounted were carried out in Sub-Saharan Africa using both Sabin and Koprowsky live virus vaccines.  None of this was mentioned by Gallo in 1986, nor by Essex and Kanki in their Scientific American article already cited.  They repeatedly scratch their heads wondering how SIV and STLV could have infected humans on such a wide scale, but never once mention vaccines, although both are close colleagues of Gallo and must have been just as aware of the Lederle vaccine enquiry and its findings.   So wide scale has been the use of live virus poliovaccine in some parts of Africa since 1961 that there is a claim that certain countries on that continent may now be poliofree. (The Lancet, 1.1.94, p.51) 

It can be argued that whereas the Japanese have high endemic levels of HTLV 1, they have relatively little 'HIV' infection, and were therefore not exposed to vaccines made using African green monkey tissues, i.e. imported US vaccines.  There are several possible explanations for this apparent lack of 'HIV' infection.  One is that the degree of risk behaviours common in the West were slow to spread to Japan, a conservative, fastidious country, and therefore they may have a concealed, dormant endemic 'HIV'.  It must be remembered that the 'AIDS test' claims to identify antibodies to activated 'HIV'.  If risk behaviours are minimal in Japan, then the latent 'virus' will not be found except by mass PCR screening.  Like most developed countries, Japan has a growing drugs problem, so 'HIV' may well start to show up in the near future.  This would seem to be borne out by a report in a Japanese newspaper.  After commenting on the apparent fall in deaths from AIDS in the US, the article goes on:  "However, the trend is in the other direction in Japan, where deaths from AIDS, the numbers of AIDS patients and HIV carriers are all on the rise." (The Daily Yomiuri, May 14, 1997, p.2)

Another possible explanation for the high HTLV1 but low apparent 'HIV'1 profile may be that Japan, like more than a dozen other countries world-wide, makes its own vaccines, incorporating the three standard attenuated poliovirus strains developed by Albert Sabin.  Rather than import African or other  monkey species for tissue cultures, they may have used the kidney cells of the native Japanese macaque, which was found in 1982 to carry an STLV 90+% homologous to HTLV.  Subsequently the Japanese macaque was found not to carry an SIV.  Thus the home produced vaccines might be contaminated with STLVJM but not SIVAGM.  This always assumes, of course, that the early HTLV1 tests did not cross-react with 'HIV' proteins, and that the Japanese study cited by Duesberg (Cancer Research, 1.3.87) showing 600,000 Japanese HTLV1 seropositives were not a mixture of 'HIV'1 and HTLV1 antibodies, which are known to crossreact.

The US vaccines mentioned by Kyle ran the risk of contamination with both viruses, and similarly produced vaccines were widely manufactured, exported and tested, in Europe, Africa, South America and the Caribbean.  In the mid-'80's, many people in these countries were found to have antibodies to both HTLV 1 and 'HIV'.  For example, Luc Montagnier, who led the team which first 'found' 'HIV', stated in 1984 at a presentation at Cold Spring Harbour that amongst his French 'HIV' (LAV) infected cultures, 13% were also infected with HTLV 1.  (Steve Connor, New Scientist, 12.2.87)

How long has 'HIV' been in humans?

In the 1995 book Molecular Basis of Virus Evolution 15, there is a chapter on The Human Immunodeficiency Viruses by Sharp, Burgess and Hahn.  The chapter is just as interesting for its admissions as for some significant omissions about the origins of 'HIV'.  In a table listing 'Primate Lentiviruses', HIV's 1 and 2 are categorised as not "natural" to their human host - in other words a recent addition to the human bloodstream - "...implying the occurrence of cross-species transmission."  In discussing the different isolate clusters of 'HIV'-1 round the world, they state: "Within the 'North American Cluster' there are also viruses isolated from Europe.... and Japan, which have probably spread from North America." (My italics)  This is consistent with widely exported US made poliovaccines, but they offer only the lamest of explanations for this spread - "...that HIV1 and HIV2 have spread, at a time coincidental with the development of biochemical techniques allowing their detection, most probably reflects recent massive increases in urbanisation and travel."   Zero mention is made of vaccine contaminants.  However the authors do state: "... we have argued that HIV1 and HIV2 have arisen in humans recently...", (My italics) and time periods of "40 years" are mentioned in their paper.

Gallo and Montagnier had admitted in a jointly written article in Scientific American (October 1988) that 'HIV' was a recent introduction into the human bloodstream "not less than twenty but not more than 100 years ago."  This meagre hint is expanded by Gerald Myers and Bette Korber in their paper The Future of Human Immunodeficiency Virus 16.   Having freely admitted the simian origins of 'HIV', they point out that at the time of writing (1994) there were globally five main subtypes of 'HIV' (currently increased to ten+).  The authors state:  "These HIV-1 subtypes appear to have diverged from one another as recently as 1960, that is to say, they may have proliferated in step with the pandemic." (My italics)   The significant date 1960 is thus given as the starting point of the AIDS 'pandemic' and is within one year of 1961 when manufacturers of live poliovaccines switched from rhesus to African greens for their incubating cell tissues, in the wake of the SV40 panic. 

The lack of candour by the scientific community on this subject is typified by the last chapter in The Evolutionary Biology of Viruses 16 by Stephen S.Morse.  In a table titled "Human intervention in viral emergence", he lists ways in which humans may have been instrumental in spreading viruses from their natural animal hosts to humans and other species.  There are three main categories - "Agriculture", "Tropical deforestation", and "Medical technology".  In this last group he includes 'HIV' and HTLV, as well as Hepatitis B and C.  He lists methods of accidental viral spread, including "Transfusions, contaminated hypodermic needles and organ transplants" and completely omits to mention vaccines, contaminated or otherwise, the most widespread method of deliberately spreading viruses devised by man.  Indeed, the whole concept of 'vaccination' stems from the use of an animal virus, vaccinia, to combat human smallpox, devised by Edward Jenner in the 18th century - the first deliberately engineered zoonosis. The other virology textbooks cited in my references all preserve a deafening silence on the subject, even those which mention, in passing, the SV40 fiasco. 

I propose that world-wide differences in 'HIV' subtypes merely reflect the proliferation of WHO and other polio vaccination programmes and the export of US and European polio vaccines globally since 1961.  The chief difference in the 'subtypes' will be generational, in that SIVAGM- infected vaccinees from 1961 in the US and Europe will have a much more evolved 'strain' of SIVAGM-'HIV' (SHIV?) than people vaccinated in more recent decades.  The degree of divergence from the SIVAGM precursor will thus be an effect of time in the human bloodstream, further modified by local endemic disease conditions and behavioural antigenic exposure, which in turn causes increased cellular activity and the consequent production of more mutations of 'HIV' in each individual.  The first strains of 'HIV' found in young gay men in countries with compulsory poliovaccination starting in infancy - the USA, France etc. found in 1982/3 will have had longer to diverge from the initial childhood SIVAGM infection.  Later recipients of SIVAGM will have a less highly diverged strain of 'HIV'.  This would give the appearance of different 'HIV' 'subtypes'.

Are there any human retroviruses?

It cannot be mere coincidence that:

a) two novel 'human' retroviruses, HTLV 1 (Type C) and HIV 1 (an unstable 'lentivirus'),

b) which both have their closest primate relatives in African green monkeys,

c) one of the few lower primates found to carry both STLVAGM  (Type C) and SIVAGM (an unstable 'lentivirus'),

d) in up to 40% (STLV) and 70% (SIV) of wild-caught African green monkeys,

e) whose cells were almost universally used in poliovaccine production since 1961,

f) were 'found' so soon after the Lederle vaccine enquiry in 1976/77 into retrovirus-contaminated     poliovaccines,

g) and wrongly alleged to cause two human diseases, 

h) as suspiciously novel (adult T-cell leukaemia, 1977 and AIDS, 1981), as the retroviruses.

No-one could believe in such an eight-fold cascade of simultaneous, unconnected coincidences, not even a Portuguese trader.  However, this is where a gullibility co-factor kicked in to the advantage of the retrovirologists.  No-one considered, then as now, that it is totally incredible that not one, but two 'human' retroviruses had been quietly lurking in the human bloodstream, passing harmlessly from generation to generation, and considerately waiting to cause two new fatal diseases until exactly the same time that medical and scientific gadgetry had progressed sufficiently to allow retroviruses to be detected and come under such intense scrutiny.  If 'HIV' is a 'deadly virus', it could not be passed down more than one generation, and the vertically transmitted 'epidemic' would have burnt itself out.  A retrovirus passed down through many generations, however, is obviously a non-pathogenic, harmless passenger virus.  Similarly, if 'HTLV'1, allegedly present in humans for hundreds of years, is the cause of adult T-cell leukemia, the disease would have been recognised as one of the commonest forms of geriatric cancer in Japan and elsewhere long before the late '70's, the same time that both HTLV1 and the cancer were found.

I suspect that in finding the first 'human' retrovirus, Robert Gallo cynically capitalised on the findings of the contaminated vaccine enquiry in 1977 and merely took a calculated risk of finding the contaminants in the cells of humans who had received the vaccines, identifying the first of two simian viruses (both subsequently found in African green monkeys) which had by then contaminated live poliovaccines for about fifteen years.  Just as before in 1975, Gallo had merely 'found' a simian retrovirus in human cancer cells, STLVAGM, and made it 'human' by calling it 'HTLV'.  The same cynical scientific legerdemain, perhaps prompted by a US governmental desire for damage containment, and to prevent the French from gaining the AIDS research initiative, turned SIVAGM into 'HTLV-111' ('HIV') in 1984.   As Lady Bracknell might have observed: "To find one simian 'human' retrovirus may be regarded as opportune, to find two seems like sheer opportunism".  Gallo's colleagues Myron Essex and Phyllis Kanki made one trip too many to the same well in 1986 and isolated 'HIV' 3, which they called HTLV-1V.  Like Gallo's first attempt to demonstrate a human retrovirus, this was again a soup of simian contaminants, including SIV, grown in human cell lines.  As Robin Weiss and Richard Tedder 17 explain: "HTLV-IV (sic) was found to represent a laboratory contamination of human cell lines with SIV and the detection of apparently specific antibodies was due to antigenic cross-reactivity between HIV2 and SIV."  (My italics)  Thus, alleged 'human' viral antibodies cross react with their simian viral counterparts.

The fact is there are still no truly 'human' retroviruses, although there may well be spent proviral debris from previous ancient infections in the human genome.  Both Kary Mullis, who won the Nobel Prize for inventing PCR, and Peter Duesberg, the world's leading retrovirus expert, have repeatedly said that humans have hundreds, if not thousands of retroviral genomes integrated into their cellular DNA, like so many burnt out microchips.  Then why is it that the only detectable human retroviruses invariably have these embarrassingly close simian relatives? All these 'human' retroviruses are merely recent simian additions to the human bloodstream, turning human blood itself into a viral pick'n'mix 'crude soup'.  The list so far includes HTLV1&2, HIV1&2, and possibly spumaviruses. Indeed, no 'human' retrovirus has yet been 'found' which cannot be connected to monkeys, principally African greens and sooty mangabeys. 

To claim that as human primates we have inherited these retroviruses from a distant common primate ancestor is a complete cop-out.  African green monkeys must be pretty remote from humans on the primate family tree, not nearly as close as, for instance, chimpanzees.  The SIV experts realised that it was hardly likely that a common ancestor virus had survived in lower primates and humans and by-passed the chimpanzees, our closest primate relatives, so they had to show that chimps were in fact infected with SIV in the wild.  Consequently, chimpanzees are now listed in all standard textbooks as infected with SIVCPZ, based principally on a handful (4!) of animals, the first of which may have escaped from the French-run primate research centre in Gabon, only to be recaptured and declared an example of a wild-caught, naturally SIV infected chimpanzee.  No-one ever suggested yet another laboratory contamination might have taken place.  The whole of 'AIDS research' is riddled with such dubious examples of Portuguese traderism.  Nor did they mention that these allegedly wild-caught SIV-infected chimps remain perfectly healthy.  Logically, if so-called chimpanzee SIV does not cause AIDS in wild caught chimps, and SIVAGM does not cause disease in African greens, why should so-called 'HIV' cause AIDS in humans if it is natural to humans? 

Is AIDS an infectious epidemic?

Almost from the outset, AIDS was not seen to be spreading exponentially like a typically infectious, genuine 'virgin soil' epidemic, and even the supposed mechanisms of horizontal spread of 'HIV', with the possible exception of transfused whole blood prior to 1985, remain expedient, widely believed but largely unproved assumptions.  A letter on the Internet showed that the chance of sexual transmission of 'HIV' is statistically as low as 4/1000 18.  More remarkably, the same source, Dr. Ian Trowbridge, an AIDS researcher at the Salk Institute in San Diego, stated that the risk of 'HIV' spread via dirty syringes and needles by drug addicts is even more remote - 3/1000.  The 'wildfire' spread between gay men via rectal sex was always more the product of mainly heterosexual epidemiologists' prurient obsession with the Riddle of the Sphincter than scientific feasibility. (see below)  The fact is that apart perhaps from via a blood transfusion, 'HIV' spreads rarely, if at all, horizontally.  If the pathogen responsible for the Black Death had been so reticent, Europe would have been spared that horror.  If 'HIV' is a retrovirus at all, its typical method of spread will be vertical from female to offspring, which could have happened since the first generation of SIVAGM-infected female polio vaccinees reached child-bearing age in the late '60's-early '70's.  However, the fact that females infected with SIVAGM in infancy should live long enough to bear children argues against the pathogenicity of the virus, unless it has an incubation period of some twenty years, or longer.  Today, 'HIV' will not pass to more than one generation, as the offspring of usually drug-using pregnant women, on diagnosis with 'HIV' positivity, will be bombarded with AZT and other poisonous anti-viral drugs and succomb before puberty.

'HIV' found in infants could very well be the result of exposure to 3 or more doses of potentially SIV-contaminated poliovaccine given in the first few months of life, rather than mother-to-child transmission.  The world was shocked by the high numbers of 'HIV' positive babies found in Rumania after the fall of Ceaucescu regime.  No-one seemed to find it odd that the babies were infected, but not, apparently, the adults.  The infection was attributed to widescale use of micro-blood transfusions in babies who showed failure to thrive, usually due to malnutrition.  However, a letter from three Rumanian doctors in The Lancet (1.1.94, p.51) reported a case of a 26 month old girl who had suffered paralytic polio apparently resulting from abreaction to poliovaccines, of which she had received four doses, at 3, 6, 9, and 15 months of age.  The child was found to be 'HIV' positive, and had been part of a local poliovaccination campaign.  The child's mother was "reported to be HIV negative."  At no stage do they offer an explanation for the 'HIV' being present in the child of an uninfected mother, and there is no mention that the child had had a blood transfusion.  It did not occur to the doctors that the vaccines might have carried SIVAGM; alternatively, that the positive 'HIV' test may have been a false-positive due to cross-reactivity with all those vaccine antigens.  They also chillingly point out that the WHO Expanded Programme of Immunization (1987) recommends vaccination against polio at birth, then again at 6, 10 and 14 weeks for all infants "including infants known to be HIV-infected". 

I hope the Clerici article (see above) is brought to the attention of the WHO.

As for those mysterious cases of people alleged to have been infected during a trip abroad, how many adults have been advised to have a battery of vaccinations, including a poliovaccine booster before going on holiday or a business trip?  Who is to say some contaminant SIVAGM was not one of the last items they packed before leaving for the airport?  Some occupations require repeated vaccination as part of conditions of employment - airline crews, armed forces, medical workers etc. 

Where is the actual virus?

Cell-free 'HIV' is never directly seen in alleged infected body fluids under electronmicroscopy.  Gallo apparently concurs with Duesberg when he admits that abundant viruses can be seen in the tissues of infected animals when they cause disease in lab conditions, but HTLV-1 could not be seen in his cancer cells 19.  Gallo found this puzzling, and devised a series of assays to detect antibodies against alleged virus-specific proteins.  Since then, evidence of human retroviral infection is always indirect, and never visually confirmed.  Again, as Lady Bracknell might have observed: "Viruses should be seen, not inferred".  Instead, 'HIV' antibodies are used as a marker for exposure to the virus.  This is a bit like assuming the existence of the yeti from its supposed footprints.

It is never possible to take a direct sample of an allegedly 'HIV infected' fluid, including blood, plasma, saliva, or semen, subject it to electronmicroscopy and see 'HIV', even from patients with alleged massive 'viral loads'.  Instead, cells have to be extracted from the fluids - e.g. monocytes stripped out of semen - and then stimulated to express reactivated 'virus' in cell cultures, totally isolated from an immune response.  With luck, after several attempts, and several weeks, some 'virus' may be 'found', i.e. in the case of semen, two studies yielded only 1 provirus after repeated attempts in only 1/25, and 'virus' in 9/95, ejaculates of semen taken from 'HIV' positive gay PWA's 20. 

Nevertheless, the orthodox dogma is that if a virus can be cultured from a fluid, it is transmissible in that fluid, presumably in an intracellular form. This in effect means that cells containing the proviral genome have to enter the new host's bloodstream and survive long enough, and under the right stimuli, to yield up expressed virus.  This might just be feasible via a whole blood transfusion, but it seems like an inefficient method of infection for a virus alleged to be sweeping through the world like wildfire.

Human SIV infection was an efficient accident.

Which is more likely and makes more sense - the orthodoxy's slow horizontal seepage model of 'HIV' transmission, which would have taken thousands of years - and rectal sexual acts per person - to accomplish, even with the help of Portuguese traders; or an efficient, twenty-five year world-wide human infection with animal retroviruses via dirty vaccines?  The key to the vaccine concept of infection with SIVAGM is the efficiency of the method of viral delivery. 

A vaccine delivered virus is direct and efficient.  Live, presumably retroviral particles, directly visible under electronmicroscopy 12, were harvested from animal cell cultures and then delivered direct to the recipient in a cell-free suspension fluid.  Your friendly vaccine makers have cultured the contaminant particles in as pure a form as possible, and unwittingly added them as croutons to their vaccine 'crude soup'.  Indeed, it may well be that the vaccine delivery method is the only efficient way retroviruses may be transmitted horizontally.  A simian retrovirus in a cell-free vaccine would effect an efficient zoonosis, and researchers have observed that human cells are readily infected by all the known SIV's. 

A serious objection to my hypothesis is that SIV delivered in an oral vaccine would have remained in the alimentary tract, without penetrating the blood or lymph systems, neutralised by gastric acids, and eventually evacuated in body wastes.  Kyle 12 gives this as one of the probable reasons the US government committee passed the contaminated Lederle poliovaccine for human use in 1977.  The Wistar committee in 1992 also offered this as a reason to doubt oral infection with SIV, although it must have known since 1986 that 'HIV' infects dendritic (skin) cells, including Langerhans and mucosal cells.  The alimentary tract is lined with mucosal cells, so the oral route could very well be an efficient route of transmission for cell-free infectious retroviruses.

My theory was precisely, if unintentionally, confirmed in studies by Ruth Ruprecht et al at the Dana Farber Cancer Institute, and Tulane and Tufts Universities, published in Science (7.6.96).  The same research teams had previously demonstrated the ease with which 'HIV' infects human mucosal cells. The Science paper, using SIV animal modelling, sought by analogy to show whether unprotected oral sex ran a risk of 'HIV' infection due to cell-free virus in semen infecting human oral mucosal cells, even in the absence of mouth lesions and gastric acid inhibitors.  The paper describes a "cell-free SIV solution" dribbled onto the tongues of SIV-free macaque monkeys, and 6 out of 7 previously uninfected monkeys were thus systemically infected.  The studies showed that the same SIV solution rectally administered by endoscope needed a concentration of virus 6000 times higher to achieve systemic infection than the orally administered virus solution.   As already stated - cell-free virus has never been found in human semen without extensive culturing, so it is impossible to extrapolate any conclusions from this study concerning 'HIV' oral transmission in semen.   However, a specially prepared "cell-free SIV solution" is exactly analogous with an SIV-contaminated, cell-free oral vaccine as described by Kyle 12.  The Sabin live poliovaccine was usually administered on cubes of sugar to be dissolved in the mouth, and that of Koprowsky was directly sprayed onto the back of the throat via nebuliser.

Furthermore, Dr. Ivan Roitt, citing an earlier in vitro study in  Essential Immunology, p.304, states: "Possibly of crucial importance has been the discovery that suspensions of single follicular dendritic cells from human tonsil can be directly infected with HIV by a process which does not involve CD4.  The infected cells permit viral replication and can reinfect T-cells in vitro." 21   My theory could be simply confirmed or disproved by combining the two experiments, and applying Ruprecht et al's "cell-free SIVAGM solution" to Roitt's "follicular dendritic cells from human tonsil" to see what happens.  If the  SIVAGM infects the cells, and the "infected cells permit viral replication and can reinfect human T-cells in vitro" as described by Roitt, it would be interesting to see how the scientific community explain that away.

Farr's Law.

Duesberg cites Farr's Law 23 as evidence that 'HIV' is an 'old' virus in the USA because the CDC estimate of 1,000,000 people infected has remained constant since 1985. This would seem to contradict the vaccine contamination theory.  However, I believe he is mistaken for several reasons.  Farr's Law is usually applied to the proven causal agent of a disease as confirmed by the number of disease cases.  This is not possible with 'HIV' because it has not been proved to be the cause of AIDS, but its antibodies are merely a surrogate marker for AIDS risk, principally in males, who indulge more in risk behaviours than females.  Moreover, the use of SIVAGM contaminated vaccines from 1961 until the mid '80's would have established a constantly replenished level of infection in an unknown percentage of new or repeat vaccinees of both sexes at least until the latter date.  Early concentration of AIDS in males in the age group 25-44 seen during the 1980's is entirely consistent with seeing reactivated SIV/'HIV' as a surrogate marker for principally male risk behaviour including drug addiction, both gay and straight, as well as being entirely consistent with the vaccine origins of 'HIV' beginning in 1961.

The anecdotal case cited by Duesberg 20 to challenge Gallo, Montagnier et al's contention of the recent African origin of 'HIV' is consistent with the vaccine origin of SIV/'HIV'.  I had been puzzled by this case when it first came to light in the late 1980s.  A boy of 16 in St. Louis, USA, known only as Robert R, died of an illness in 1968 which today would be clinically diagnosed as AIDS .  Subsequent examination of his stored tissues alleged to find 'HIV' proteins, but this would be quite consistent with his being one of the earliest recipients of an SIV-contaminated poliovaccine as a child.  The earlier 1959 'Manchester sailor' case frequently cited, including by the Wistar vaccine enquiry in 1992, to predate 'HIV' infection to before live poliovirus vaccination became standard  is also discountable because by 1995 it was shown that his stored tissues had been tampered with and the strain of 'HIV' allegedly found in his tissues was either a lab contaminant or a deliberate plant 22.  Duesberg further attributes the 0.03%-0.3% regular rate of 'HIV' positivity found in 17-19 year old inductees - both male and female - into the US armed forces between 1985 and 1990, to vertical transmission from mother to child 20.   However, this rate far more likely represents the extent of contamination in compulsory previous polio vaccinations sufficient to produce a systemic, productive infection in both sexes, independent of their mothers' 'HIV' status. 

If Duesberg is right about 'HIV' being a long established virus in the US, where are the older infected people, the parents of those younger men and women found 'HIV'-positive in their twenties, thirties and forties?  Where especially are  the 50, 60, 70 year old 'HIV'-positive mothers, who supposedly infected their children via mother-to-child vertical transmission?  Even those old people immunosuppressed as a natural consequence of senescence are seldom found to be 'HIV' positive.  Where such cases occur, they can usually be explained by 'HIV' transmission in a blood transfusion, more common in the elderly, using the blood of younger, polio vaccinated donors.  (Despite official assurances to the contrary, I suggest that a dormant SIV/'HIV' infection would not be detected by blood-donor screening.)  Alternatively, 'HIV' antibodies could have resulted from a reactivated SIV infection as a result of adult poliovaccination between 1961-85.  Moreover, where are the older Africans,  over the age of 65 (i.e. adults 'infected' prior to 1960) with 'HIV'1?   So far they haven't been found.  The evidence all points, both in Africa and the West, to a recent - as I believe, since 1961 - simultaneous introduction of a simian virus, SIVAGM, into the human bloodstream.  Whilst I am totally convinced by Duesberg's other arguments that 'HIV' is not  the cause of AIDS, there is no hard scientific evidence that 'HIV' has been handed down through many generations.  Although harmless, 'HIV' infection is as new and as widespread as the use of the live poliovaccines, and Farr's Law does not apply.

The appearance of AIDS in the former Soviet Union and its Eastern bloc satellites since the collapse of Communism, is also entirely consistent with the recent spread of drug addiction reactivating an endemic SIV infection resulting from previous contaminated poliovaccinations.  Indeed, AIDS in former 'Iron Curtain' countries is only seen in those areas where drug addiction is now rife, and exactly mirrors the drug-driven AIDS epidemic in the West, with the appearance of 'HIV' antibodies as a surrogate marker for  this specific risk behaviour, and mainly prevalent in exactly the same age groups - 14-18, 19-25, 26-35, 36-45 - as in the West. (Pauli Leinikki, letter, The Lancet, 28.6.97, p.p.1914-1915)  'HIV' infections there in over 50's, as in the West, are infrequent in drug addicts.

An SIVAGM contaminated vaccine origin of 'HIV' would prove conclusively that it does not cause AIDS.  Contaminant viruses/proteins/prions/DNA/RNA etc. in polio and other vaccines infected millions of males and females world-wide since the 1950's, typified by SV40.  As Robin Weiss kindly pointed out to me, the human foamy agents (spumaviruses) associated with Graves' disease may also be simian retroviruses transmitted to humans in the same way (personal communication).  In the vast majority, any genomically integrated DNA encoding 'foreign' proteins would have remained dormant unless subsequently reactivated into barely detectable, low-level expression, by other infections (particularly STD's), subsequent vaccinations and medicinal or recreational drugs in vivo; and by culturing techniques in vitro.  This expression would then be restricted efficiently to latency once again in vivo, leaving a detectable antibody level using ultra-modern technology, and wrongly interpreted as a recent infection.  A study by Jaffe et al published in The Lancet (16.9.89 pp.637-639) monitored the duration of the so-called 'window period' between supposed 'HIV' infection and seroconversion.  It was found to be as long as 35 months in one instance in a different, carefully monitored study, confirmed later by PCR; so why not a 'window period', or latency, of 30 years or more, as with SV40? 

Why were the epidemiologists wrong? 

Almost all the AIDS epidemiologists have been consistently misled by the 'HIV' test into believing that the numbers of people showing antibody positivity reflect the total number of people recently infected, whereas at best they merely show a percentage of those with a reactivated old infection, leaving the true cumulative number of silent, dormant infections underestimated and unknown.  The suppositions about horizontal spread were consequently distorted and often completely wrong. 

For example, 'clusters' of AIDS cases were attributed to a transmissible agent, forgetting or wilfully ignoring the clustering seen previously in supposedly 'infectious epidemics' e.g. pellagra, scurvy, and beri beri, all of which were subsequently shown to be caused by acute vitamin deficiencies, and not an infectious agent.  Further, it soon became clear that whereas AIDS was a suspiciously circumscribed infectious epidemic in the developed world, restricted to 'high risk' groups, the epidemiological profile in Africa and other countries was totally different.  Whilst admitting the anomaly in this apparent difference between the two epidemics, most epidemiologists just gloss over it, although it is an obvious weakness in the whole 'HIV'=AIDS theory.  To explain the presumed rampant sexual spread of 'HIV' in Africa, even reputable scientific journals published all sorts of vile, racist rubbish citing sexual promiscuity in Africa on a gigantic scale, and even hinting at sexual abuse of monkeys. 

Neither epidemiology nor any other branch of medical science has explained the mechanism of the sexual transmission of 'HIV' satisfactorarily.  It is widely acknowledged that it is much rarer for a woman to transmit 'HIV' to a man than vice versa.  Similarly, it is assumed that the receptive partner during gay rectal sex acts runs the greater risk of 'HIV' infection.  To date, there is still not one credible, scientifically proven explanation for the exact mechanism whereby a non-infected insertive partner can be infected with 'HIV' by a receptive sexual partner, whether vaginally, rectally or orally receptive.  For a typically sexually transmitted organism to survive, it must be capable of efficient bi-directional transmission. This has never been demonstrated in the case of 'HIV', and all assumptions about sexual transmission, of even supposed cell free virus, from receptive to insertive partners, remain just that - assumptions, totally unsupported by scientific evidence.  Had they done their homework properly, epidemiologists would have realised from the outset that the animal lentivirus model was singularly inept as a basis for assumed sexual spread of 'HIV', and that sexual transmission plays little or no part in the transmission of retroviruses-lentiviruses. 

As Ruth Ruprecht and her colleagues have shown (see above), SIVAGM, and by analogy, 'HIV', are 6000 times more likely to cause systemic infection via oral rather than rectal sex - but only if virus could be shown to be present in sufficient cell-free numbers in semen, which so far has never been achieved, in or out of a test tube.  However, the 'safer sex' messages about condom use may be well worth following, not because they prevent the spread of 'HIV', but they may help to impede the spread of STD's which reactivate dormant SIV/'HIV', leading to a 'positive' test result and the lethal psychological damage that can cause.  By the same argument, as much emphasis should be placed on the avoidance of toxic drugs as on the use of clean needles and syringes.

Several studies have shown that only those prostitute women in the West who take drugs have alleged 'HIV' antibodies.  This group includes many women who never injected, or shared needles, and some who only ever smoked crack cocaine; this suggests strongly that hard drugs, whether injected, ingested or inhaled, may have a mitogenic effect on cells, stimulating a dormant retrovirus into expression.  Reactivating factors such as herpes simplex, hepatitis agents and other STD's believed to be cofactors in 'HIV' expression 8,9,10 are highly infectious and easily spread, unlike retro/lentiviruses.  Because drug consumption and common STD and other pathogens are widespread in a section of the gay community it was assumed that 'HIV' positive tests in gay men were the result of a recent 'HIV' infection via rectal sex, rather than an earlier, dormant, perhaps even childhood oral SIVAGM infection via a contaminated vaccine, reactivated by a later herpes or other sexually acquired  infection, or the consumption of recreational drugs.  A very high number of reactivating pathogens will also be endemic in tropical and eastern countries where contaminated poliovaccines have been used.  

More crucially, correct interpretation of the means of transmission of an organism should help epidemiologists accurately to predict the future course and extent of a disease.  If predictive epidemiology is inaccurate, either the AIDS epidemiologists are bad at their job; or they have just been misled by or have misinterpreted scientific data; or it was expedient to lie.  In 1999, where is the sexually generated heterosexual epidemic in the West confidently predicted by the epidemiologists?  The actual AIDS figures have invariably been much lower than those predicted, but no-one ever officially admits the predictions got it wrong.  This may be because epidemiological assumptions about the methods of horizontal spread of 'HIV' are wrong.  Alternatively, the original apocolyptic predictions of AIDS cases may have been based on the NIH epidemiologists' early realisation that 'HIV' is really SIVAGM and had potentially infected millions in vaccines; a worst-case scenario would then be prudent.  An  unconfirmed report suggests that an anonymous female employee at the NIH freely admitted recently that 'HIV' was generally acknowledged to have been a contaminant in poliovaccines as long ago as 1988.

To suggest that an infectious epidemic can be confined to 'high risk groups' in the West, as it still largely is today, but will eventually spread from those groups to the general population to equal in scale the epidemic supposed to be sweeping Africa, is alarmist, self-serving nonsense.  We were warned that AIDS would spread from 'risk groups' via 'bridging groups' - bisexual men, drug addicts, prostitute women etc. - into the wider population, but so far this just hasn't happened.  Typically, infectious epidemics spread exponentially through the entire general population, which includes all the 'risk groups', although the 'risk groups' may indeed show a higher susceptibility towards infection and disease symptoms.  However, to suggest that a sexually transmitted epidemic begins in 'risk groups' and spreads via a presumably one-way bridge outwards to the rest of the population is like arguing water can flow naturally uphill.  Moreover, no STD pathogen has ever originated in gay men or any sexual minority group. 

An objection to my hypothesis may be raised by gay men who have had many sex partners, repeated STD's and high drug consumption but who did not get 'HIV'.  Many of my gay friends fit this category, and some even express a kind of guilt that they did not get 'the AIDS virus' whilst their friends did - "Why them and not me?"  It's probable they just didn't get a batch of SIV contaminated poliovaccine.  It would also explain the apparent paradox of 'discordant couples' in which one partner is infected with 'HIV' and the other remains 'HIV' negative despite sometimes years of unprotected sex - gay or straight. This would particularly seem to apply to married haemophiliacs supposedly 'HIV' infected by their clotting factor. Very few of their wives become infected, and even those who appear to be are far more easily explained by the transmission of an SIVAGM-reactivating pathogen than 'HIV' itself. 

The haemophiliacs are far more likely to have been given SIV in vaccines than 'HIV' in Factor V111.  The trail of misconceptions about haemophiliac infection with 'HIV' may again lead back to sloppy epidemiology.  Robert Gallo had stated early on that the fact that haemophiliacs were starting to get AIDS meant that they were being given the causative agent in their clotting factor.  This narrowed the hunt to a virus, as the blood product is passed through a filter too fine to allow anything larger than a virus to pass through it.  Subsequently, when a high percentage of haemophiliacs showed antibodies said to be specific to 'HIV' proteins, this looked like the clinching factor for 'HIV' being the causative agent of AIDS.  However, whole, viable, infectious 'HIV' particles have never been found in even those stored clotting factors which consisted of 99% alloantigenic contaminants.  Moreover, the clotting factors are prepared by freeze drying (cryoprecipitation) and as the official 1994 CDC pamphlet states: "Drying of HIV-infected human blood or other bodily fluids reduces the theoretical risk of environmental transmission to that which has been observed - essentially to zero." 18 

As Duesberg first suggested in his elegant paper in Cancer Research, 'HIV' antibodies are no more than an indicator of AIDS risk.  What must be understood is that the 'risk' has always been one of immune suppression due to behavioural, socio-economic, inherent disease and geographical factors - not 'HIV' infection.  'HIV' meets every one of the four classic criteria of a harmless passenger virus, listed in Duesberg's paper in a previous issue of Continuum.  'HIV' antibodies are found using flawed testing procedures, especially in the Third World, against a background of rising, and increasingly intractable, levels of endemic old diseases (Africa, India) and drug addiction (Thailand, the former Soviet Union, Eastern Europe, India etc.).  Indeed the only epidemiologist who has consistently predicted the correct number of AIDS cases occurring in both the USA and Britain to within 10% of subsequent actual totals is Professor Gordon Stewart, whose predictions are based on incidence of risk behaviours rather than incidence of 'HIV' infection.  (Genetica 95: 173-193 1995)

The current BSE/CJD fiasco proves, if any further proof were needed, the folly of man's cross species genetic tinkering, and the inadvisability of accidental man-made zoonoses typified by vaccines.  A further example may suffice to illustrate this dangerous activity.  Since the 1970's, all Western dogs have had to receive a vaccine to protect them from a cat virus, the feline parvovirus, which contaminated canine vaccines prior to that date and infected a whole generation of dogs.  Thus, an extra vaccine is now necessary to protect their descendants from the result of a previous vaccine contaminant.  If the world population is persuaded to use a vaccine against 'HIV', a harmless previous vaccine contaminant, vaccine history will merely be repeating itself. 

In February 1994, a civil suit was filed in the US federal court on behalf of a girl of twelve, with no known risk factors, who tested 'positive' for 'HIV' in "about 1992", claiming that she "...was infected with the Human Immunodeficiency Virus by way of an FDA-approved live oral poliovirus vaccine she received on April 9, 1982; June 25, 1982; and August 20, 1982. The live oral poliovirus vaccine was produced, tested, and approved by the United States Food and Drug Administration pursuant to measures inconsistent with accepted standards of medical practice ... the product was FDA-approved despite the known presence of contaminants, including retroviruses such as HIV." (24) (My italics)  By June 1995, Judge Ronald Hedges ruled that American Cyanamid, the manufacturer, had to allow the plaintiffs to test samples of their vaccine for HIV-1, despite stated FDA denials that the vaccines could have been contaminated.  A result of the tests was scheduled for November 1995.  I would be grateful if anyone has an update on this landmark lawsuit.  Was there, I wonder, an out-of-court settlement?

In the meantime, what is urgently needed is a full-scale, totally independent, international enquiry into the manufacture of polio and any other vaccines involving simian cell lines from 1955 to the present day.  The enquiry should seek to know exactly which pharmaceutical companies, in which countries, were involved; which monkey species' tissues were used in their product; which countries exported or imported the vaccines; which countries have compulsory polio and other vaccinations, and what is their level of 'HIV' infection; how many 'HIV- positive people were never vaccinated against polio; and to demand full access to stored reference vaccine batches and poliovirus seedstocks for examination using the most up-to-date scientific methods (PCR etc.) to detect the presence of contaminant viruses.  Providing not too much evidence has conveniently disappeared into the shredder or down laboratory sinks since 1976, the results could prove very interesting.  Much more importantly, it is vitally urgent that some of the billions currently being wasted on studying 'HIV' be allocated to the study of the complexities of the immune system, and how it really works, in the hope we may discover how to repair and rebuild the damaged systems of PWA's.  If we do not, then we may well reach the situation foreseen by Robert Root-Bernstein and others of a day when we have totally eradicated 'HIV' but not AIDS.

It is very doubtful that the authorities will ever admit that the 'probable cause of AIDS' was a vaccine contaminant.  No-one could shoulder the huge burden of guilt, or the astronomical financial cost of compensation arising from such an admission, so the story will obviously be kept hushed up or buried in obfuscatory scientific debate.  This is not a new situation.  In the published text of his 1966 Heath Clark Lectures on the subject of The Hazards of Immunization 25, Sir Graham Wilson has this to say in his Introduction:  "The woeful record I present of the accidents attendant on immunization and the ways in which they have arisen will not be complete. Far from it in fact. Even if I had had time to comb the whole of the relevant literature, I should still not have been in a position to give a complete record. This is mainly because a large number of accidents - I suspect the majority - have never been reported in print, either through fear of compensation claims, or of giving a weapon to the anti-vaccinationists, or for some other reason. Admittedly most of the larger accidents have been reported, but even with some of these attempts were made to keep knowledge of them from the public." (My italics) 

It must be remembered that 33 years ago, when that was written, no-one knew how retroviruses really worked, or that they infected monkeys being used in the production of poliovaccines.  When I have raised this subject with AIDS experts I have always received the same answer - a swift denial, followed by an equally swift "... and what does it matter anyway where 'HIV' came from - it's here now and we have to deal with it."  Ironically, we remain beholden to the very 'experts' who allowed SIV to infect humans to try to get rid of it and its presumed effects.  Consequently, I naturally view with grave misgiving the WHO's plan for global eradication of polio.  Even now they are debating whether to use Salk killed or Sabin live virus vaccines.  Either way, let us hope the WHO does not obtain its poliovaccines from Portuguese traders.

There may be light on the horizon.  A letter to The Lancet, (6.6.1998, p. 1705), from V.A.Morosov of the Russian Cancer Research Centre in Moscow, and S. Lagaye of the Institut Pasteur in Paris, is entitled "Latent foamy and simian retroviruses in healthy African green monkeys used in biomedical research."  The letter concludes: "... On the basis of our data, we suggest that during preparation of poliovaccines on AGM cells, retroviruses may have been activated in cells of some symptomless carriers, and contaminated poliovaccine stocks.  RT-PCR analysis of old stocks are required to clarify this point."  So far, Kyle and other writers like Tom Curtis have called for the same tests to be done without result.  Let's hope Morosov and Lagaye have more success.  If it can be shown that SIVAGM was the precursor of 'HIV', then the whole "HIV=AIDS" nonsense can be flushed down the lavatory with its propounders, and we can start to tackle the real fight against the raft of diseases which are classified as AIDS.

I should like to thank Alex Russell for productive discussions and invaluable help in researching this article; Prof. Robin Weiss for critical and useful comments on an earlier draft; and Peter Duesberg for his customary astringent scepticism.  I also apologise to the traders of Portugal for my tasteless jokes, and to the people of Africa for Robert Gallo's scandalously racist libel.

References:

1.            Vaccination - The Medical Assault on the Immune System, Viera Scheibner Ph.D, Privately printed in Australia, 1993. 

2.           Vaccination and Immunization - Dangers, Delusions and Alternatives, Leon Chaitow, The C.W.Daniel Co. Ltd., Saffron Walden,1987.

3.            The  Pathogenesis of Infectious Disease, Prof. C. Mims, Academic Press, London, 1987, p.319.

4.             Biohazard, booklet published in 1987/88 by the National Anti-Vivisection Society, £5 from 0181-846-9777 . 

5.             Science, Vol 273, 9.8.96, pp 746-747.

6.             Science, Vol.257, 24.7.92, p.478. Jon Cohen, Monkey-Human Viral Hybrid is NewWeapon in AIDS Fight.

7.             Fields Virology, 2 Vols, Raven Press, 2nd Edition 1990.

8.              Gonzalez-Scarano et al, AIDS Research and Human Retroviruses (1987) 3 (3) 245-252.

9.             Mosca et al, PNAS, (1988) 84 (21) 7408-7412.

10.           Tong-Starksen et al, PNAS (1987) 84 (19) 6845-6849.

11.            Peter H. Duesberg - Personal communication 1996.

12.           Simian retroviruses, poliovaccine, and origin of AIDS, W.S. Kyle, The Lancet, 1992, 339, 600-601.

13.           Cellular Receptors for Animal Viruses, Cold Spring Harbour Laboratory Press,  Chap 2 Human Receptors for Retroviruses by Robin Weiss 1994,  pp19-21.

14.            Acquired Immune Deficiency Syndrome, UCLA Symposia on Molecular and Cellular Biology, Volume 16, Alan R.Liss, Inc., New York, pp. 9-27.

15.            Molecular Basis of Viral Evolution, edited by Gibbs, Calisher and Garcia-Arenal, Cambridge University Press, 1995.

16.           The Evolutionary Biology of Viruses, edited by Stephen S. Morse, Raven Press,   1994, p.330

17.            Retrovirus Infections of Humans, by Richard Tedder and Robin Weiss, Topley and Wilson, Principles of Bacteriology, Virology and Immunity, Eighth edition,   Vol 4 - Virology, pp 632-655. Published by Edward Arnold 1990.

18.           On needle exchange, by Mark Gabrish Conlan.  Zenger's, December 1996, p 2.

19.           The First Human Retrovirus by Robert Gallo, Scientific American, Dec. 1986.

20.          Duesberg - Pharma. Ther. Vol 55, pp 201-277, 1992.

21.           Dr. Ivan Roitt, Essential Immunology, Eighth Edition, 1994, Blackwell Scientific Publications, Ch.15, p.304.

22.           Steve Connor, The Independent, 24.3.95. p.1  The World's first AIDS case was false.

23.           Duesberg, Inventing the AIDS Virus, Regnery Publishing, Inc., 1996, pp.191-192.

24.           Immunization - Theory vs. Reality, by Neil Z. Miller, New Atlantean Press, Santa Fe, New Mexico, 1996. p.55.

25.           Sir Graham S. Wilson, The Hazards of Immunization,  University of London - The Heath Clark Lectures 1966. Pub. The Athlone Press, 1967. pp. 4-5.

*The address from which Louis Pascal's paper may be obtained is: 

                                                Department of Science and Technology Studies,

                                                University of Wollongong

                                                PO Box 1144

                                                Wollongong NSW 2500, Australia. 

                                                Ask for Working Paper No.9 by Louis Pascal, Dec.1991

©  MICHAEL VERNEY-ELLIOTT, FINAL DRAFT Thursday, July 1, 1999

Author's Note. 

This article is dedicated to those who persist in believing in the existence of disease-causing 'human' retroviruses, despite evidence to the contrary demonstrated in this and previous issues of CONTINUUM.  My arguments are based on the orthodoxy's assumption that human and simian retroviruses have been proved to exist, and have been isolated, characterized and sequenced, and my references are mainly culled from the orthodox literature.  I believe the best way to overturn the views of the orthodoxy is to use their own arguments against them.

                                                                   Robert Laarhoven, M.V.E., Peter Duesberg, Joan Shenton, Volker Gildemeister, Alfred Hässig, Harvey Bialy in 1993

Aids - 20 years on - A string of false assumptions

by Michael Verney-Elliott

Immunity Resource Foundation  2005

Writer, producer and editor, has been at the forefront of the Aids debate since he brought his doubts about the Virus/Aids hypothesis to Meditel Productions. There followed four network documentaries on the subject for Channel 4. The first, Aids – The Unheard Voices, on which he worked as associate producer and reporter won the Royal Television Society Journalism Award, 1987.

Michael’s background in the arts – English at Magdalen College, Oxford and then the London Academy of Music and Dramatic Art has richly contributed to his incisive challenge of the Aids scientific establishment combined with his unerring wit.

On April 23rd 1984 President Ronald Reagan’s Secretary for Health, Margaret Heckler told the assembled international press that “The probable cause of AIDS…” had been found - a novel ‘human’ retrovirus initially called variously LAV, ARV, and HTLV-III. Subsequently, in 1986, despite a complete lack of convincing scientific evidence, which persists to this day, that such an organism causes immune suppression, in a pre-emptive move the retrovirus was named the Human Immunodeficiency Virus - (HIV) - by an international committee. It was generally accepted that after a period of latency, some infectees start to manifest symptoms of AIDS, and that this average length of asymptomatic infection was some ten years; once the symptoms appeared, the patient would inevitably die, with a totally destroyed cellular immune system.

The HIV hypothesis of AIDS causation was based on a set of assumptions, most if not all of which would be proved over the next ten years to be totally wrong. For instance, it was assumed that HIV was sexually transmitted, principally in semen. However, some twenty years later, not one HIV particle has been seen in, or recovered from, a freshly acquired semen sample taken from an HIV positive man. Moreover, the original assumption has never explained the precise mechanism whereby an insertive male becomes infected by his receptive partner, male or female.

It was assumed that HIV infects its target cells by means of the ‘spikes’ of glycoprotein 120 studding its outer coat. These spikes supposedly hook on to CD4 receptors on the target cells’ outer membrane, allowing the virus to attach itself prior to inserting its genetic RNA into the cells. It is now abundantly clear that as the virus buds out of an infected cell, it sheds its ‘spikes’ and, according to the originally supposed method of cellular infection, cannot therefore infect further cells.

It was assumed that HIV would cause a global pandemic that would be more damaging than the Black Death that carried off a third of Europe’s population in the 14 th century. It was supposed that AIDS would spread from the initially infected minority groups – gay men, IV drug users, transfusion recipients etc. - via so called bridging groups - bi-sexual men, needle sharing drug addicts etc. Having spread to the heterosexual population, AIDS would escalate rapidly and, according to a statement from TV chat star Oprah Winfrey by the year 2000 the whole of the USA would be infected. This did not happen, and in the USA, some twenty years later, AIDS is still largely confined to gay men, drug addicts and malnourished people in low socio-economic groups – mainly black and Hispanic.

It was assumed that the exponential spread of AIDS would continue until HIV ran out of victims. However, the actual number of AIDS cases as originally defined started to decline in the late1980’s. By then some 29 known diseases were classified as indicative of AIDS if found in the presence of HIV positivity – and still the numbers of AIDS cases had to be re-assessed downwards. In order to boost the numbers, and keep the AIDS terror going, new diseases had to be added into the syndrome, the largest increases being brought about by the addition of pulmonary tuberculosis and, to keep the women from feeling excluded, cervical cancer in HIV positive patients. Thus a new first was claimed for the versatile, all singing and dancing HIV – it could destroy the all important white T4 cells whilst simultaneously fostering the unstoppable proliferation of cervical cancer cells, yet another of the ludicrous claims made on behalf of HIV. There is no evidence that immune suppression is a necessary prerequisite for cancer.

Despite all the finagling with AIDS definitions and juggling of figures, the numbers of predicted AIDS cases still refused to rise to predicted levels. By the early 1990’s the epidemic was simply running out of steam. Most of the AIDS hype was merely apocalyptic theatre anyway, designed to sell expensive, lethal so-called anti-viral drugs, and the pharmaceutical companies viewed with alarm the prospect that the billions spent on R&D of said drugs would not show a good return if the show was beginning to fold too soon. So it was decided to take the AIDS circus on a third world tour. By sneakily re-packaging the fatal endemic diseases that have always killed Africans for generations - tuberculosis, malaria etc. – as AIDS, even without an HIV test, it could be claimed that sub-Saharan Africa was doomed, unless they could be subsidised by the developed world, who would pay for expensive anti-viral drugs. Similar AIDS panics are even now being fostered in India and Asia.

© 2005 Michael Verney-Elliott & IRF  

                                                                                  Ellner, M.V.E., Shenton, Lauritsen at the Alternative AIDS Symposium, Buenos Aires, April 1995.

A Highly Important New Paper from Western Australia 

Debunks AZT

The Perth group in collaboration with Helman Alphonso of Colombia and Todd Miller of Florida, Miami, have published a very important paper, A critical analysis of the Pharmacology of AZT and its Use in AIDS, in Current Medical Research and Opinion.

By Michael Verney-Elliott 

Continuum Magazine, Vol. 5, No. 6 - Summer 1999 

The article, issued as a 45 page supplement to the journal, cites 121 references to support their conclusion: "A critical analysis of the presently available data which claim that AZT has an anti-HIV effect shows that there is neither theoretic nor experimental evidence which proves that AZT used either alone or in combination with other drugs, has any such effect."  Their study shows that the use of the drug, whatever claims are made on its behalf, to be as irresponsible, having due regard to its admitted toxicity, as it is ineffectual in stemming the production of the virus.

It is currently supposed, especially by doctors prescribing AZT (Zidovudine etc) to treat both people with AIDS  and people testing 'HIV-positive', that the drug will block the virus' capacity to infect cells.  As the Perth group clearly shows, this belief is totally unsupported by data from in vitro (lab cell culture) or in vivo (living patient) studies. The Perth group cautions very forcibly against attempting to extrapolate from in vitro studies to an in vivo context.

The original justification for using AZT, a drug previously demonstrated by cancer researchers to be highly toxic, to treat 'HIV' infection was based on studies which purported to show that the drug acted as a DNA chain terminator.  For 'HIV' successfully to infect a cell, after entering the cytoplasm of a permissive target cell, the virus must, with the aid of an enzyme commonly called reverse transcriptase (RT) transcribe its genetic information, carried in the form of RNA, into a double strand of DNA, which it then proceeds to integrate into the cell's nucletic DNA.  Thereafter, whenever the cell is stimulated into activity, more virus will be generated.  It was claimed, on the basis of in vitro studied carried out in 1985/6, that AZT (azidothymidine) was able to inhibit the reverse transcriptase enzyme, thereby stopping the transcribed DNA chain from being completed.  Moreover, it was alleged that the AZT is selective in inhibiting the supposed virus-specific reverse transcriptase without damaging other cellular enzymes or interfering with necessary cellular DNA synthesis.

The Perth team first tackle the question of triphosphorylation of AZT to AZTTP.  Only this form of AZT is deemed effective in inhabiting RT activity.  However, it is acknowledged, even by AZT's promoters, that this form of AZT is far too toxic to administer to patients directly, so a series of studies were carried out seeking to show that the cells metabolised AZT into AZTTP naturally, thereby conferring an anti-HIV capability of the drug.  All these studies were flawed, and indeed later studies showed that the AZT remained ineffective in stopping the reverse transcription of viral RNA into proviral DNA.  Moreover, as the group point out in the Comments on this section of the paper, AZT is very efficiently monophosphorylated intracellularly, and there is clear evidence that this results in "decreased cellular DNA synthesis".  This of course was always one of Peter Duesberg's most telling arguments against the use of AZT- that in order to forestall the virus the drug would have to destroy healthy cells.  equally damaging to the cell's metabolism is the evidence that the Group quotes to show AZT destroys mitochondrial DNA synthesis, which inevitably results in destruction of the cell.

As the Perth group point out, if the theory behind the use of AZT is correct, then this should be reflected in the rapid diminution of the number of viral particles supposed to be found in the blood of alleged 'HIV' infectees.  However, according to the kinetics of David Ho's 1995 model of 'HIV' viral replication, billions of viral particles are continuously generated daily after infection, and AZT apparently does nothing to prevent this.  If the claims made for AZT are correct, then the viral load should diminish rapidly with the use of the drug; and the death of the productively infected cells, which live for only a few days, should see a complete clearance of the infection as no further cells can be infected.  None of this has been shown to be the case. 

In summary, 'HIV' experts seem to agree that AZT inhibits reverse transcription of 'HIV' RNA into proviral DNA, but only in vitro in the form of AZTTP, which cannot be given to patients because of its lethal toxicity; any conversion of AZT into AZTTP occurring intracellularly is below the level needed to inhibit RT.  Thus, the drug does not have an anti-'HIV' effect at all, but has well documented toxic effects on mitochondria, without which the cell cannot survive.  Moreover, the drug is known to cause hideous side-effects in some patients, including severe megaloblastic anaemia, unbearable headaches, nausea, muscle wastage and a huge increase (46.4%!) in the risk of non-Hodgkin's lymphoma.  

The Group acknowledge that there is evidence that AZT may have anti-viral and anti-bacterial capabilities - but this leads to complications in the assessment of how successfully the drug treats 'HIV'.  Is AZT considered to have helped the patients by a direct effect on the 'HIV' infection or was the efficacy more indirect in that the drug effectively treated opportunistic viruses and bacteria?  Could ever improving patient management be responsible for the improvement in the patients, despite the toxicities of AZT?  The true risk-benefit ratio in the use of AZT must be thoroughly re-examined, and urgently.  

For reasons of space, this is only the briefest overview of this exhaustively researched and closely argued paper, but I hope it conveys something of its seminal importance.  Even now, parents in America and pregnant women worldwide are being cajoled, pressured and even legally coerced into taking, or giving tot heir children, a drug o more than doubtful benefit but proven toxicity.  This paper, by the Perth group and their colleagues, should be required reading by all G.P.s's and so-called 'AIDS' specialists who are in a position to prescribe AZT.  It should also be acquired by all lawyers specialising in drug injury cases.

Eleni Papadopulos-Eleopulos, Valendar F. Turner, John M. Papadimitriou, David Causer, Helman Alphonso and Todd Miller: A Critical Analysis of the Pharmacology of AZT and its Use AIDS - Current Medical Research and Opinion Vol. 15, Supplement 1, 1999.

                                                                                                                        Peter Duesberg with M.V.E at the University of California, Berkeley

 'Virtual Viral Load' Tests  

   Seeing is believing - it's time to call their bluff!

    "...infectious units, after all, are the only clinically relevant criteria for a viral pathogen."

     Peter Duesberg and Harvey Bialy (Nature, 375, 1995, p. 197)

    Continuum Magazine, Vol. 5, No. 5 - Mid-Winter 1998/1999 

    By Michael Verney-Elliott 

Mediaeval theologians were obsessed with how many angels danced on the head of a pin. Virtual virology is a more recent phenomenon which persuades non-critical virologists that huge quantities of 'HIV' particles exist in the blood of people deemed 'HIV positive', and cause the thirty or so diseases currently supposed to make up the syndrome known as 'AIDS'.

Today, the curious mixture of virtual virology and theology which passes for orthodox 'AIDS' research is obsessed with how many demonic 'infectious units' are found in a cubic millilitre of blood. This obsession gave rise to the 'virtual viral load' test. The fact that the demons, just like the angels of old, can never be seen worries no-one, and 'AIDS' science depends more on gnosis than empirical observation. Paul Valery reminds us "What has been believed by all, always and everywhere, has every likelihood of being untrue."

As Peter Duesberg pointed out in his ground-breaking paper (Cancer Research 1.3.87), Retroviruses as Pathogens and Carcinogens: Expectations and Reality, one of many reasons why 'HIV' could not be the cause of 'AIDS' is that such a virus is never 'found' in sufficient quantity to have any pathogenic significance in those supposedly infected. Typically, viruses which cause disease are found at very high titre at the time the disease is active, but this just did not seem to be the case with 'HIV', either in those people said to be incubating 'AIDS' for ten years or those with the full-blown condition. By contrast, supposed 'HIV', if detectable at all, is only ever 'found' in minute trace quantities, and even then only by stretching laboratory culture techniques to their limit. This is one of the chief characteristics of a persistent, harmless passenger virus. The currently accepted evidence for the presence of active 'HIV' depends on surrogate markers, 'signals', non-specific antibodies etc., and what Jon Cohen calls "...HIV RNA's - a proxy for the amount of free virus ...". ( Science, 13.1.95, p.179) Thus the 'HIV' viral titres are deemed to be present by inference rather than direct observation as is usually the case with other disease causing microbes. As Lady Bracknell might have said: "A proxy? Viruses should be seen, not inferred!"

Duesberg's point about the scarcity of detectable virus in the blood of PWA's may have infuriated the orthodox 'AIDS' establishment, but until 1995 they were unable to argue with him. This was when they decided to switch from sloppy science to sharp practice. In 1995, David Ho and Xiping Wei published separate papers in the same issue of Nature (373, pp. 123 et seq. and 117 et seq.) claiming that far from being the indolent virus supposed during the previous 11 years of 'AIDS' research, 'HIV' was hyperactive, and soon after infection, high titres of virus were circulating continuously in the peripheral blood of 'HIV' positive individuals. Although these high titres had never been seen before by any other 'AIDS' researchers, by amplifying 'viral RNA' using PCR and using the resulting DNA's as a "proxy", the two papers claimed that the corresponding 'viral RNAs' represented the amount of cell-free virus in the blood. No-one spotted the absurdity that if there were that much virus present in the blood you would not need to amplify it by PCR in order to detect it. To claim to have found so much cell-free virus by using sequence amplification is as ludicrous as 'finding' a previously invisible inflatable elephant with a bicycle pump. However, the scientific community uncritically accepted this purely hypothetical gung-Ho theory of 'HIV' dynamics as conclusive evidence for it being the cause of 'AIDS', to the extent of making these papers the basis for the so-called 'viral load tests' currently used, and the prescription of 'anti-viral drugs' like protease inhibitors and AZT. Both papers have been thoroughly debunked by Duesberg and Bialy (Nature, 375, 1995, p.197), and Paul Philpott and Christine Johnson (Reappraising AIDS, Vol.4, October 1996), and more recently by Roederer et al. (Nature Med. 4, 145, 1997), and Hellerstein et al. (Nature Med. 5, 33, 1999), as well as in articles in Continuum.

Prof. Etienne de Harven, a distinguished expert in electron microscopy, has written two articles in Continuum (Vol. 5, No 2, Winter 97; Vol. 5, No.3, Spring 98) describing the standard method he developed in the 1960's for visual detection and morphological identification, in the fresh plasma of leukemic mice, of "RNA tumour viruses", as retroviruses were known prior to the discovery of 'immunodeficiency viruses'. The procedure can be carried out quite simply in any lab equipped with facilities for centrifugation, micro filtration and electron microscopy (EM) as follows:

A blood sample suspected of containing a pathogenically significant quantity of cell-free retroviruses is centrifuged to spin out the red and white blood cells, leaving just the plasma, the basic fluid in which the cells float. The fresh plasma is then diluted 1/1 with cold heparinised Ringer's solution. Heparin is an anticoagulant, added to thin the plasma and render it more suitable to pass successively through two millipore filters of diminishing size, first using 0.6 then 0.22 micrometer pore size diameter filters. These filter out any debris larger than the size of the viral particles being sought. The last filter used will be slightly larger than the 100-120nm diameter of a retrovirus. The final filtrate is then spun in a centrifuge at 30,000 g for two hours. This has the effect of concentrating any virus in the plasma into a tiny pellet which can be recovered from the bottom of the test tube. The pellet is then fixed, embedded in an epoxy resin block and shaved into ultra thin slices which can be mounted on copper grids and examined under EM.

Figure 1. Electronmicrograph of densely packed particles with retroviral morphology identified as the Friend murine (mouse) leukaemia virus. Pathologie-Biologie, Vol. 13, pp. 125-134

A perfect illustration of de Harven's purification technique is seen in Fig.1. This electron micrograph by de Harven was published in 1965, (Pathologie-Biologie, Vol.13, pp. 125-134) and shows densely packed particles with retroviral morphology identified as the Friend murine (mouse) leukaemia virus. The densely packed particles, identical in shape and size, were pelleted down from fresh plasma using the method described. The magnification is 19,500 x and it can be seen that there is very little extraneous material contaminating the final pelleted isolate, indicated by three arrows. The Friend virus is classified morphologically as a Type C oncovirus, one of a small group of retroviruses which encode a cancer-causing gene in their RNA. The ultra thin slice through the pellet clearly shows the dense core in bisected virions, as round black dots.

As Dr. de Harven explains in his second Continuum article, even by the late 'sixties there was a growing tendency to abandon the use of EM, on the pretext that it was cumbersome and time-consuming, in favour of the purification and identification of possible viruses using other means, chiefly the use of the sucrose density gradient without EM, allied with indirect surrogate markers. Already, the virologists were starting to cut corners. Moreover, after 1970, when the race was on to find human retroviruses which cause cancer, there was a very good reason why clear, EM visualisation of such human oncoviruses was abandoned. The simple truth was that they were unable, then as now, to find high titres of cell-free retroviruses in fresh human blood or plasma.

It is worth stressing at this stage that in the entire 15 years of 'HIV'/'AIDS' research, no micrograph has ever been published purporting to show purified, densely packed 'HIV' particles, recovered from the fresh plasma of 'HIV positive' subjects. Indeed, no such picture exists of any so-called human retrovirus, not even HTLV-I, the alleged cause of adult T-cell leukaemia. That is not to say that micrographs of alleged 'HIV' have not been published, but they invariably came from cell cultures grown sometimes for weeks, in the total absence of an immune system (it is worth remembering that 'HIV infection' is most often diagnosed on the detection of antibodies supposedly specific to 'HIV'), and involving co-culturing with known cancerous cell-lines such as H9 or CEM, and stimulated with mitogens, hydrocortisone and other chemical activators - the standard laboratory methods of reactivating latent viruses.

Figure 2. "Purified HIV-1 preparations are contaminated by cellular vesicles. Purified vesicles from H9 cells (a)..".Gluschankof, P. et al. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virology, 1997; 230:125-133

There is no better way to show the degeneration into sloppy imprecision in science characterised by the 'AIDS' war than to compare de Harven's micrograph with Fig. 2, a micrograph published in 1997 of material banded at 1.16.gm/ml in a sucrose density gradient. Prior to its publication, by Gluschankof et al. (Virology, 230, pp 125-133, 1997), it was claimed that material banding at this level represented pure retrovirus. However, this study, and another in the same issue by Bess et al., finally came clean and admitted that all sorts of debris and extraneous matter banded at the retroviral density in the sucrose medium, principally cellular microvescicles, something that de Harven had observed even in the 1960's.

Whereas de Harven has to use three arrows to identify impurities in Fig.1, Gluschankof et al by total contrast have to use three arrows to identify three 'viral' dots, which may or may not be retroviruses, in their culture-derived rubbish tip in Fig. 2. This comparison strikingly illustrates the precision and superiority of de Harven's method of purification to currently used methods.

Undoubtedly, sedimentation in sucrose density gradients has its uses, particularly in confirming viral identity. Viruses have specific buoyant densities, and it is indeed known that purified retroviruses form a distinct sedimented band at 1.16 gm/ml, but it is a major error to suppose that all material contained in the gross supernatant from a cell culture which bands at that level is pure retrovirus, as Fig.2 makes clear. Moreover, in plasma samples containing more than one variety of active virus, as in PWA's with several, concurrently active viral infections, distinguishing them by their morphology under EM may be difficult, so subsequent buoyant density tests may be needed. Even the use of surrogate markers may be legitimate, but only when numerous laboratories have established that a large quantity of virus particles, of identical shape and size, are invariably present in diseased tissues and the virus has been proved beyond any doubt to be the cause of the disease. Then, and only then, can markers or proxies be trusted to indicate viraemia. However, 'HIV' fails all these tests.

If Ho and Wei are correct, it must be possible to pellet down fresh plasma from a person or persons who have had a recent 'high viral load' test result and clearly see tightly packed identical viral particles using EM, in a quantity consistent with the amount of virus indicated by the 'viral load' test. The application of the de Harven methodology will clearly demonstrate the presence or absence of actual rather than virtual particles, and do away with bogus mathematical models, inappropriate use of PCR, proxies, surrogates and all the other trappings of modern scientific obfuscation. If the virus particles cannot be seen, then they are just not there, whatever the test may claim. If it is claimed that there are indeed 'HIV' particles in the plasma, but too few to form a pellet, then there is obviously not enough virus in the sample to be pathogenically significant. Had 'AIDS' researchers been able to photograph high titres of cell-free 'HIV' in fresh plasma using the de Harven method during the last fifteen years, undoubtedly they would have done so and published their results, even if only to silence critics like Peter Duesberg. There are no such micrographs in the entire 'AIDS' literature.

When assessing how much virus - viable, enveloped, infectious virion units - should be visible from the amount of :

" 'HIV' RNA's" determined by a currently used 'viral load test', important scientific evidence shows that the 'proxy' viral RNA's represent very few actual potentially infectious particles. As Duesberg and Bialy state in the heavily censored version of their 'viral load theory' critique published in Nature (ibid):

The senior researcher [George Shaw] of the Wei et al paper has previously claimed that the method they used overestimates by at least 60,000 times the real titre of infectious HIV [Piatak et al, Science, 259, pp 1749-1754, 1993]. 100,000/60,000 is 1.7 infectious HIV's per ml ... Further, Ho and a different group of collaborators have just shown [Cao, et al New Eng. J. Med 332, pp 201-208, 1995] that more than 10,000 'plasma virions', detected by the branched-DNA amplification assay used in their Nature paper, correspond to less than one (!) infectious virus per ml . And infectious units, after all, are the only clinically relevant criteria for a viral pathogen. [my emphasis]

A transcript of a public question and answer session at the 1998 World AIDS Conference in Geneva shows the following exchange between Huw Christie and David Ho:

Huw: .....If people have a viral load of 200,000 per millilitre, it should be possible, shouldn't it, to demonstrate particles, viraemia? Why is it necessary to use a technique which is designed for amplification of numbers?

Ho: This indeed has been supported by other forms of assays, including assays that do not amplify the target that you're trying to measure. For example, using the branched chain DNA technology the same type of results have been generated, and compared head to head and published in numerous scientific papers.

David Ho is curiously silent about the findings of the paper he co-wrote with Cao et al cited above by Duesberg and Bialy.

Thus it may be seen that the 'viral load test' at best translates into a barely, if at all, detectable level of virus-like particles which can have little relevance in 'AIDS' pathogenicity; at worst it is a specious argument to pump asymptomatic people full of expensive drugs which may cause more harm than good in the long run.

CALLING THEIR BLUFF - £10000 challenge

So confident am I that no such EM evidence can be produced by adhering strictly to the de Harven methodology, I am prepared to offer the sum of £1000 to the first person to submit just such a micrograph, prepared under stringent laboratory conditions. These are:

1. Only plasma centrifuged from fresh whole blood may be used in the experiment. No material derived from cultured cells will be considered, to rule out 'viral particles' which may be merely cultural artefacts.

2. The donor blood/plasma must be taken from a person/persons with a recent 'high-viral load' test result, and evidence for the date and result of the test (the number of 'HIV'- RNA's alleged) must be submitted, obviously with the name of the person/persons deleted to preserve donor confidentiality.

3. The donor must not be in receipt of protease inhibitors, AZT or any antiviral drugs.

4. Only cold heparinised Ringer's solution may be used to dilute the plasma 1/1 ( i.e. 50%).

5. The diluted plasma shall be first filtered by aspiration-filtration, through a 0.6 millipore membrane. The resulting filtrate #1 will then be filtered again, this time using a 0.22 millipore membrane and filtrate #2 will be submitted to ultracentrifugation.

6. Centrifugation at 30,000 g for two hours will be used to prepare a pellet, likely to be extremely small. This pellet will be fixed with glutaraldehyde and osmium, then carefully detached and embedded in epoxy resins following routine EM procedures.

7. The electronmicrograph shall be at least 19,500 x magnification, and must resemble that published in Fig.1 of this article for particle size and shape, but with one notable and important variation. 'HIV' has been deemed to be a lentivirus, possessing a dense core of truncated conical shape. An ultrathin slice of randomly packed lentiviruses must inevitably show a number of particles bisected to show this core lengthwise, as well as end-on, with a resultant apparent mixture of round and 'rod-shaped' dense cores. Any micrograph which does not clearly show this feature will be deemed not to represent the lentivirus 'HIV'.

8. This challenge is open to any qualified scientists, or microbiology students/lab technicians with the necessary lab skills and facilities to carry out the work.

Photos of the required electronmicrograph(s) plus full details of the methodology, along with brief details of the senders' qualifications, must be sent, preferably with proof of date of postage, to me c/o the Continuum office at the address in the magazine. The first submission received which fulfils the above requirements according to qualified scientific scrutineers will be presented with £1000, in cash or by cheque, whichever is desired. There is no time limit, and the offer will remain open indefinitely.

Although not qualifying for the £1000, reports of failure to detect significant quantities of virus in the fresh plasma of 'HIV' positive donors, under the above conditions, would be most welcome, and considered for publication in Continuum. Medical and scientific journals are notoriously reluctant to publish reports which disprove a currently held paradigm, thereby preserving their role as the upholders of orthodoxy. Modern science doesn't seem to be about debate any more. However, I should be very interested to hear from anyone who has tried to establish a visual record of the viremia predicted by a 'high viral load' test result - and failed. Hitherto, the 'AIDS Dissidents' have had to restrict themselves to picking holes and spotting paradoxa in the orthodox 'AIDS' literature. Surely it cannot be beyond the wit and resources of people like the Reappraising AIDS group in California to carry out this experiment. Many distinguished scientists in that group, possessed of more than enough expertise, could easily carry out the lab work, if they could get access to a lab and the relevant donor plasma samples. Instead of commenting on the orthodoxy's work, why can't dissident scientists do some of their own? As de Harven says, when he wanted to do just this in his lab in Toronto in the mid '80's, his students threatened a walk-out. Short of barricading ourselves in a hijacked lab, can any reader come up with another way to kick virological ass?

Modern microbiologists and virologists have developed, and continue to develop, a bewildering array of techniques to aid them in pursuit of their disciplines. However, the increasing sophistication of the technology carries with it a proportionally increased need for scrutiny and analysis of their lab results. Modern culture techniques, involving mitogenic stimulation, other chemical additives, co-culturing with known cancerous cell-lines, the use of sucrose density gradients - all these valuable modern tools of science can easily produce results open to misinterpretation, accidental or deliberate. Add to this the pressure from financial interests typified by pharmaceutical companies seeking quick results to order, and pressure on labs to secure grant funding etc. and it is not difficult to see how a few 'virus-like particles', inevitably dredged up in cell cultures, can be parlayed into a massive viraemia by using 'proxies' and mathematical prestidigitation.

The uncritical acceptance of the gung-Ho 'viral load' theory has led to some patently risible studies. The latest absurdity comes from Farzadegan et al. in The Lancet (7.11.98), who carried out a long-term study based on blood samples taken from 650 male and female injecting drug users principally African Americans, using three different methods of measuring 'viral load'. The results of their trial claim to show that the women progress to 'AIDS' at the same rate as men but with only half the amount of 'viral load'. In other words, 'HIV' is supposedly twice as pathogenic in females as males - yet another pathogenic first for 'HIV'. At no stage do they mention the possibility that the harmful effects of the continuous use of illicit drugs far more logically explains the seeming equality of progression to AIDS in both sexes, irrespective of apparent differences in HIV kinetics between the sexes based on ambiguous 'viral load' tests. Unless their data are confirmed by similar studies of 'HIV positive' African, Asian and European males and females who are not IDU's, what does their study prove? Chillingly, the paper suggests that as the virus appears to be doubly pathogenic in women, they should be urgently considered for early drug cocktail therapy as soon as diagnosed.

In the final analysis, the only way to establish a true, in vivo viral titre in peripheral blood is by recovery of virus from a measured quantity of fresh, suspect plasma, and seeing the packed particles in a micrograph. Seeing, in this instance at least, is believing. As de Harven has explained (ibid), an aliquot of the unfixed viral pellet may be resuspended in Ringer's solution and used for titration by the precise, traditional method. Virus counting under EM may be tedious, but would, of course, reinforce the observations made. If few or no viral particles can be seen in the above conditions, then certain questions must be asked:

1. If not whole infectious viral particles, what is the 'viral load' test measuring?

2. What are the 'proxy' RNA's representing?

3. After administration of protease inhibitor drugs, and alleged decrease in 'proxy' RNA's, what has in fact been inhibited?

4. If little or no infectious virus is found in plasma of supposed viremic people, how did the haemophiliacs become infected by their plasma-derived clotting factors?

If, as I predict, no pathogenically significant amounts of virus can be visualised after pelleting down fresh plasma of donors previously deemed to be highly viremic by a 'viral load test', then perhaps we may be on the way to getting a re-examination of the whole concept of 'viral loads'; David Ho will have his Man of the Year award rescinded; the action of protease inhibitors can be reassessed in terms of a realistic risk-benefit ratio; and we can finally say "A pox on all your proxies!" 

Acknowledgements: I should like to thank Dr. Etienne de Harven for his invaluable help in correcting and clarifying the technical aspects of the electron microscopy, and Alex Russell for diligent research, and Peter Duesberg for his usual kindness and common sense.

                                                                           Jad Adams, author of AIDS: The HIV Myth with Michael Verney-Elliott

AIDS - Oh what a phoney war!

Continuum Magazine, Vol. 5, No. 3  Spring 1998

By Michael Verney-Elliott

"We fought in nineteen-seventeen And drove the tyrant from the scene. We're in a bigger, better war For your patriotic pastime. We don't know what we're fighting for But we didn't know the last time. So load the cannon, draw the blade, Come on, and join the Death Brigade." 

George and Ira Gershwin.

These are the opening words of one of George Gershwin’s most rousing songs - "Strike Up The Band". They were invariably omitted as being too bitter, too cynical. I can’t get them out of my head as I write about the war against AIDS

I was nearly two years old when the first ‘Phoney War’ began. The term 'phoney war' was coined by historians to describe the six month lull, between the declaration of war by the British government against Nazi Germany on September 3 1939, and the start of the real fighting. During that period, the British busily dug defences, stripped out iron railings to make munitions, filled sandbags, distributed gasmasks, dispatched the first infant evacuees to safer areas, and generally got ready for the serious business of repelling the invading hordes. The Americans stood on the sidelines, apparently justifying their nickname of ‘Doughboys’ - kneaded at the beginning of World War 1, but not rising until halfway through. Still, it wasn’t a fight most Americans understood, as Ira Gershwin’s lyric shows, and a sizable portion of the US population were of German origin, with understandably torn loyalties.

Forty-odd years later, the world was stampeded, this time largely by America, into another phoney war, this time against ‘HIV’, "the probable cause of AIDS". A principal difference between the two wars is that the first ‘phoney war’ was the overture to one of the bloodiest conflicts the world has seen, culminating in the revelation in 1944 of the horrors of the concentration camps and the obscenities of Hiroshima and Nagasaki in 1945 before final victory. The AIDS war, by contrast, is still, some 14 years later, a phoney war, a looking glass war directed against a non-existent enemy retrovirus, ‘HIV’. It has already cost tens of billions of dollars, and shows no sign of being won. AIDS stands for Acquired (as opposed to congenital) Immunodeficiency (as judged by failure to combat normally harmless pathogens) Syndrome (a collection of diseases with a linking factor), and affects different groups of people for group specific reasons.

Who contrived this phoney AIDS war? By 1981, the US Centres for Disease Control (CDC) had not had a major epidemic to deal with since its inception following the polio epidemic in the late 40’s, and by the late 70’s, their track record stank. After the 1976 twin debacles of the wrongly predicted swine flu epidemic which left hundreds paralysed after the use of an inappropriate vaccine, and legionnaires’ disease, which was blamed on an ubiquitous bacterium found in soil and air conditioning units, for political reasons the CDC needed a genuine epidemic fast - by the late 70’s, there was talk of closing down the inefficient facility. Meanwhile, the National Institutes of Health (NIH) were under pressure to find the cause of an apparently new aggregation of previously barely noticed illnesses proving fatal amongst gay men and drug addicts. The National Cancer Institute, a tentacle of the NIH, also needed a boost to its flagging reputation. Very expensive labs had been set up as part of Nixon’s War on Cancer, but with the exception of claims by Dr. Robert Gallo to have found a viral cause of leukaemia, (subsequently completely debunked by Prof. Peter Duesberg), the National Cancer Institute was deemed by the early 80’s to have lost the war against cancer, and there was talk of closing, or at least mothballing some of those labs. In an uneasy alliance, the CDC and NIH, joined forces to combat a proposed AIDS ‘epidemic’, initially called GRID (Gay Related Immune Deficiency). Can anyone seriously believe that the largely homophobic staff at both agencies really cared that some gay men or drug addicts were dying of a rare pneumonia, and a form of blood vessel cancer usually associated with elderly men - the two original AIDS-defining diseases? The NIH’s interest in sick gays and drug addicts secured funding, keeping the labs working.

The first casualty in any war is truth, closely followed by common sense and rationality. The CDC-led propaganda machine was not helped by the fact that the two principal risk groups, gay men and drug addicts, were marginalised by society, and nobody cared very much what happened to them. The ‘risk groups’ were rather like the Czechs whom Hitler invaded at the start of his quest for lebensraum - the rest of Europe didn't care much, and Czechoslovakia was thought of as merely a small far away country, about which people knew little, and cared even less. How do you whip up enthusiasm and funding for a war which seemed to most middle-Americans to be fought solely on behalf of faggots and junkies, whose illness was perceived by many to be self-inflicted?

The first task was to make the public aware of AIDS as a general threat to the population at large. When haemophiliacs started to show signs of immune suppression, as well as recipients of blood transfusions, the CDC stressed that here were cases of the mysterious plague outside the original risk groups; some people may remember the clumsy description by Princess Anne of the ‘innocent victims of AIDS’. The impression was fostered that gay men and drug addicts had donated their blood and plasma to hospitals and the manufacturers of haemophiliac clotting factors, and infected innocent bystanders. No-one mentioned that the blood products were made from commercially acquired plasma, including imports from countries like Haiti, Senegal, Brazil, Belize and Zaire, as well as from drug addicts in America. I couldn't find any evidence that gays were in the habit of selling their blood or plasma, but the propaganda machine made no mention of that. The CDC played on popular fears and terror, and soon the world was convinced we were in for a deadly plague which would wipe out millions by the end of the century.

Gallo and his colleagues claimed a transmissible agent, probably a virus, was involved, and started to rummage in the 'retroviral' ragbag established in 1970 when Temin and his team revealed the phenomenon of reverse transcription. Virologists in other countries were also fashionably hunting for a viral cause of the new immune suppression syndrome, and very soon laboratories in France, Britain, America, Sweden, and Germany claimed to have come up with variants of the indirect markers that would come to be known as ‘HIV’ in co-cultures of cells from the tissues of patients, mostly gay men suffering from lymphadenopathy and irregularities in their T-cell subsets.

The Oxford English Dictionary defines the word ‘epiphenomenon’ thus: "Secondary symptom, mere concomitant of something else not regarded as its cause or result" - a perfect description of ‘HIV’, as the last fourteen years have shown. That claims of detection of variants of ‘HIV’ should be made almost simultaneously in several labs world-wide seemed like confirmation that scientists were on the right track. However, this was not the first time that different experts came to the same wrong conclusion, as the history of diseases like beri beri, pellagra and smon shows. I try to put myself in their place, given a first class ticket to ride the AIDS War gravy train. If I were the first to realise that train was steaming in the wrong direction, would I have had the guts to pull the communication cord? When Margaret Heckler’s announcement in 1984 that the ‘probable’ cause of AIDS had been found was welcomed unquestioningly by an anxious world, the enemy had been identified, and war could be declared. No-one asked why human retroviruses had waited for thousands of years until some seven years after Temin’s discovery of reverse transcription to start to cause diseases.

After an assay to detect alleged ‘HIV antibodies’ was patented, the CDC and NIH cast their net wider, and started to test blood samples in the Third World, Africa, South America etc. and sure enough they struck gold. The non-specific tests reacted in some members of all these populations, and AIDS went global. The discovery that ‘HIV antibody positivity’ was distributed world-wide finally guaranteed enormous funding for a global anti-‘HIV’ war. The World Health Organisation joined the fray, and by the late 80’s, was predicting 20 million people infected with 'HIV' by the year 2000, and 6 million AIDS cases. AIDS was being touted  as an even bigger threat to the world than the Black Death which had wiped out a third of Europe's population in the middle ages. By comparison with AIDS, we were assured, the Black Death would seem a minor blip in health history.

From the outset, not everyone was happy about the proposal of an HIV=AIDS=death scenario. Dr. Joe Sonnabend had been treating immune suppressed gay men in New York for a plethora of STD’s all through the 70’s, and he was convinced that AIDS was the result of an antigenic overload. The same patients who had continually come back to him for antibiotic and other treatments for a whole raft of herpes, hepatitis, syphilis and other STD’s then were among those who first came down with AIDS-defining conditions in the early 80’s. They had ignored his warnings that they were permanently undermining their health. The complacent belief in the efficacy and low-to-no risk of antibiotics had led most gay men to regard STD’s and their treatment as a mere recreational  hazard. Today, however, we are continually being told that antibiotics are losing the fight against such diseases as tuberculosis, and even in the 70’s there was a known strain of gonorrhoea allegedly brought back from Vietnam, and known as Saigon Rose, which was highly resistant to treatment. Sonnabend founded a journal called AIDS Research, to publish original research into feasible causes of AIDS that could not find publication in orthodox scientific journals. The magazine was soon taken out of his hands, re-funded by Burroughs Wellcome, and retitled AIDS Research and Human Retroviruses. Such is the neurosis of the propaganda machine during a war that even one small enquiring journal had to be  silenced, and converted to yet another cog in the disinformation machine. One of the most powerful weapons in any war is censorship.

One of the the first scientists to stick his head above the parapet and state his disbelief in what was by then officially called HIV as the cause of AIDS was Dr. Peter Duesberg, the world’s foremost retrovirologist. He was commissioned to write a paper for Cancer Research about the role of human retroviruses in disease, the expectation and the reality, and in an elegant work published on March 1 1987, he demolished not only the Gallo theory that HTLV1 was the cause of Adult T-Cell Leukaemia, but stated in the last third of the paper that from the available evidence ‘HIV’ could not be the cause of AIDS. His paper was a bombshell, and swiftly earned him the condemnation of the fat cats in the AIDS War - he was treated as a fifth columnist or saboteur because he had dared to break ranks and tell the truth as he saw it. The subsequent list of such ‘saboteurs’ reads like an Honour Roll -Kary Mullis, Nobel prize winner for the invention of polymerase chain reaction; Prof. Walter Gilbert, Nobel prizewinner for his work on bacteriophages; Prof. Harry Rubin, winner of the prestigious Lasker Award for his work in virology; Prof. Serge Lange, the greatest mathematician in the USA; and Britain’s Prof. Gordon Stewart, who has repeatedly been refused publication of letters to  leading medical journals, despite the fact that his predictions of the numbers of AIDS cases have been consistently and uncannily accurate. All these prominent scientists and doctors, and numerous others, expressed their unease about the premature consensus which labelled ‘HIV’ the sole cause of ‘AIDS’.

The fact is that once the ‘HIV’-AIDS war machine was rolling, no-one on board wanted to dismantle it and lose not only credibility but all the money and prestige that being an AIDS ‘expert’ generate. For example, The Boston Globe reported as recently as April 18 1998:

"Two scientists who have fought bitterly over discovery rights to the virus that causes AIDS will share a $ 100,000 prize for their joint achievements. Dr. Robert Gallo of the University of Maryland and Dr. Luc Montagnier of the Pasteur Institute in Paris and Queens College in New York are scheduled to share a podium at Boston’s Four Seasons hotel on April 30 to accept the 10th annual Warren Alpert Foundation Award."

The booty may console Gallo for the fact that even now, the US Government is thinking seriously whether or not to extend funding to his posh new institute in Baltimore, due to end officially on June 30th. (Nature Medicine, p.541, May 1998).

For some time, evidence has been growing that there are efforts afoot to ‘downsize’ or even call off the AIDS War. By the end of the 80’s, the propaganda department at the CDC were having to duck and dive to maintain the AIDS panic. Even by finagling the estimated ‘HIV’ positivity figures, which see-sawed up and down from 1 million constant for several years, to a low of 600,000, and adding new diseases into the syndrome, the US AIDS cases failed to live up to their inflated predictions. Still it dawned on no-one that if the estimated, or even real, numbers of 'HIV'-positives never reflect the actual numbers of AIDS cases, they had the wrong presumed bug in their gunsights. AIDS was the first recorded example of a virgin-soil epidemic in which the numbers of people supposed to be infected by an exponentially spreading pathogen were remaining stable or even diminishing.

I remember being puzzled when Margaret Thatcher cut off £350,000 funding for the projected Medical Research Council HIV positivity survey planned for 1993. This was designed to try to estimate the number of ‘HIV’ infectees in Britain. Had she been told by one of those secret, black and midnight Think Tanks who advise governments, that there was no heterosexual AIDS epidemic, and that the money would be wasted? Many people had been pointing out since the late ’80’s that the threatened heterosexual epidemic had not materialised, and that all the government advisers had been totally wrong about projected AIDS figures. They were roundly denounced as homophobes, out of touch with reality. As it transpired, the AIDS War free loaders, speculators, profiteers, spivs, hangers on and camp followers in 1993 needn’t have worried. Wellcome came to the rescue with a sack of gold to fund the study - when you make anti-‘HIV’ drugs, you need punters, so they paid for the MRC to find them. There weren't many.

By the mid 90’s, it seemed most people were beginning to treat the AIDS War rather like one of those desultory, incomprehensible little civil wars rumbling on in the Balkans or the former satellite states of the dead USSR - self-absorbed and self-inflicted, hardly worth a glance as you turn the pages of the newspaper to find the footie results. The WHO, realising that AIDS had passed its panic-by date in Europe, but still trumpeting a worst-case scenario for AIDS in the 3rd World, nevertheless gave the boot to 750 workers in the Global AIDS Programme in April 1995. After all, if AIDS cases in the West are falling, even in the absence of a cure or a vaccine, then AIDS cannot be an infectious epidemic at all.

What I interpret as the winding down of the AIDS war, much akin to America’s slinking out of Vietnam, is reflected in an article in The National Journal, May 9, 1998, Pg. 1062; Vol. 30, No. 19. Entitled The AIDS Initiative, One Year Later, by Garance Franke Ruta, it is worth quoting at length:

"Last May 18, in a commencement speech at Morgan State University, President Clinton declared the development of an AIDS vaccine a national priority, saying, "I am prepared to do all I can do to make it happen." He called for the development of a vaccine within a decade, likening the endeavour to the race to land on the moon. One year later, the National Institutes of Health (NIH) has yet to name a director to set up the new Vaccine Research Center Clinton announced. The search process had to be reopened after everyone in the first crop of candidates was deemed inadequate or withdrew from consideration. And that’s not the only important vacancy at NIH: The Office of AIDS Research (OAR) has not had a permanent director since November, when the former head, William E. Paul, decided to return to his immunology lab. And the directorship of the vaccine and prevention research program at the National Institute of Allergy and Infectious Diseases (NIAID) has been empty ever since Patricia Fast left last November to join Aviron, a California-based biotech firm. The Administration has been slow to fill positions throughout the government, and this is just another example of that," said Jeff Jacobs, director of government affairs at AIDS Action, a Washington-based advocacy group. "If the Administration has an intent to have this vaccine on line, they need to move as quickly as possible to make sure the director of the vaccine center is on line at the NIH."

This smacks of rats, sinking ships, and dodging the poisoned chalice. To head the department which doesn’t come up with a vaccine against ‘HIV’ won’t look good on anyone’s CV.

The growing dissatisfaction amongst gay men in particular with the way in which AIDS funding is administered by AIDS charities has become even more marked since this article by Erin McCormick appeared last year in the San Francisco Examiner (26.4.97). British AIDS charities should take note:

"Michael Petrelis wants to know what happened to the $1.5 billion the United States spent on AIDS last year. The 39- year-old AIDS patient, and a growing number of activists like him, have been willing to bang on locked boardroom doors, rifle through file cabinets and generally raise hell to make sure money raised for AIDS goes to fight the deadly disease and not to overhead expenses and high salaries for charity executives. Now they are taking their crusade public with an Internet Web site that will allow donors and people with AIDS to follow the money that goes to the dozens of charity relief efforts around the country. "There’s a new phenomenon of people with AIDS living longer, which means we're asking more questions about services," said Petrelis, who said since he started prodding organisations for financial information he has been banned from receiving full services at three Bay Area AIDS charities. "We’re now questioning where the money goes from the AIDS Walk, the AIDS Redound the AIDS Dance-a-thon because we would like to have services like hot meals and housing," he said. The Accountability Project Web site (www.accountability project.com), which reveals IRS tax filings and other financial information about major U.S. AIDS charities and other non-profit (organisations), makes it possible for Internet surfers to get instant information about how they spend their money. The project, an offshoot of the in-your-face AIDS activist group, ACT UP Golden Gate, is also pushing for laws to require open board meetings, democratic management and greater financial scrutiny for the nation's rapidly growing non-profit sector."

A more recent piece posted on the Rethinking AIDS website (16.4.98) from Tom Hudson concerns the huge funding for Gay Men’s’ Health Crisis, the original AIDS self-help group in New York.

"I just received in yesterday’s mail a reply from the New York State Department of Charities. I had requested a copy of the financial status of the Gay Men's Health Crisis of West 20th street here in New York. For the last fiscal year available - ending June 30, 1996 the GMHC had received $28.3 million dollars in contributions, including $5.2 million in government grants. GMHC spent that year $5.1 million in FUNDRAISING expenses, which is $21.4% of their budget. They have a full time public relations and media research staff. My dear friends, what could we do with $28.3 million a year? Think of it. I also have before me an article in a local newspaper written by several people including former GMHC employees who say that the place is a joke. If they hand out a leaflet they call it patient counselling on their reports. Case after case of clients asking for the help promised in the leaflets and posters are turned away and phone calls are not answered whilst within the organisation they live like royalty. GMHC owns two office buildings and occupies three others as well. They have a huge staff of hundreds. Can you just imagine what could be done with this huge amount of money for truly honest and health producing information? Gary Null once said that it sure pays to sell out your integrity. Shocking as his statement was, it is proven over and over again. Now the GMHC leaders are weeping that the CDC is reporting large decreases in AIDS deaths. They are lamenting the news. I won’t say why, but could it be because their funding is based upon AIDS deaths?"

Nearer home, a letter to Pink Paper from Pete Forest (May 15,1998) commented on the 3 directors of the Terrence Higgins Trust (THT) on £43,000 a year and the secret salary of the Chief Executive Nick Partridge. On May 19, a very concerned Susie Parsons, Chief Executive of the London Lighthouse, was inter-viewed on BBC TV news about the threat to close the ‘flagship hospice’ She was obviously deeply distressed and who wouldn’t be at the thought of losing her Director’s salary reported to be £60,000. That’s a lot of moolah for dispensing tea and sympathy. If nothing else, the AIDS war has certainly inflated the price of altruism. For as long as diamond studded vivandieres like Liz Taylor, Elton John and the late Princess Diana could guarantee that the donations rolled in, the AIDS charities were awash with money and could fulfil their function as the AIDS War’s deluxe equivalent of the Women’s Voluntary Service (WVS) but when the phoney war finally peters out, once the party’s over, who’ll take care of these overpaid caterers? All the hands-on work with PWAs is done by dedicated, unpaid volunteers or low paid workers, so we need feel no sympathy for the executive greedies. Partridge worked hard for the Troops Out of Ireland movement before cashing in at the THT, so perhaps he’ll be quite philosophical about being demobbed.

The world is getting ready for the biennial AIDS conference in Geneva, where the nostrum floggers will be out in force, glossy brochures at the ready. I wonder if they will spare a thought for the ultimate fate of the 1500 chimpanzees, bred specifically for AIDS research, and now regarded as surplus to requirement, but costing the US Government $7.3 million a year to house and feed. All those people currently earning unjustifiably fat salaries on the backs of PWA’s would do well to monitor just what happens to their primate cousins. Perhaps they could get jobs looking after the chimps in the sanctuaries proposed by Newt Gingrich to the US House of Representatives on May 5th.

It would be nice to think the real war against the AIDS phenomena could begin once the phoney war against ‘HIV’ has been exposed for the grotesque con trick it is, but I’m not hopeful: Phil Johnson of Rethinking AIDS posted an article from the San Francisco Weekly (May 13 1998) by Tara Shioya dealing with the wave of ‘Circuit Parties’ sweeping the gay scene in the USA. She describes the parties on a circuit which takes in Palm Springs, Fire Island, Miami, Atlanta, New Orleans and Montreal, where up to 7000 gorgeous young men party non stop for three days :

"During a circuit party weekend, the dancing usually begins around 9 p.m. and goes until 3 a.m., followed by various after-parties that run till midmorning. Most Circuit-goers will rely on drugs - poppers (a gold-coloured liquid sold legally as "liquid incense," which causes a high when the fumes are inhaled); crystal methamphetamine, popularly known as crystal, "Tina," or "Crissy"; and to a lesser extent, cocaine - to stay awake for the parties. Then there's an alphabet soup of other illegal drugs that heighten the emotions and senses. Ecstasy ("X"), or MDMA, is at the heart of the scene because of its relaxing and, some say, aphrodisiac effects; it's usually taken in combination with one or more other drugs. Ketamine ("Special K" or just "K") is an anaesthetic veterinarians use on cats and "subhuman primates"; partygoers usually dry or bake it into crystal form, and then crush it into a fine white powder that's inhaled in "bumps" from a small glass vial with a rounded plastic cap, called a "bullet." Users feel happy and relaxed - unless they overdose and fall into a "K-hole," a temporary trance-like state. GHB ("G"), Gamma hydroxybutyric acid, a liquid anaesthetic with effects similar to Special K, is taken orally: While some users report a better high from G, its effects are unpredictable. (Health food stores once sold GHB as a growth hormone supplement, but the FDA took it off the market.) Too much G can induce any number of effects, including violent vomiting or a "G-coma," which lasts hours. Combined with alcohol, the drug can be lethal."

This list of drugs is highly reminiscent of that described by Larry Kramer in his novel Faggots in the late 70’s, just before the appearance of the first gay AIDS cases, as well as the list given by John Lauritsen in the Meditel/Channel 4 documentary The AIDS Catch in 1990. The different combinations of these drugs, accompanied by repeated infections with - is it? - eight different herpes viruses, who knows how many hepatitises, and bacterial STD’s, plus the mass of antibiotics used to treat them, are going to make a lot, if not all, the sad young men very sick. When Michael Callen described the identical lifestyle he led in the late 70’s, before subsequently developing various AIDS-defining illnesses, he was honest enough to admit that this was the cause of his illness. As he said to me, the wonder was that he had the strength to crawl to Joe Sonnabend’s surgery for treatment. Shioya’s article mentions the reservations of "AIDS experts" who ".... fear the prevalence of drug use on the Circuit - particularly, crystal - leads to dangerous sexual practices that will increase the spread of HIV." Wearing a condom as thick as a wellington boot will not save anyone who repeatedly turns their body into a toxic battlefield or sticks a loaded gun to his head and pulls the trigger? Could it be that the CDC and NIH now know they can never win the War against AIDS by fighting ‘HIV’ and are preparing to make gays the scapegoats for their failure?

Real victory over the illnesses grouped as AIDS can only begin when gay men can be honest and admit that in our case, AIDS is a hedonistic holocaust brought on by our own excesses, and stop passing the buck to a harmless irrelevant epiphenomenon called ‘HIV’. They can either get real or get dead. The choice is theirs. The fight for gay liberation was surely about more than an inalienable right to drug-fuck each other to death. Lest I be misunderstood, the war against AIDS-defining illnesses is a just war, a must war, and worthy the winning; but the phoney war against ‘HIV’ is a wicked waste of time, blood, hope and treasure.  

                                                                     M.V.E in St. Petersburg, Florida, 1991 filming Meditel's AZT Cause for Concern

AIDS  Vaccines - The Cruel Delusion 

Dissenting View  Continuum Magazine, Vol. 5, No. 2  Winter 1997/8

By Michael Verney-Elliott

The theory of vaccinating against a disease requires that one must find its true cause, and if it is an organism like a virus or a bacterium, a vaccine perhaps may be constructed which will raise prophylactic antibodies to neutralize the bug, should it infect, before it can cause the disease. None of this applies in the case of AIDS and ‘HIV’. AIDS is not a specific disease but a collection or syndrome of some thirty old diseases; the so-called AIDS-virus, ‘HIV’, has never been properly isolated, let alone shown to cause immunodeficiency; AIDS develops only after some ten years of an effective antibody defense against the constellation of some nine or ten proteins alleged to constitute the AIDS ‘virus’, which itself may not be a virus at all. The idea that an AIDS vaccine will be found at the end of the rainbow, like the proverbial pot of gold is merely a crock of shit.

Even the AIDS Junta are sharply divided over the use of an anti-’HIV’ vaccine. One section are realistic enough to admit that there can never be a vaccine. The other group want to waste time and treasure in raising hopes whilst lining their own pockets. This latter group are getting ready to attempt the old vaccine scam. According to Nature (15.1.’98) San Francisco-based veteran AIDS researcher Don Francis is embarking on a Phase III trial using some 7500 "healthy" volunteers in the USA and Thailand in a $20 million three year project using a vaccine based on glyco-protein 120, an alleged component of ‘HIV’. John Moore, of New York’s Aaron Diamond AIDS Research Centre, rightly describes this trial as a "total waste of time and money." (Nature 15.1.’98)

The vaccine scam works like this. Identify and magnify an ‘epidemic’ disease, whip up world panic, and devise a vaccine against the supposed causative agent. Administer the vaccine, preferably just before the epidemic starts to wane naturally, and then, when the cases of the disease start to diminish, claim the vaccine has worked and the pharmaceutical company who manufactures it will get the credit for saving mankind. There will be bouquets and Nobel prizes all round and every one makes a lot of money. One has only to look at the cases of the anti-poIio and anti-smallpox vaccine campaigns to see the classic modus operandi in taking credit for ending epidemics, which in the manner of all self-limiting phenomena, were already dying out before the vaccine was introduced.

In the USA during the late ‘forties, there was a noticeable increase in polio cases. This prompted the authorities to pay a bounty of $25 to GP’s reporting any suspected case of polio, treating it as a notifiable disease. The numbers of cases of ‘polio’ shot up, causing a national panic. Any stiff neck or slight limp was reported. Curiously, at the same time, the official number of cases of aseptic meningitis, which shares some symptoms with polio, and previously reached some 25,000 annually nationwide, disappeared completely. A whole disease just vanished. Subsequently, when the polio epidemic had abated, the credit being given to Salk and Sabin’s polio vaccines (which frequently caused polio ! ) the numbers of meningitis cases returned to their previous level. Professor Gordon Stewart explained to me that the same thing happened in India when people were paid a few rupees to report cases of smallpox during the WHO’s anti-smallpox campaign As a result, official figures for chickenpox disappeared during the campaign, but reappeared with a bang after smallpox was declared eradicated in 1980. The trick is to make sure you get in with the vaccine just before the numbers of cases of the disease start to diminish. In the case of polio, the definition of the disease was later tightened up to exclude illnesses with similar symptoms - meningitis, encephalopathies etc. - and presto, there was a dramatic drop in the official polio cases. Hooray, the vaccine worked. Unfortunately for the AIDS Junta, the epidemic is clearly already on the wane, at least in the West, and there is the worrying little detail of the ten year incubation period. The latest official German annual AIDS- deaths figure for 1997 is 35 (thirty-five!) out of a population of some 81,000,000 (eighty one million!) so does Germany really need a vaccine? Does anyone? Indeed, will it ever be possible to devise a single vaccine against a syndrome which seems to vary in intensity, incidence and symptoms throughout the world and even from city to city? Watch out for the inevitable redefinitions of AIDS, either to make the threat seem more widespread than it is, or to have just the reverse effect, by diminishing the number of AIDS-related illnesses and make it look as if AIDS is on the wane, thanks to a vaccine or the latest ‘miracle’ drugs.

In April 1984, the world was told that the ‘probable’ cause of AIDS had been found - a novel ‘human’ retrovirus called variously LAV, ARV, and HTLV-III. Subsequently, despite a complete lack of convincing scientific evidence, which persists to this day, that such an organism causes immunosuppression, in a pre-emptive move the claimed novel retrovirus was named ‘HIV’ (Human Immunodeficiency Virus) by an international committee (1986). It was accepted that after a period of latency, some infectees start to manifest symptoms of AIDS, and the average length of asymptomatic infection was some ten years. Therefore, any trial of an ‘anti-HIV’ vaccine must run for at least ten years to show whether the vaccine will prevent disease after infection with the alleged viral cause of AIDS. To date, none of the vaccine trials has run for more than a few months, and Francis’ trial is scheduled to run only three years.

Vaccination will be a singularly inappropriate method of countering ‘HIV’/AIDS. A vaccine uses either a killed pathogenic micro-organism or a specially weakened (attenuated) live form to induce a prophylactic antibody response. However, vaccination is primarily used to protect against pathogens which cause diseases of rapid onset. Organisms which replicate very rapidly to high titre may cause a disease before the body can mount a successful antibody response. Vaccination against a pathogen primes the body by tricking it into generating antibodies in advance of a natural infection. This antibody titre then subsides, but leaves behind memory cells which can mount an almost instantaneous response on subsequent exposure, as opposed to having to wait for the body’s humoral immune system to analyze the intruding pathogen and then synthesize an appropriate antibody. However, according to the orthodox view of ‘HIV’/AIDS, disease only develops after the body has already been generating neutralizing antibody against ‘HIV’ for roughly a decade. Indeed, it is these antibodies which are alleged to show infection with ‘HIV’ in the first place. All those rapacious AIDS researchers seem to be unaware of the irony that the very clue which reveals ‘HIV infection’ protects from any ill-effects allegedly caused by the ‘virus’. As Peter Duesberg explained eleven years ago (Cancer Research, 1.3.’87) once you are producing the antibodies which give an ‘HIV’+ diagnosis, you are already vaccinated. However, we are now constantly being told of the lightning-fast mutability of ‘viral strains’, usually to explain why the latest miracle drugs cease to work. This has excused the failure of AZT, other nucleoside analogue drugs and protease inhibitors, and will no doubt be used to explain the failure of anti-’HlV’ vaccines, including Don Francis’. Once again, the brilliant ‘HIV’ will have mutated to outwit the vaccine.

The difficulties surrounding the production of a vaccine against ‘HIV’ are too horrendous for it ever to be a possibility. The putative virus is alleged to mutate so rapidly that a single individual is said to produce many different strains of virus simultaneously. Which one do you vaccinate against? How could any vaccine protect against a constantly moving target? Should one use an attenuated live viral strain or a killed fully pathogenic one to generate an antibody response? It is also supposed, since a group of eleven ‘HIV’ infected people were found in Australia who have failed to develop AIDS after some 13 years, that not all strains of ‘HIV’ are pathogenic. Would a vaccine-derived antibody raised by using such a non-pathogenic strain in a vaccine afford protection against a fully virulent strain of ‘HIV’? What of those scientists like Montagnier, who as early as 1985/6 was suggesting that the antibodies against ‘HIV’ were autoimmune antibodies and may themselves be the cause of the decline of the immune system. Could a vaccine cause AIDS, as the polio one undoubtedly did? Even in the more than unlikely event of a successful vaccine being devised, the implications are alarming for a country’s blood supply. If there is nothing to distinguish vaccine-generated antibodies from an acquired infection, and antibody-positive blood is screened out of the blood supply, this suggests that countries with widescale vaccination, i.e. in the Third World, will have large shortfalls in blood supplies for transfusion. Will vaccinees be told not to donate blood, setting up a form of ‘positive’ discrimination?

What of the "healthy volunteers" in Francis’ study? Are they from the ‘high risk’ groups? The AIDS epidemics in the USA and Thailand have entirely different profiles, cases being more evenly distributed between the sexes in the latter area, but the linking factor amongst heterosexuals in both countries seems to be drug addiction, especially in sex workers. How will the volunteers be encouraged to challenge the vaccine? Will they be encouraged to have unsafe sex and indulge in heavy recreational drug use with shared needles in the hope that they will become infected with ‘HIV’, thereby challenging the vaccine to protect them against AIDS ten years - not the planned three years - down the line? This would obviously be stupid as well as completely unethical, but the fact remains that a vaccine trial must challenge the vaccine to protect the recipient. When Walter Reed wanted to demonstrate the efficacy of his yellow fever vaccine, he vaccinated himself and then deliberately infected himself with the mosquito-borne arbovirus which causes the disease to demonstrate that his vaccine worked. Are Francis’ "healthy volunteers" in ‘high-risk activity’ groups, or just Mr. and Mrs. Average? Mr. and Mrs. Average do not get AIDS. A recent feature article in the Sunday Times Magazine (14.12.’97) made much of a group of celebrity and other volunteers for an anti-‘HIV’ vaccine trial, with varying degrees of risk behaviour, but short of using deliberate injection with a strain of ‘HIV’, what risk do they have of ‘infection’? These people obviously mean well, but their altruistic gesture is as futile as nuns volunteering for a vaccine trial against syphilis. The fact remains, ‘HIV’ is not highly infectious like the polio or measles viruses, yet another reason why a vaccine is wholly irrelevant.

The only certain way to test the efficacy of a medicine or a vaccine is by double-blind placebo testing. Such testing is totally impracticable, ostensibly because it would be unethical to give a placebo to a group of volunteer controls when dealing with an allegedly fatal pathogen. This excuse is entirely specious. In a double-blind controlled study, the volunteers would have to agree to be infected with the pathogen - in this case ‘HlV’ - and then it could be shown whether the recipients of the vaccine received protection from ‘HIV’, whilst those who got the placebo would succumb to AIDS. According to the orthodox view it would take anything up to a decade or longer for AIDS symptoms to show up in those who didn’t get the vaccine after being infected with ‘HIV’, so such a trial would not only be unethical but also impractical from a time point of view. What the AIDS Junta really fears is that neither group of volunteers in a double-blinded controlled study would develop AIDS, because they are aware that ‘HIV’ is not the cause of AIDS but a marker for risk.

                                                                               Michael Verney-Elliott & Eleni Eleopulos at AIDS: A Different View, Amsterdam, 1992.

A Reappraisal of the HIV/AIDS Hypothesis

by Michael Baumgartner, Alex Russell and Michael Verney-Elliott

Petition submitted to the United Nations, Geneva 1997

In 14 years, 'HIV' has still not been proven to be the cause of the 29 'AIDS' defining illnesses. The 'HIV' hypothesis has been unproductive and non-predictive because 'AIDS' is neither an infectious epidemic nor caused by 'HIV'.

To date, 'HIV' has never been isolated as a unique, exogenous 'retrovirus', Dr. Robert Gallo and Prof. Luc Montagnier, the alleged co-discoverers of 'HIV', did not follow the rules and standard protocols designed for 'retroviral' isolation set out in 1973 by the Pasteur Institute of France (see Sinoussi in Spectra 4, 1973): The steps for 'retroviral' isolation are:

1.  Culture of putatively infected tissue,
2. Purification of specimens by density gradient ultracentrifugation,
3. Electro micrographs of particles exhibiting the morphological characteristics having condensed inner bodies (cores) and knobs and dimensions almost spherical; in shape and in a diameter of 100 - 120 nM of retroviral particles at the sucrose density of 1.16 gm/ml and containing nothing else, not even particles of other morphologies or dimensions.
4. Proof that the particles contain reverse transcriptase,
5. Analysis of the particles, proteins and RNA and proof that these are unique,
6. Proof that points 1 to 5 are property only of putatively infected tissues and cannot be induced in control cultures.
7. Proof that the particles are infectious, that is, when PURE particles are introduced into an uninfected culture or animal, the identical particle is obtained as shown by repeating steps 1 to 5.

There will never be a cure or a vaccine against 'HIV' because it does not exist as a unique 'exogenous lentivirus'. There is no Universal Gold Standard 'HIV' test to prove 'HIV' positivity. The 'HIV' antibody test does not detect a 'virus' but an assortment of proteins that are non-specific to the hypothetical 'HIV' In Current Medical Research and Opinion, vol. 13, no. 10, August, 1997, and Bio/Technology, June, 1993, 'AIDS'-analyst and biophysicist, Dr. Eleni Eleopulos and colleagues exposed the non-specificity and unreliability of the 'HIV' antibody test. Dr. Eleopulos's critique supports the argument for the international banning of the 'HIV' antibody tests.

It was admitted ten years ago that there is no such thing as a typical 'HIV' isolate, therefore, there can be no Gold Standard 'HIV' test because there is no Gold Standard  'HIV' isolate. On each continent there are different criteria for 'HIV' positivity and 'AIDS' definition. All evidence of 'HIV' positivity must be confirmed by pure culturing of a patient's lymphocytes and detection of whole, cell-free viral particles; so far this has never been achieved. 'HIV',  like all known 'lentiviruses' is not known to be sexually transmitted: cell-free viral particles have never been found directly in semen. Therefore 'HIV' is not a typically sexually transmitted entity; no 'lentivirus' is. Epidemiologists claim that a degree of correlation between 'HIV' and 'AIDS' proves causation. However, just as correlation does not prove causation, epidemiology cannot prove etiology.

Far from defeating 'AIDS' the 'HIV' hypothesis has escalated the epidemic by the global promotion of 'antiviral' drugs (AZT, ddI, ddC, 3TC, etc.) which are proven to be a major cause of 'AIDS' conditions. By focusing exclusively on 'HIV' researchers, counselors and doctors have failed to examine and halt the recreational drug-driven 'AIDS' epidemic that has hit London, New York, Paris, San Francisco, Amsterdam as well as countries like the former Soviet Union, the Ukraine, Romania, Thailand, Myanmar, Laos, Vietnam and Korea. The 'AIDS' epidemic reveals that 'AIDS' would be entirely preventable and in part curable, if:

1. AZT, protease inhibitors and all other 'antiviral' drugs and 'HIV' vaccines were banned,
2. a global educational programme were instigated concerning the health risks of illicit recreational drugs,
3. and the non-specific 'HIV' antibody testing procedures (Elisa, Western blot) were to be withdrawn. Therefore patients may be treated for any 'real' illnesses rather than for the being 'treated' by cyto-toxic 'antiviral' drugs on the outcome of an arbitrary 'HIV' antibody test.

Yet there are a number of obstacles, 15 years in the making, that block the possible solution of 'AIDS' based on the drug/'AIDS' hypothesis:

1. The World Health Organization, the Centers for Disease Control, the National Institutes of Health, plus thousands of 'AIDS' organizations (as well as scientific reputations) focus exclusively on promoting the 'HIV' hypothesis.
2. The colossal commercial interests in 'HIV' tests, with over 20 million tests per year at $50 or more in the USA alone.
3. As well as the huge financial profits from 'HIV' vaccines and anti-'HIV' drugs. Figures published in early August, 1997, of the half-yearly accounts of pharmaceutical giant Glaxo-Welcome showed the multinationalâs drugs sales of AZT (Retrovir) and 3TC (Epivir) exceeded £4 billion for the half year. With vast profits like these, 'anti-HIV' drug manufacturers want to hold onto the 'HIV' hypothesis at all costs.
4. The numerous negligence and malpractice law suits against the 'HIV/AIDS' orthodoxy from those who were told they are destined to die based on the fraudulent 'HIV' tests or whose friends/relatives died from iatrogenic-'AIDS' ('AIDS' caused by 'antiviral' drugs).
5. The prospect of a profound loss of confidence of the global community in its medical-scientific institutions once the world's media expose the 'HIV' fraud.
6. Annually $8 billion are spent on 'HIV' treatment, research and education on the unproductive 'HIV' hypothesis paid for by the US taxpayer. The US Government cannot afford to admit at this late stage that they have made a tragic blunder and wasted $46 billion in 14 years. Continuum urgently request that the United Nations to instigate an enquiry into a full reappraisal of the 'HIV/AIDS' hypothesis under an international, independent scientific committee.

References:
Eleni Eleopulos, et al., 'Is a Western blot proof of HIV infection?' Bio/Technology, June, 1993. Peter Duesberg and David Rasnick, 'The Drug-AIDS Hypothesis', Continuum, vol. 4, no. 5, 1997.

Copyright 1997: Alex Russell, Michael Verney-Elliott, Michael Baumgartner, Continuum

                                                                                                                                                  Michael Verney-Elliott playing Hamlet in 1957  

The Drug-AIDS Hypothesis

by Peter Duesberg & David Rasnick

Michael Verney-Elliott introduces the major new paper that forms this issue’s Supplement

Continuum Magazine, Vol. 4, No. 5  February - March 1997

Peter Duesberg, the world’s foremost retrovirologist, has declared since 1987 that HIV is a conventional retrovirus, without a disease-causing supernumerary gene, is not sexually transmitted, and is principally transmitted by female to offspring. He states that what is called HIV, for these and many other reasons, is not and cannot be the cause of AIDS. He is currently engaged in a debate, principally in this magazine, with other leading scientists as to whether HIV has really ever been proved to exist as an isolated virus, which he believes it has. Even if this is not so, both sides of that debate agree that what is called HIV cannot be the cause of AIDS.

Having since 1987 refuted the idea that a human retrovirus can be the cause of AIDS, Duesberg has searched the epidemiological evidence for an alternative cause for the acquired immune deficiency syndrome ("AIDS"). He has propounded the drug-AIDS hypothesis for some time, and in this latest paper he and co-author David Rasnick have presented his arguments in exhaustive detail, with 338 references. The paper is very persuasive.

The authors begin by expounding the scientific credo of Richard Feynman, who states that good science will present all the relevant facts concerning an hypothesis, not merely those which support it, and leave the readers to make up their own mind. This means that the true scientist must be his own Devil’s Advocate, and state the con’s as well as the pro’s in presenting a scientific theory. My personal experience of Duesberg is that he has always obeyed this precept, whilst the vast majority of so-called ‘AIDS experts’ have consistently and wilfully presented only the specious arguments which seem to support their frequently illogical theories, sometimes deliberately obfuscating or suppressing contradictory evidence.

Duesberg gives a perfect example of this scientific chicanery, citing a paper published by Nature purporting to show AIDS in non-drug-using patients which, in fact, showed nothing of the kind, and all the patients in the study had in fact used recreational drugs. A line on an illustrative graph claimed to represent non-drug users, but the text mentioned no such patients. The line was an artefact, used to support a shaky, flaky piece of research. Even worse, a subsequent independent study of the database used in the paper revealed in the same cohort of patients, 45 HIV negative drug users with AIDS defining diseases. These were not mentioned in the paper, obviously because they would have shown that the drugs caused the diseases and HIV was irrelevant. Unfortunately, this rotten science has prevailed since the beginning of ‘AIDS’, and shows no sign of abating.

Space allows for only a few of the many points which particularly struck me in Duesberg’s hypothesis. Duesberg gives a list of diseases known to afflict long-term drug addicts and their babies since an earlier drugs epidemic at the beginning of this century in the USA. "These diseases include immunodeficiency, pneumonia, tuberculosis, dementia, candidiasis, weight loss, diarrhea, fever, night sweats, congenital abnormalities, mouth infections, impotence, epileptic seizures, paranoia, Iymphadenopathy, hemorrhages, hypertension and many others." (12 refs. cited) This looks almost identical to a list of ‘AIDS’ defining diseases. Moreover, "Patients and deaths from drug diseases... show essentially the same sex and age distribution..." (as AIDS).

When AIDS first appeared, drug causation was widely suspected and supported by scientists like Blattner, Curran, Friedman-Kien, Goedart and Jaffe, all of whom did a volte face and joined the HIV junta in 1984. Despite the fact that, epidemiologically, drugs are a much more convincing explanation for AIDS than a retroviral infection, these men still show solidarity with an increasingly threadbare scientific theory, "without even offering a refutation of the drug hypothesis."

In the best Feynman tradition, Duesberg does not shirk the objection that not all drug users develop AIDS. He illustrates his thesis that "The dose is the poison" by pointing out the following: "In adults it takes about ten years of injecting or oral use of heroin, cocaine and amphetamines to develop tuberculosis, bronchitis, pneumonia, irreversible or hardly irreversible weight loss and other drug-induced diseases. [8 refs. cited.] The time lag from initiating a habit of inhaling nitrites to acquire Kaposi’s sarcoma has also been determined to be 7-10 years [4 refs. cited]." The ten year use of drugs is remarkably reminiscent of the embarrassingly elastic ‘HIV incubation’ period.

In a particularly telling section, the paper lists 11 examples from the literature of the devastation caused by AZT/nucleoside analogues cynically minimized, wilfully misinterpreted or disregarded by conductors of drug studies. For instance, Samuel Broder, who first pushed AZT as an antiviral drug, when confronted by the 46.4% increase in Iymphoma in patients taking AZT claimed it as a victory for AZT, in that it kept the patients alive long enough for half of them to develop cancer.

The dishonesty in failing to admit the link between drug use/addiction and AIDS reaches right up to Government level, as this paper shows. Despite paying lip service to the War Against Drugs, the US government restricts their efforts largely to token drug seizures and pursuing dealers. They have consistently failed to stress the illnesses caused by drugs, as has been done in successful campaigns against smoking. As far as AIDS and drug users are concerned, the message has been rather ‘Say no to shared needles’ than ‘Say no to drugs’, (which tragically should include AZT/DNA synthesis inhibitors). The American government for reasons of its own fails to realize that to link the wars against drugs and AIDS would stand a better chance of winning, rather than losing, both. Obviously, to undermine the prevailing view that HIV is the sole cause of AIDS would damage the already tarnished scientific reputations of the "HIV" junta, and to focus on drugs would rouse the ire of powerful drug cartels – both recreational and pharmaceutical.

This paper is exhaustively researched, fully referenced and convincingly argued. Anyone interested in the true cause and nature of ‘AIDS’ – Acquired Immunosuppressive Drug Sickness – should read it several times. Duesberg’s hypothesis is testable – studies of heavy drug users, using HIV positive and negative controls, should reveal identical immune deficiencies, disease incidence and early mortality. To date no-one has carried out such a study. It is long overdue.

Peter Duesberg, Department of Molecular and Cell Biology,
229 Stanley Hall, UC Berkeley, Berkeley, CA 94720
phone (510) 642-6549, fax (510) 643-6455, email: duesberg@uclink4.berkeley.edu

David Rasnick, Resident AIDS investigator at UC Berkeley,
229 Stanley Hall, UC Berkeley, Berkeley, CA 94720
phone (510) 642-6549, fax (415) 826-1241, email: rasnick@mindspring.com

                                                                                                                                                                     Michael Verney-Elliott  in 1958   

HHV8: missing KS infectious agent or...

Blind Alley

Continuum Magazine, Vol. 3, No. 6  March - April 1996 

Michael Verney-Elliott

Since intensive study of the phenomenon of AIDS began, it has been claimed that three 'new' human herpes viruses have been found. The latest, HHV8, has been linked to Kaposi's Sarcoma. Michael Verney-Elliott asks are the virologists right, or are we taking too much on trust?

Prior to the AIDS era, there were five well understood, characterised human herpes viruses.  All these viruses are  persistent infections, believed to last for life, and well studied decades before AIDS.  These are: herpes Simplex 1 - causing cold sores around the mouth, usually in the same place when recurring. Herpes Simplex 2 -  referred to as genital herpes, easily transmitted sexually, and  causing recurring lesions and painful blisters.  The spread of this variety gathered momentum in the '60s and was epidemic in both the gay and straight populations in the USA and Europe in the '70s. This was the panic epidemic preceding AIDS, believed to infect some seven million Americans at its peak.  Epstein Barr virus - which causes mononucleosis. Being easily transmitted via saliva,  it is sometimes known as the kissing virus, and infects particularly during puberty.  It has also been implicated in causing cancer, but never proven.  Varicella Zoster virus - causing two distinct diseases: chicken pox in the young, and subsequently shingles, usually in middle age.  Cytomegalovirus - which can cause brain damage and blindness.  This was suspected early as a cause of AIDS by some doctors and virologists, but as it is distributed equally among the sexes, it cannot explain why homosexuals are particularly affected by AIDS.

All these persistent viral infections are known to flair up when the immune system is low, or the person is feeling run down or under stress. In 1986, Robert Gallo claimed to have found a sixth human herpes virus - HHV6.  Having previously stated that HIV is sufficient to cause AIDS without co-factors,  he gradually, and in the most face-saving way possible, acknowledged that this 'new' herpes virus might contribute to the syndrome.  Currently, this all-singing, all-dancing, all-purpose virus is considered to cause cell death in many types of cells - T4, CD8, etc.  HHV6 can infect and damage a wide variety of organ tissues, including brain, spinal chord, lung, lymph node, heart, bone marrow,  liver, kidney, spleen, tonsil, skeletal muscle, adrenal glands, pancreas, and perhaps most significantly for PWAs, the thymus. 1  It is also believed that the virus can cause something similar to graft-versus-host disease, a form of auto-immune reaction found in some cases of organ transplant patients, and suffering from lupus.

Of particular note is that an almost simian herpes virus is found in nearly 1005 of African green monkeys, the principal source of kidney cells used in the manufacture of polio and other human vaccines since the late 50s.  Could it be that this 'new' herpes virus found its way into the human bloodstream as a contaminant in vaccines?   Not many scientists want to talk about this possibility, as this would obviously be a man-made disaster on a huge scale.  We do know that simian virus  40 (SV40) contaminated the Salk, Savin and Koprowski polio vaccines, and infected hundreds of thousands of vaccinees world-wide before the virus was discovered and isolated in 1960.  This tiny (even by viral standards) double stranded  DNA virus can integrate into the human genome, just as HIV is alleged to do, and is known to cause cells  to become immortalized - pre-cancerous.  Anyone wanting to pursue this scary story of the ease of vaccine contamination  should read Monograph 29, published by the National Institutes of Health, December 1968.   You won't sleep at nights! 

Subsequently, a seventh human herpes virus was said to have been found,  thought to be  a variation of HHV6.  Recently, HHV8 was announced by husband and wife team Drs Patrick Moore and Yuan Chang of the Columbian Presbyterian  Medical Centre at a press conference  on December 15th 1994. 2   They claimed to find an almost 100% correlation between "DNA viral fragments" and cases of Kaposi's Sarcoma (KS).  Cautiously Dr Moore stated that even if the DNA fragments do prove to be another herpes virus, this is not proof that it is the cause of KS.  He, unlike so many other AIDS "researchers", has remembered the golden rule - correlation does not prove causation!  He also stated that the virus may merely be colonising the KS lesions after something else has triggered the illness; a typical opportunistic virus.  Curiously, the small fragments of DNA identified by these researcher closely resemble the genome of another monkey virus - herpes saimiri.  Did that little goody contaminate vaccines?  It is worth remembering that virtually all animal species whose tissues are used to manufacture human vaccines are infected by varieties of herpes virus.  It was also speculated that HH8 may work in tandem with HIV.  Either HIV infection wakens the dormant HHV8, or vice versa.  However, Moore and Chang also caution that both these viruses may merely appear as a result of AIDS, but neither contribute to causation.  Their discovery caused a major sensation.  Nobody explained why this virus seems to gravitate to gay men who use poppers, although even Robert Gallo admits that the correlation between nitrite use and KS in gay men is "significant  enough to be investigated further".  HHV8 is considered quite widespread in the general population - as it would be if it were a contaminant in vaccines - but AIDS-related KS is principally a gay problem. 

Some nine months later, Jay Levy, the third virologist to "isolate" HIV, wrote a piece in The Lancet (Sep. 23, 1995) which I quoted in the last issue of Continuum.  He states that HHV9 has  never been fully characterised, or photographed under electronmicroscopy.  In other words, it has not been isolated, so its very existence as a herpes virus is still uncertain.  In the twelve years I have been researching AIDS, there have been many hopeful  "breakthroughs" which have invariably been shown to be  without foundation, merely optimistic trips down scientific cul-de-sacs.  Make me to see HHV8 isolated in pure cell culture with clear electronmicrographs of identically shaped viral particles, unimpeded by any other microscopic debris, and I will suspend my disbelief.  Meanwhile, I can hardly contain my indifference.

References:

1. Knox, Carrigan.  Disseminated Active HHV6 Infection in Patients with AIDS, Lancet 343.577, March 5, 1994.

2. Chang Yuan et al Identification of Herpes--Like DNA Sequences in AIDS-associated Kaposi's Sarcoma,  Science 266: 1885, December 16, 1994.

                                                                                              Michael Verney-Elliott acting in the late 1950s

DEATH CAMP: No. 14  Nov/Dec 1996 

Interview: Michael Verney-Elliott talks to Alex Russell, Editor of Death Camp. 

Death Camp: "In 1986, when you first became interested in the causes of 'AIDS', what made you doubt that 'HIV' was the cause?"

Michael Verney-Elliott: "Well, it was too neat an explanation... call it Cartesian reductionism or whatever you like... but if an exotic bug should come from nowhere and appear to target gay men something about that whole set up struck me as odd and one of the first rules of science is always look to the odd. Of course in those days they were confidently predicting that HIV had targeted gays first and would soon target the whole of the human race. Think of those lurid adverts warning straights that they were at risk. In the developed world there is still not heterosexual epidemic ten years on despite all their juggling with the figures."

D.C.: "Why is it then, that 'HIV' journalists like Steve Connor, Liz Hunt, Chris Mihill, Simon Garfield, Jon Cohen, Simon Watney, Peter Scott, Keith Alcorn and Edward King still use the alarmist rhetoric of a global doomsday scenario of an 'HIV' epidemic?"

M.V.E.: "Because they are only hacks and do it for the money."

D.C.: "Or is it, that they genuinely believe in the handouts dished up to them by the WHO, CDC, NIH and our Department of Health?"

M.V.E.: "Perhaps they do, but if so, it does not say much for their critical faculties. If they are merely prepared to hand out propaganda on behalf of pharmaceutical companies, epidemiologists, etc., who are out to make a buck or a reputation then that's a matter for their own conscience. Of course they may be sincere, but my experience with journalists' apparent sincerity should be treated with the utmost caution. When you consider what some of these scribblers earn, you have to admit that the Compassion Industry pays very well."

D.C.: "Can you tell me about the hostile reception that your TV programme 'The AIDS Catch' received in 1990?"

M.V.E.: "We were reported to the Broadcast Complaints Commission and were accused of "being unfair to the subject of AIDS" because we had dared to question the received wisdom. But as Prof. Walter Gilbert said in that programme, consensus science is bad science. Meditel were invited up to the Edinburgh Television Festival to discuss that programme but there was no discussion, just a lynch mob orchestrated by Duncan Campbell and Sheena McDonald. It must be galling for both of them to realize now that everything we said in that programme has been subsequently shown to be true. One positive thing that seemed to have emerged from our visit to Edinburgh was a chat with Derek Jarman, when we warned him never to take AZT; however, due to pressure from his doctor, he ignored our warning, took AZT and is now dead. It is my contention that Jarman, like so many gay men, died of AZT poisoning."

D.C.: "John Curry, Oscar Moore, Denholm Elliott, Arthur Ashe, Kimberley Bergalis, Ryan White, Kenny Everett and Freddie Mercury, like Jarman, were murdered by the 'HIV/AZT' establishment; all died unnecessarily from 'antiviral' drug poisoning. Why are journalists still flogging the redundant 'HIV' hypothesis and lethal so-called 'antiviral' drugs?"

M.V.E.: "Because they are too cowardly to admit they've made a mistake. On the other hand the world's greatest retrovirologist, Peter Duesberg, still maintains that HIV could not cause the destruction of the immune system by direct or indirect mechanisms and even Luc Montagnier, the alleged discoverer of 'HIV', admitted to me in 1990 that 'HIV' does not cause AIDS on its own. Once the possibility of co-factors is raised then all bets are off..."

D.C.: "The argument seems to have moved on that 'HIV' does not even exist. How does this affect the way you feel about Duesberg's views, as he is seen to be locked into the retroviral paradigm that he helped pioneer?"

M.V.E: "First let me state that Peter Duesberg is a personal friend, he is also my guru. Whether or not 'retroviruses' exist is a matter of debate; Peter believes that they exist and is the foremost expert in the field. Therefore, if the foremost retrovirologist in the world still maintains that 'HIV' is not, and cannot be, the cause of the destruction of the cellular immune system, then on a retrovirological level, I trust him completely. When I interviewed eminent scientists during the making of the various AIDS programmes for Channel 4 television, two of them--eminent virologist Professor Beverley Griffin and editor of Bio-Technology, Harvey Bialy, said of Peter Duesberg that they had never known him to be wrong. When I put it to Duesberg the last time we met in Berlin in 1995, that Dr Stefan Lanka maintains that 'HIV' has never been isolated and that I wondered whether 'retroviruses were an over interpretation of aggregated molecular particles, he replied: 'Anything is possible in science.' This shows the open mind of a great man who stands head and shoulders above his fellow microbiologists. Remember that Duesberg said as early as 1987 that 'HIV' antibodies may be no more than a surrogate marker for a disease condition. My own view is we must not mistake a marker for a causative agent. Measles spots do not cause measles, they are a marker, a symptom."

D.C.: "How do you feel about ACT UP, SF dumping 25 lbs of cat shit over wealthy SF AIDS Foundation Executive Dictator, 'Fat Cat' Pat Christen's head as a political strategy?"

M.V.E.: "As pathetic as it is dangerous. Not only does cat shit contain the toxicara worm found in dog shit which can cause blindness in humans, it is also a common transmitter of toxoplasma gondii, which in a weakened immune system can cause toxoplasmosis and brain abscesses leading to dementia and death. This latter condition is one of the 29 diseases included in 'AIDS' grab-bag. It would be interesting to check how many gay men with 'AIDS' developed this condition had had extensive contact with cats as domestic pets. I would also suggest it is unsafe for anyone diagnosed with 'AIDS' to keep pet birds, after all, another disease in the 'AIDS' list is mycobacterium avium intercellulare which is transmitted by birds."

D.C.: "How do you feel about this new treatment involving Interleukin II?"

M.V.E.: "It is claimed that this treatment can dramatically increase the number of T4 cells, even double them. However, as Anthony Fauci himself admits, despite observing a dramatic increase in T-cell 4 numbers there is no apparent clinical benefit observed in the patient, therefore what is the point of the treatment...if you are positively bulging with T4 cell levels and still die from AIDS? Even the NIH admitted in the late '80s that T4 Cell levels should not be used for prognosis as they are extremely untrustworthy."

D.C.: "Is this recent fetishism of Viral Loads another con trick to entice simple minded people to be poisoned by protease inhibitors and 'antiviral' cytotoxic drugs?"

M.V.E.: "Absolutely. When David Ho and others claimed to be able to detect massive viral activity held in check by equally massive cellular activity, the methods used were complete rubbish. The mathematical model used was garbage. They used PCR to measure viral loads forgetting the Kary Mullis is on record as saying 'Quantitative PCR is an oxymoron.' He should know - he invented it. I remember thinking at the time with so much virus allegedly swirling about, why has nobody ever seen it before in the first ten years of so-called 'HIV' research?"

D.C.: "Eleni Papadopulos-Eleopulos's revolutionary paper showing that 'HIV' has never been shown to exist as a unique molecular entity, was not celebrated by our 'AIDS' organizations or our gay press and the so-called 'HIV' community? Surely such a liberating paradigm shift away from the 'HIV' death culture should have been a merciful release?"

M.V.E.: "I once put this question to Joe Sonnabend. His answer struck me as being very perceptive. 'HIV absolves gay men from any responsibility for their own condition.' The 'experts' said 'AIDS' could happen to anybody...we were all supposed to be at risk...gays were just unlucky. However, X years later, what we have to ask ourselves as gay men is, why are we still the largest group of 'unlucky' ones in the Western World and why hasn't it happened to everybody else? Gay men must accept the fact that their lifestyle has put them at risk, not the Virus from Hell, and it will continue to do so as long as they indulge in drugs, poppers and over-dependence on
antibiotics and remain complacent about STDs. The received wisdom states that super-bugs are out-witting antibiotics faster than we can devise new ones."

D.C.: " 'HIV' propagandists argue that straights consume as many street drugs as gays, but don't get 'AIDS', and Fred Cline has argued that many women, particularly in Latin countries, have anal sex (17% of French women have anal sex) yet they do not develop 'AIDS'?"

M.V.E.: "They also do not get nearly as many STDs as gay men and are not nearly so dependent on antibiotics. Moreover, even gay men will have to admit sooner or later that rectal and oral sex, however pleasurable, are extremely efficient methods of transmitting all known STDs. Ask yourself this question: how many simultaneous infections can your immune-system cope with at any given time, especially if your immune-system is weakened by antibiotic and drug use?"

D.C.: "What do you think of so-called 'AIDS' treatments at the moment?"

M.V.E.: "As a general rule, any treatments that were previously devised to combat cancer will fail disastrously in the treatment of 'AIDS'. Cancer is the unstoppable production of cells; 'AIDS' would appear to be the unstoppable diminution of cells. Thus protease inhibitors, nucleoside analogues and indeed the whole ball of wax devised to stop production of cells can only have a disastrous effect on people who are already losing cells in an unstoppable way. This basic error to apply cell inhibitory treatments was devised against cancer and invariably abandoned because of their toxicity. My belief, that if they were not good enough to treat cancer, then they sure as hell are not going to work against 'AIDS'. We must stop using inept anti-cancer drugs (AZT, ddI, ddC) on people with 'AIDS.' The future of 'AIDS' research must lie in rebuilding a damaged immune system and not in the fruitless pursuit of a clapped-out phantom non-isolated 'virus'."

D.C.: "In a nutshell, why do you think they persist in pursuing the 'HIV' paradigm?"

M.V.E.: "Because a lot of people are making a lot of money out of it. As Karl Marx said, 'All great fortunes are based upon a great crime.' I think this is apt because 'HIV' careerists are greedy criminals. As I've always prided myself that gay men are more perceptive than most, I'm astonished that more of my fellow gay men have not yet rumbled the 'HIV' hoax. When Joan Shenton and I were invited to Bristol University, to defend the programme 'The AIDS Catch,' we faced an audience of some three hundred very hostile 'HIV' counselors, 'HIV' monitors, and other ancillary 'AIDS' carers and workers. AT that time the official figure for the number of 'AIDS' cases in the West Country was 18! One young man with 'AIDS' said he seldom got any peace and quiet and virtually had to beat off these 'HIV/AIDS' carers with a stick when they invaded his flat. He had an army of 'HIV' home-help busy bodies banging on his door 24 hours a day. He had an 'HIV' meals-on-wheels, and 'HIV' social-worker, and 'HIV' psychologist, and 'HIV' MacMillan nurse, an "HIV' buddy, and 'HIV' masseur barging into his flat day and night brandishing their compassion like Smaritans with attitude. If nothing else, 'HIV' has certainly created a lot of jobs, which is exactly what the CDC intended when they invented the 'AIDS' epidemic. Still it's an ill-wind that blows no one any good."

D.C.: "No wonder so many vested-interest groups fear the non-existence of 'HIV'; thousands of people will lose their 'HIV' fat salaries, expense accounts, grants and be made redundant." [end]

                                                                                                           Michael Verney-Elliott in the late 1950s

The Stonewall Experiment; A gay psychohistory  

Ian Young

Cassell UK/USA 1995, 312 pages ISBN 0-304-33270-0.

Continuum Magazine, Vol. 3, No. 3  September - October 1995 

Reviewed by Michael Verney-Elliott

This is an easy, and uncomfortable, book to read. The ease is afforded by Ian Young's pellucid prose style; the discomfort lies in the sadness of his account of the betrayal of gay hopes following so soon after the Stonewall rebellion, and the consequence of that betrayal - the seeming inevitability of AIDS.

Young gives a brief account of the pioneers of gay culture, headed by Walt 'Dad' Whitman, with his Platonic ideal of male love and comradeship. This had a profound influence on the Englishman, Edward Carpenter, who became outspoken in his championing of homosexual emancipation. He lived openly with his lover, George Merrill, at Millthorpe in the North of England, and even after Wilde's trial and disgrace, he remained steadfast to his 'Uranian' ideals, when more timorous writers kept a low profile. Until virtually the 1960's, writers fought shy of open expression of gay sympathies, but there were exceptions in the previous decade - Gore Vidal with The City And The Pillar, James Baldwin with Giovanni's Room, spring to mind. Things then started to get more graphic - and even more depressing and pessimistic - with the works of John Rechy. By the 70's, Young says ".... the mystical/political patrimony of Whitman and Carpenter had been largely forgotten." The rest of his book explains how and why.

A 1979 screenplay by William Burroughs (a relative of the Mr.Burroughs who teamed up with Mr. Wellcome to form the company which eventually brought us AZT!) presents an uncannily prescient description of AIDS. "The hero of the story is Billy, a gay man who is a 'blade runner', a courier of medical contraband. His attempts to spread the word about a new medicine are hampered by the atmosphere of distrust and paranoia generated by the official Health Control as well as by an illness he has contracted - pneumonia."

Long before the word 'homosexual' was coined by Karl Benkert in 1867, gays had been persecuted and demonised. In his chapter on 'The Myth of the Homosexual', Young states:

"The homosexual was thus installed in a rogues' gallery with other mythical creations of Western diabolism: the Vampire, the Leper, the Witch, the Gypsy, the Werewolf, the Jew - figures concocted out of the fears, folk memories and repressed desires of a civilisation, aspects of Christian society's dark unconscious, its shadow side."

Gays have been systematically classified as sick by the medical profession, criminalised by governments and brutalised by police, abused and derided by heterosexuals. Young draws a parallel between the gay urban ghettos of the 60's and the plague-stricken city of 'Death in Venice', and has this to say:

"The Stonewall Experiment began in the untutored hands of gay people who had had enough of being second-class citizens, partial people, never fully human. It was an experiment in reclaiming full humanity from the medical/governmental establishment. Within a few years, control of the experiment had fallen into other hands, and the initiators found themselves in the position of experimental animals. The new phase of the experiment involved the development of a commercial gay scene that could be test-marketed as a prototype of the urban lifestyle of the future."

Young unflinchingly depicts the cynically commercialised hedonism of the bathhouse and backroom bar 'culture' which ironically came to symbolise gay 'liberation', using descriptive passages from novels like Faggots by Larry Kramer. Other writers extolled the virtue of promiscuity, and even STD's, as proof of homosexual political commitment; drugs and poppers became an indispensable part of the gay scene; the Mafia took over the pornography market; whether a gay man was 'deep' or 'wide' defined whether he could take one forearm up his arse to the elbow, or two fists simultaneously. Crisco and nitrite inhalants became the anointing oil and incense of the new religion.

"The impulses that led young men to join in these darkly alluring activities had something in common with feelings that an older writer of the time recalled encountering in himself as a young man, decades earlier. 'It seemed to me', he wrote, 'that I had passed a threshold, and that in passing it, I was dimly dismissing something from where I had come: my land, my past, the traditions of my country. But these men fascinated me and I wanted to incorporate myself there. I perceived them as strong, generous and pitiless: beings without weakness who would never putrefy.' The words are those of the French author Christian de La Mazi, remembering his emotions when, thirty years earlier, he joined the Waffen SS."

Young's descriptions of AIDS are very moving. His own partner, Jamie, died aged 32, on World AIDS Day, 1993, as this book was nearing completion. His understanding and summation of the dissident views of Duesberg, Lauritsen and others who have never been blinded by the official 'explanations' for the malady, are quite the best and most comprehensive I have been privileged to read.

"Piece by piece, the stone wall of orthodoxy was crumbling. But the ruins were heavily defended. Over a decade into the epidemic, the public was still being told by newspapers and television, and all but a tiny handful of physicians, that a positive result from an HIV antibody test showed present and lifelong 'infection' by the virus; that the virus was certain or very likely to lead to AIDS; and that AIDS was universally fatal. None of these assertions had been proven. Yet the psychological effect of believing them could be catastrophic.... In the post-1984 world, a growing number of people considered their allotted blood 'status' as the key to both their identity and their fate."

In not purporting to be a "history of homosexuality, the gay movement, or the health crisis'" but merely the observations of a poet with a "particular interest in images, verbal messages and psychic undercurrents...", Ian Young is being modest. His book is all these and much, much more. Whatever his intentions, he has written a wonderful book, and Cassell Lesbian and Gay Studies have published an important one. This book should be read by all those concerned about the truth and the tragedy of AIDS - gays, lesbians and straights. They may make what they will of Young's last sentence: "The experiment continues."

                                                                                                                    Michael Verney-Elliott in 1959

Meditel replies to Simon Watney 

Capital Gay  September 1996 

We wish to take issue with the virulent attack by Simon Watney (Capital Gay, September 10th) on Professor Peter Duesberg and what Mr Watney describes as his "cronies" in the "lunatic fringe of the mass media". 

Firstly we must point out that Watney has grossly misrepresented Duesberg  by putting several fabricated sentences in quotes as though they came from Duesberg. 

"Don't bother to use condoms" is one example. Duesberg has never said this. He has said that condoms protect against STDs and unwanted pregnancies but do not guarantee that you are protected from developing AIDS defining illnesses.

"It's all drugs and promoscuity" is also a serious misrepresentation of Duesberg's case.  He maintains that AIDS diseases in the West result from non-contagious risk factors that include drug consumption, blood transfusion and anti-HIV drugs, and in Africa from protein malnutrition, poor sanitation and subsequent endemic parasitic  infections.

We, as Meditel, presumably qualify as Watney's "lunatic fringe", since we have now made five network documentaries reflecting Duesberg's hypothesis. May I point out that we have won eight major awards for our work, including the Royal Television Society Award for Journalism in 1987, for our first Channel Four film on AIDS and a British Medical Association Education Award  in 1993 for our film AZT - Cause for Concern.  As specialists in the field of science and medicine, I strongly object to this slur on our professional integrity.

Watney also criticises Graham McKerrow for pointing out that the gay press has been exercising forms of self-censorship in the past. It is to McKerrow's credit that he is able to write about this so powerfully from his own invaluable sense of historical perspective.

Watney says "we have an ethical responsibility to counter cranks and bigots" and goes on to call Duesberg and his "cronies" dangerous.  Perhaps he should look into his own glass house and root out the long standing bigotry that has exited there. If he continues to suppress open debate about the HIV/AIDS hypothesis by making cheap jibes which totally fail to address the scientific issues, he is himself endangering lives.

Joan Shenton

Michael Verney-Elliott

Meditel

London WC2

                                                                Aged 16 M.V.E showed Huw Weldon his hand made dolls on BBC TV's ALL Your Own

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