'SIV' AND POLIOVACCINATION: A SHOT IN THE FOOT?
by Michael Verney-Elliott
© MICHAEL VERNEY-ELLIOTT, FINAL DRAFT Thursday, July 1, 1999
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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, noone 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 artifact of human and simian cell cultures.
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.
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.
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 nonessential, 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 'AIDSlike' 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 polio vaccination. Secondly, Britain abolished conscription in the early '60's at about the same time that African green-generated polio vaccines 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 polio vaccine mentioned by Kyle 12. However, Britain has also been heavily dependent on imported polio vaccines 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 uninfected simian cells could dislodge, dredge up or reactivate previously 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 retroviruscontaminated 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 zoonoticallyacquired 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 socalled '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 cross-react.
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)