HIV=AIDS=Death: A Killer Myth


David Pratt

Aug 2006, last revised Sep 2010


Contents

Introduction
AIDS & HIV: the missing link
A logic-defying virus
AIDS is not contagious
Africa: fact vs. fantasy
Poisoning the patients
Challenging the establishment
Risk factors and survival
Sources


Introduction

‘There is no question HIV is the cause of AIDS. Anyone who gets up publicly and says the opposite is encouraging people to risk their lives.’ – David Baltimore, Nobel laureate

‘Years from now, people looking back at us will find our acceptance of the HIV theory of AIDS as silly as we find the leaders who excommunicated Galileo.’ – Kary Mullis, Nobel laureate

Contrary to popular belief, Acquired Immune Deficiency Syndrome (AIDS) is not a global pandemic caused by the Human Immunodeficiency Virus (HIV); rather, it is one of the biggest and deadliest medical scandals of modern times. There is no convincing evidence that ‘HIV’ plays any role whatsoever in impairing the immune system, let alone that it is the sole cause of AIDS. There is compelling evidence that ‘HIV’ is not readily transmitted sexually, and that AIDS is not contagious.

HIV/AIDS is above all a multibillion dollar industry, in which so many scientists and organizations have acquired a stake that the views of researchers who challenge the orthodox position are vigorously suppressed. The constant message propagated by the world media, high-profile science journals, and AIDS propagandists is of course that there is ‘overwhelming evidence’ that HIV causes AIDS, and that those who deny this are a public health menace and deserve to be silenced. But it is a telling fact that all the catastrophic predictions made since the early 1980s on the basis of the HIV=AIDS=Death dogma have failed to materialize.

In the early days of rampant hysteria, it was predicted that AIDS was about to explode into the general population, and that 1 in 5 heterosexuals could be dead within three years. In 1987 the US President’s AIDS Commission stated that by 2001 there could, hypothetically, be 10 billion people infected – a number far greater than the world population, meaning that the human race would become extinct! Needless to say, nothing remotely like this has happened. In fact, the number of HIV-positive people in North America and the UK has not increased since the HIV test came into general use in 1985 and AIDS cases have fallen since the early 1990s. In the West, AIDS remains confined predominantly to the same risk groups as 20 years ago: highly promiscuous gay men, heavy users of ‘recreational’ drugs, and blood transfusion recipients.

In the name of fighting HIV/AIDS, hundreds of thousands of lives have been and are being destroyed. People who test positive on the highly unreliable ‘AIDS test’ – including those who are otherwise perfectly healthy, among them babies and young children – are ‘treated’ with extremely toxic and deadly drugs, which ruin the immune and digestive systems and cause several AIDS-defining conditions, while giant pharmaceutical companies rake in the profits.

HIV is supposed to be 100% lethal. Yet the World Health Organization (WHO) admits that 95% of people worldwide described as ‘having HIV’ live in good health. In the early 1980s, it was claimed that death followed only months after infection, but this ‘latency period’ has since been increased to 10 or 15 years or more. Some HIV-positive people have actually survived for at least two decades and remained healthy – but only if they have refused to take toxic ‘antiviral’ drugs.

HIV is said to be a retrovirus, but no other known retrovirus is able to kill cells. There is so little HIV present in the bodies of AIDS victims that it is generally impossible to detect it. Instead, people are tested for the presence of antibodies to HIV. But in the case of every other virus except HIV, the presence of antibodies is regarded as a sign that the virus in question has been defeated and the person concerned is probably immune!

The mainstream position is that HIV is an exception – a new kind of retrovirus with unique properties, which behaves in ways that no one can explain, despite two decades of research and more than $100 billion spent on AIDS by US taxpayers alone. But, as we will see, there is no need to invoke ‘HIV’ to explain immune deficiency. In fact, the very existence of ‘HIV’ as a genuine invasive virus has never been conclusively demonstrated. In the developed world, drugs are the main factor causing ‘AIDS’, while in the developing world the key factors are malnutrition, poor sanitation, and tropical diseases.


AIDS & HIV: the missing link

According to the latest definition of the Centers for Disease Control (CDC), 29 familiar illnesses and conditions – including yeast infection, herpes, diarrhoea, some pneumonias, certain cancers, salmonella, and tuberculosis – are classed as AIDS, but only if they occur in people who test positive for antibodies to HIV. This means, for example, that people who die of tuberculosis are said to have died of AIDS if they are HIV-positive, but to have died of tuberculosis if they are not!

‘HIV’ is the only virus which is said to cause a group of diseases caused by other viruses and bacteria rather than causing its own disease. Moreover, AIDS patients do not have any one of the 29 AIDS-defining diseases in common. In fact, AIDS diseases such as dementia, wasting syndrome, and cancers do not even involve immunodeficiency. AIDS researchers have not bothered to conduct large-scale controlled studies to test whether the incidence of AIDS diseases is higher among individuals infected with HIV than among the general uninfected population.

If HIV caused AIDS, the prevalence of HIV and AIDS should be closely correlated – but they are not. In the US, HIV infections have remained more or less constant at about 1 million since widespread testing began in 1985, whereas AIDS cases increased from 1981 to 1992 and have declined ever since. HIV testing by the US military has consistently reported near equal numbers of HIV-positive results among male and female new recruits, yet 80% of AIDS patients in the US and Europe are males. Between 1981 and 2000, the ratio of black Americans to white Americans reported with AIDS trebled, while the ratio of positive HIV-tests in the two groups remained the same – again contradicting the purported link between HIV and AIDS.

The CDC has expanded its definition of AIDS three times since 1981, with each change boosting the number of AIDS cases. In 1993 the definition was expanded to include people who have no illness or symptoms but have a CD4+ T-cell count of 200 or less (T-cells play a key role in the immune system). This caused the number of AIDS cases in the US to double overnight. Since then, more than half of all new AIDS cases diagnosed each year have been among people who are not ill. However, Canada, like most of Europe, does not recognize the American T-cell count criterion for AIDS. This means that 182,200 American AIDS patients – more than 25% of all the people in the US ever diagnosed with AIDS – could be cured instantly simply by crossing into Canada!

In most of Africa, WHO guidelines allow patients to be diagnosed with AIDS if they have a combination of three or four symptoms such as chronic diarrhoea, prolonged fever, persistent cough, weight loss of 10% or more, and generalized itching. No test for HIV or HIV antibodies is required.

The proclaimed link between HIV and AIDS dates from 1984. In April of that year, Robert Gallo, a researcher employed by the National Institutes of Health (NIH), called an international press conference together with the US Department of Health and Human Services, at which he announced his discovery of a new retrovirus described as ‘the probable cause of AIDS’. This was a case of science by press conference, since the announcement was made before any scientific evidence confirming the virus theory had been published. Later the same day Gallo filed a patent for the ‘AIDS test’. By the following day the media were calling HIV ‘the virus that causes AIDS’, and the presence of HIV (or rather antibodies to it) quickly became part of the definition of AIDS. Many researchers who had previously favoured the hypothesis that recreational drug use was the cause of AIDS dropped the hypothesis to work on the new ‘AIDS virus’. One leading researcher later explained the reason for his conversion: ‘That’s where the money is’ (Duesberg et al., 2003, p. 388).

The first publication from Gallo’s group in support of the theory that HIV causes AIDS reported finding that 18 out of 21 ‘pre-AIDS’ patients (86%) tested HIV-positive, but only 26 of 72 people (36%) who had full-blown AIDS. This makes no sense if HIV is cause of AIDS. Nor was any proof offered that HIV differed from other retroviruses, which are all harmless and unable to kill cells. But the HIV=AIDS hypothesis received no widespread critical scrutiny because it fitted in with the prevailing microbe-hunting mentality, and the juggernaut started to roll. All funding for research into other potential causes came to an abrupt halt, and only discussions on how HIV causes AIDS were tolerated, but not on whether HIV causes AIDS.

A Congressional investigation later found that Gallo had presented fraudulent data in his HIV paper, and that the virus he claimed to have discovered was the same one he had been sent by Luc Montagnier of the Pasteur Institute in France. The French and American governments finally negotiated a compromise, with Montagnier and Gallo sharing credit as co-discoverers of HIV and ownership rights to the ‘HIV test’. Gallo and his collaborators receive $100,000 annually in royalties.

Kary Mullis, who won the Nobel Prize for Chemistry in 1993, tried to find out why scientists had become so convinced that HIV caused AIDS. He realized that the detection of antibodies to HIV in a person suffering from AIDS does not prove that HIV causes AIDS.

Antibodies to viruses had always been considered evidence of past disease, not present disease. Antibodies signalled that the virus had been defeated. ... There was no indication in these papers that this virus caused a disease. They didn’t show that everybody with the antibodies had the disease. In fact, they found some healthy people with antibodies. (Mullis, 2000, p. 173)

Mullis proceeded to ask AIDS experts he met at conferences to tell him in what article he could find the proof that HIV caused AIDS.

Everyone said something. Everyone had the answer at home in the office in some drawer. They all knew and they would send me the papers as soon as they got back. But I never got any papers. Nobody ever sent me the news about how AIDS was caused by HIV. (p. 174)

Finally, he had the opportunity to ask Montagnier himself:

    With a look of condescending puzzlement, Montagnier said, ‘Why don’t you quote the report from the Centers for Disease Control?’
    I replied, ‘It doesn’t really address the issue of whether or not HIV is the probable cause of AIDS, does it?’
    ‘No,’ he admitted, no doubt wondering when I would just go away. ...
    ‘Why don’t you quote the work on SIV [Simian Immunodeficiency Virus]?’ the good doctor offered.
    ‘I read that too, Dr. Montagnier,’ I responded. ‘What happened to those monkeys didn’t remind me of AIDS. Besides, that paper was just published only a couple of months ago. I’m looking for the original paper where somebody showed that HIV caused AIDS.’
    This time, Dr. Montagnier’s response was to walk quickly away to greet an acquaintance across the room. (Duesberg, 1996, pp. xii-xiii)

Mullis became a member of the Group for the Scientific Reappraisal of the HIV/AIDS Hypothesis, whose petition has now been signed by over 2300 professionals. He points out that retroviruses are everywhere, and are passed from mother to child, but they’ve never been shown to have killed anyone. He comments wryly: ‘HIV didn’t suddenly pop out of the rain forest or Haiti. It just popped into Bob Gallo’s hands at a time when he needed a new career’ (Mullis, 2000, p. 178). Gallo had previously been involved in the search for genes that cause cancer (oncogenes), and, like numerous others researchers, had become frustrated by the lack of success.

All the old virus hunters from the National Cancer Institute put new signs on their doors and became AIDS researchers. Reagan sent up about a billion dollars just for starters, and suddenly everybody who could claim to be any kind of medical scientist and who hadn’t had anything much to do lately was fully employed. They still are. (p. 177)

As HIV came to be automatically equated with AIDS, anyone testing HIV-positive qualified as a disaster victim eligible for treatment at public expense, which meant lucrative consultation and testing fees, and treatment with drugs that have proved highly profitable for the pharmaceutical industry. County health authorities receive $2500 per year for every reported AIDS case.

The ‘evidence’ that HIV causes AIDS is purely epidemiological: persons infected with HIV develop AIDS and those not so infected do not. But since AIDS is now defined as requiring a positive HIV test, it’s hardly surprising that everyone with AIDS is HIV-positive! It has become increasingly clear over the years that very few HIV-positive people ever become ill, and that by no means all patients with AIDS symptoms test HIV-positive. The scientific literature documents 4621 confirmed cases (to 1992) of HIV-free people dying of AIDS symptoms. To preserve the dogma that HIV causes AIDS, a new condition was invented to cover these cases – ‘idiopathic CD4-lymphocytopenia’. This is just a scientific-sounding way of saying ‘we haven’t got a clue’, but it has the advantage of allowing these paradigm-busting cases to be excluded from official AIDS statistics.

Strictly speaking, there is no such thing as a test for AIDS. ‘AIDS tests’ do not identify or diagnose AIDS and cannot detect HIV. The Elisa and Western Blot tests commonly used to diagnose HIV infection detect only interactions between proteins and antibodies assumed to be related to HIV, not HIV itself. Newer ‘viral load’ tests, too, do not measure levels of actual virus in the blood.

All HIV antibody tests are highly unreliable because the proteins they look for are not specific to ‘HIV’. Even with the same individual, it is not uncommon for successive HIV tests to switch back and forth between positive and negative results. False-positive HIV tests can result from almost 70 medical conditions, e.g. a variety of infections (including flu), flu vaccination, interferon therapy, many antibodies, blood transfusions, autoimmune diseases, haemophilia, hepatitis, herpes simplex, leprosy, malaria, certain cancers, rheumatoid arthritis, tuberculosis, tetanus vaccination, and multiple pregnancies. HIV antibody tests are between 41 and 76% accurate for people with AIDS conditions, and between 0 and 16% accurate for those with no symptoms. In one study, 50% of blood samples from healthy dogs reacted positively on HIV antibody tests. The tests were originally developed for screening the blood supply, where false positives hardly matter. All the test kits are accompanied by disclaimers in which the manufacturers warn that the tests should not be used to diagnose HIV infection.

A key problem is that none of the proteins detected in HIV antibody tests are specific to HIV. Out of 30 or so possible retroviral proteins, about 10 were selected as being specifically from HIV and nothing else, even though there was no way of knowing this for certain since HIV had not been properly isolated. ‘So, in an amazing display of circular logic, they simply selected the proteins that most commonly reacted in blood samples of AIDS and pre-AIDS patients. No wonder there is a correlation between testing HIV-positive and developing AIDS in some patients’ (Culshaw, 2007, p. 38).

HIV test kits are calibrated to ensure that most healthy people test negative, but there are no international standards for deciding what constitutes a positive result, and someone could switch from positive to negative simply by changing countries. In the Elisa, the serum reacts with a mixture of the selected proteins to cause a colour change. But there are varying degrees of colour change, and the cutoff value between ‘positive’ and ‘negative’ is not universal but is determined by the testing venue and depends on what the test is intended for. Moreover, the serum is first diluted 400-fold, otherwise everybody would test positive. The result of the Western Blot takes the form of a series of reactive protein bands, and depending on the lab or the country in which it is located, different combinations of two, three, or four bands are sufficient to diagnose HIV infection. In the US, a positive HIV diagnosis based on the Elisa test must be confirmed by a Western Blot test. In the UK, diagnosis relies on repeat tests with various types of Elisa, as the Western Blot is regarded as too unreliable.

AIDS patients have typically been exposed to a vast number of infections and recreational drugs, which induce antibodies and impair the immune system. The antibody tests may, at best, be measuring a condition called hypergammaglobulinemia, which means having too many antibodies to too many things. Microbiologist Phyllis Evelyn Pease (2005) provides evidence that the antibodies detected may be autoantibodies, directed against some of the body’s own cell constituents, as a result of cells being infected with alien DNA carried into the body by certain types of bacteria. Unfortunately, according to orthodox thinking a positive result on the nonstandardized, nonspecific HIV test is equivalent to a death sentence, and therefore has a devastating impact on the individual concerned.


A logic-defying virus

HIV is supposed to be lethal retrovirus, widely believed to have originated in Africa, that gradually destroys the cells of the immune system, so that victims eventually die from the inability to resist a variety of well-known diseases. AIDS victims suffer slow, painful deaths from pneumonias, yeast infections, cancers, uncontrollable diarrhoea, and dementia from brain degeneration.

However, retroviruses are harmless; they don’t kill cells because they depend on viable cells for replication. There is no convincing evidence that HIV is any different. On average, HIV only infects 1 in 1000 T-cells; over 99% of T-cells in persons with AIDS are not infected. So even if HIV really could kill T-cells, it would not be able to deplete them and cause AIDS. The cell-killing viruses that are believed cause herpes are found in millions of T-cells (up to half), yet they are still unable to cause T-cell depletion and AIDS. As Harvey Bialy says, ‘the problem of massive cell killing by minuscule amounts of virus ... remains the central unanswered question about the HIV=AIDS equation’ (2004, p. 79).

Since ‘HIV’ is genetically unremarkable, and, like other retroviruses, doesn’t even kill defenceless cells in culture, why should we imagine that it does so in the body when it is effectively neutralized by the human immune system? The orthodox response is that HIV is a new kind of retrovirus with special new properties – including, apparently, the ability to defy the rules of science and logic! It has been claimed that, even when it is not present, HIV somehow programmes T-cells to commit suicide at some later time. Some researchers claim that HIV exploits special receptors on human T-cells that, due to a hypothetical genetic mutation, many ‘Caucasian Europeans’ lack, but most Africans have. Curiously, many gay men also seem to possess these mysterious receptors, as do intravenous drug users and transfusion recipients! As Celia Farber (2006) says, ‘Such unproven hypotheses about the ingenuity of HIV proliferate in the popular and scientific media like seasonal flu.’

In 2001 the science magazine Nature conceded that ‘much remains left to the imagination’ when it comes to understanding how ‘HIV’ causes immune deficiency. In 2006 Benigno Rodriguez et al. published a paper in the Journal of the American Medical Association which concluded that HIV cannot be responsible from more than 5-8% of the loss of CD4 immune cells that is necessary to cause AIDS. This flatly contradicts the mainstream position that HIV is the sole cause of AIDS.

To isolate a retrovirus, a sample thought to contain it is added to a tube containing a sugar solution whose density increases from top to bottom. The tube is placed in a centrifuge and spun at ultra-high speeds for many hours, so that the particles band according to their density; retroviruses band at a density of 1.16 g/ml. Images of the relevant band are then made with an electron microscope. All retroviruses apart from HIV have been properly isolated in this way.

HIV has never been observed under an electron microscope in the uncultured blood plasma of AIDS patients (De Harven, 2003, 2010). Particles claimed to be HIV have only been observed in cell cultures that have been stimulated by certain chemicals or irradiated. The first and only electronmicrographs of ‘purified HIV’ were published in 1997 by two groups of scientists – a US team led by Julian Bess and a Franco-German team led by Pablo Gluschankof. They accepted that the purity of ‘HIV’ preparations had not previously been verified. Eleni Papadopulos, leader of the Perth Group, comments:

In other words, for fourteen years the community of HIV experts claimed to have obtained purified HIV, and then used this material to obtain proteins and RNA as if it were unique to a retrovirus HIV, and employed it time and time again for research and producing and patenting various diagnostic tests. All without a shred of proof it contained even one particle of any description let alone a retroviral-like particle. (Papadopulos, 2006, p. 110)

The US and Franco-German teams admitted that the vast majority of their own ‘purified’ material consisted of microvesicles, i.e. cellular fragments, but claimed that some particles looked like retroviruses and were ‘HIV’. Yet none of these particles had all the morphological characteristics of retroviruses, or even their principal characteristics: a diameter of 100-120 nanometres (officially reduced to 80-100 nm in 2000), and surface spikes and knobs. In the Franco-German study the average ‘HIV’ diameter was 136 nm and no particles were smaller than 120 nm. In the US study the corresponding dimensions were 236 nm and 160 nm. In other words, the American ‘HIV’ is about twice the diameter of the European ‘HIV’. In addition, of the 12 proteins that allegedly compose HIV, only three were detected by Bess et al., yet they were found not only in the material supposedly containing ‘HIV’ particles but also in the material without it – only the quantities were different. The Perth Group concludes: ‘This is as good an evidence as one can get that nobody has: (1) proven the existence of the “HIV” particles; (2) purified the “HIV” particles; (3) proven the existence of “HIV” proteins and RNA’ (Papadopulos et al., 2008).


Electronmicrograph of ‘HIV’ published by Bess et al. in 1997. Particles marked ‘MV’ are said to be normal microvesicles and those marked ‘V’ are said to be HIV. Pure HIV has still not been isolated.


Based on the genetic fragments, assumed to be related to HIV, that are found in patients’ blood, AIDS scientists estimate that 100 million or more genetically distinct variants of HIV are present in any one patient. Some researchers consider HIV to be a ‘quasi-species’ of virus, while others believe that it has an extraordinary and unprecedented ability to mutate. The Perth Group, on the other hand, argues that much of the genetic material attributed to HIV is in fact DNA or RNA from decaying cells, which are capable of producing retroviral-like particles when stressed or dying in large quantities. In other words, we are looking at chaotic genetic activity from within disordered cells rather than a unique, invasive viral entity. In their view, ‘HIV’ is simply ‘a metaphor for a lot of quasi-related phenomena’, and a consequence of challenged health rather than its cause.


One of many colourful, computer-generated images of what ‘HIV’ might look like if it really existed.


Pease (2005) argues that failure to make proper use of the electron microscope has had a disastrous impact on AIDS research. Researchers have failed to take account of contaminants such as mycoplasmas – bacteria lacking a cell wall which can easily escape detection. She shows that the cell-killing capacity attributed to ‘HIV’ is actually due to mycoplasma contamination. Montagnier carried out experiments on a cell line in which it was thought that HIV’s cell-killing properties had been demonstrated, but was surprised to find that when the cell line was treated with an antibiotic the cells grew undamaged; Pease explains that the antibiotic blocked the growth of contaminating mycoplasma. Gallo claimed to have developed a cell line called H9 that allowed HIV to grow, supposedly because it had become resistant to the virus. Pease contends that the cells had actually become resistant to the contaminating mycoplasma; she reproduces electronmicrographs of an H9 cell culture used as a control for HIV which clearly show mycoplasma elements, growing without any noticeable effects on the cells. Hodgkinson (2007, p. 600) comments: ‘Even after it became clear that mycoplasmas had contaminated the cultures used by HIV’s protagonists, and that they were the cause of the cell-killing for which HIV was being blamed, no one wanted to know.’

It has so far proved impossible to develop an AIDS vaccine, despite the billions of dollars thrown at AIDS research. In fact the hopes for a vaccine are irrational. A vaccine works by triggering the production of antibodies. But AIDS patients already, by definition, have HIV antibodies in their blood. Moreover these antibodies are so effective that no HIV is detectable in AIDS patients. That’s why ‘AIDS tests’ look for antibodies rather than actual virus. If a vaccine were developed and given to people who are HIV-negative, they would become HIV-positive and therefore, by definition, AIDS patients. In other words, everyone would become an AIDS case, and the prediction of a global pandemic would come true!

The four classical tests of whether or not a microorganism is the cause of an infectious disease are known as Koch’s postulates. First, the microbe must be found in all cases of the disease – but there are over 4600 cases of HIV-negative people dying of AIDS symptoms and all that can be found in patients’ blood is antibodies to what are assumed to be ‘HIV proteins’, not HIV itself. Second, the microbe must be isolated from the host and grown in pure culture – but no isolation of HIV has ever been achieved which meets the standards that virology normally requires for retroviruses. Third, the microbe must produce the original disease when introduced into a susceptible host – but scientists have not managed to infect chimpanzees with HIV. Fourth, the microbe must be found present in the experimental host so infected – since the third condition has never been met in the case of HIV, this is irrelevant.

Until HIV appeared on the scene, the period from infection with a virus to the onset of disease depended on the generation time of the virus. Since HIV is believed to replicate in two days, like all other retroviruses, and since an infected cell produces over 1000 viruses every two days, HIV should cause AIDS just as fast as other viruses cause disease. However, the latency period attributed to HIV has steadily increased over the years: first it was a few months, then it was extended to 2 years, then 5, then 10 or 15 years, and more recently, even to entire lifetimes.

The situation was becoming so embarrassing that in 1995 a new hypothesis, known as ‘viral load’, was invented. Proponents claim that HIV goes on the offensive from the very moment of infection, and that the immune system of a person who tests positive is engaged in a perpetual struggle to keep the virus under control, but that after 5, 10, or 15 years or more, HIV eventually wins the battle. A person’s ‘viral load’ is determined by means of the polymerase chain reaction (PCR) test. But this test does not detect actual virus. It amplifies millions of times small genetic segments assumed to be associated with ‘HIV’ so that they become detectable, and these fragments of genetic material are then assumed to correspond to counts of actual virus. Evidence suggests that these fragments are actually associated with human endogenous retroviruses (HERVs) (De Harven, 2010). Using PCR, an average of over 100,000 HIVs per millilitre of blood are found in AIDS patients. However, when standard virus-counting methods, are applied, a viral load of 100,000 is found to correspond to less than 10 infectious units of ‘HIV’ – far too little to induce illness.

Viral loads have been measured in people who are HIV-negative and in AIDS patients who test HIV-antibody positive but have no HIV. Low viral loads do not correlate with high T-cell counts or good health, while high viral loads do not correspond with low T-cell counts or sickness. Kary Mullis, who won the Nobel Prize in 1993 for inventing PCR, says that the conclusions being drawn from PCR’s use in these tests are worthless. Some critics have bluntly characterized this new hypothesis as ‘a viral load of crap’.


AIDS is not contagious

AIDS propagandists are adept at using misleading and inflated statistics to maintain the AIDS scare. Rather than giving numbers of new AIDS cases each year (as is done with all other diseases), AIDS reports typically quote cumulative totals: the number of cases or fatalities in any particular year is added to the sum total of all AIDS diagnoses or deaths that have ever occurred. This makes it possible to cite ever-growing numbers for AIDS even as AIDS is actually declining. Frequent use is made of estimates and projections. For instance, the 1999 United Nations AIDS Report estimated that 2.5 million people throughout the world died of AIDS in 1998. Yet the November 1999 WHO Weekly Epidemiological Record reported that only 2.2 million people worldwide have ever received a diagnosis of AIDS – and this includes many people who remain alive and well. The UN estimate received widely publicity while the actual WHO case count was neglected.

In 1986 it was predicted that 3 to 5 million Americans would be HIV-positive and 1 million would have died from AIDS by 1996. However, HIV has been found in about a third of 1% of the US population – i.e. in about 1 million people – since 1985, and is therefore clearly not a spreading infection but an endemic condition. The number of Americans dying of AIDS reached 410,800 in 1998, and this includes death from any cause – accidents, noncontagious illnesses, drug side effects, etc. To put things in perspective, AIDS is not among the 10 leading causes of death in the US. In annual death rates, it lags behind motor vehicle accidents, nonvehicular accidents and other adverse events, flu and pneumonia, diabetes, septicaemia, Alzheimer’s disease, and homicide. From 1981 to 1998 car accidents killed over 800,000 Americans. Suicides exceed AIDS fatalities by over 100,000. And deaths from the side effects of properly prescribed and correctly taken drugs outnumber AIDS deaths in America by more than 1.3 million.

Portraying AIDS as the biggest health threat means that it receives greater funding than problems affecting far higher numbers of people. NIH research expenditures in 1992 averaged $1160 for every American who died of heart disease, $4700 for each one who died of cancer, and more than $43,000 for every death in a person diagnosed with AIDS.

In 1985 the UK’s Royal College of Nursing predicted that 1 million people in Britain would have AIDS in six years unless the killer disease was checked. 15 years later, the annual number of AIDS deaths was 263 – less than the number of people who died from falling down stairs. Around 25,000 people are currently diagnosed as HIV-positive in the UK – half to a quarter of the totals estimated in the 1980s.

In the US, AIDS cases increased from 1981 to 1992 and have since declined, whereas HIV infections have remained more or less constant – so HIV is clearly not the cause of the AIDS epidemics of the early 1980s. The failure of AIDS to progress exponentially shows that it is not a contagious disease caused by an infectious virus. Instead it has acted like lifestyle diseases, such as lung cancer from smoking. If contagious, it would also have spread randomly through the population, like all viral/microbial epidemics in the past. Instead it is highly nonrandom with regard to sex (80% of patients are male), sexual persuasion (over 60% are homosexual), and age (85% are aged 25-49). After nearly two decades, AIDS in western countries has still not entered the general population, but remains predominantly confined to the original risk groups: male homosexuals, injection drug users, and blood recipients.

In the US, AIDS was first noted around 1980 in New York, Los Angeles, and San Francisco; HIV is alleged to have arrived in those communities about 10 years earlier. Tests for HIV have been widely carried out since 1985, and straight away HIV-positive people were found in every sector of society and in every part of the US. It is highly unlikely that HIV could have spread so rapidly into the general population across the country. For a start, the geographic distribution of HIV does not look like a spread from the AIDS epicentres; HIV has always been more prevalent in the east and south of the US than in the west, and is least prevalent in northern and central parts. The conventional view of HIV/AIDS is unable to explain this asymmetry, for ‘one would hardly expect a sexually transmitted infection to display so unvarying a geographic distribution’ (Bauer, 2005, p. 582).

Studies show that ‘HIV’ is not readily transmissible by either infected needles or sexual intercourse. Only about 1 in 1000 unprotected sexual contacts ‘transmits HIV’. Since only 1 in 275 US citizens is HIV-infected, an average uninfected citizen would therefore need 275,000 random sexual contacts to get infected and spread HIV – an unlikely basis for an epidemic! The risk of transmitting genuine sexually transmitted diseases (STDs) is hundreds of times higher. While the number of HIV-positives has failed to grow, rates of venereal disease have increased over the same period and far surpass cases of AIDS. This contradicts the idea that ‘safe sex’ has prevented HIV from spreading. A fairly steady number of under a million Americans are believed to be infected with HIV – far fewer than the estimated 4 to 8 million new infections annually with chlamydia, 500,000 with genital herpes, and 400,000 with gonorrhoea. It has been found that the use of condoms does not significantly affect the rate of HIV transmission, whereas it does decrease transmission of venereal diseases.

If HIV were transmitted sexually, there would be a correlation between exposure to prostitutes and the probability of testing HIV-positive – but no such correlation exists. Prostitutes typically become infected with syphilis, gonorrhoea, and herpes, but almost never become infected with ‘HIV’, unless they abuse intravenous drugs. Likewise, the wives of haemophiliacs don’t get AIDS. Nor are there any confirmed cases of medical workers contracting AIDS from patients, whereas thousands of healthcare professionals working among people with cholera, hepatitis, syphilis, influenza, or rabies have been infected with these diseases. The 57 possible cases by 2001, about three per year, are entirely consistent with the hypothesis that there is a spontaneous incidence of HIV from a variety of not-necessarily-serious health challenges. In other words, all the evidence shows that ‘HIV’ is extremely difficult to ‘transmit’ to a healthy individual, and there is actually no compelling proof that a genuine virus is being transmitted at all.

Further evidence that ‘HIV’ is not a sexually transmitted infection is provided by comparisons of the incidence of AIDS in different population groups and the variation of ‘infection’ rate with age (Bauer, 2006a). Newborn babies test HIV-positive about 4 times more often than children from about one year of age to the pre-teen years, and about 10 times more often than children in their early teens. From the teens on, the ‘infection’ rate in all studied groups follows the same course, increasing into the middle adult years and then declining again towards old age, more so for men than for women. Psychiatric patients test ‘HIV-positive’ significantly more often than people attending clinics for sexually transmitted diseases, or clinics providing HIV tests and counselling. The prevalence of HIV is much higher in critically ill emergency-room patients than in the least ill patients, and among tuberculosis patients it is about the same as, perhaps even higher than, among those visiting STD clinics. In general, the fitter and healthier the group, the lower the prevalence of HIV.

The frequency of positive HIV tests also correlates with racial category (Bauer, 2006b). In every occupational, social, or other group tested in the US, at all ages and for both sexes, the prevalence of HIV increases in the order: Asian – white – Native American – Hispanic – black. Data from South Africa display a similar sequence: white/Asian-Indian – coloured – black. The only explanation under the current paradigm is that blacks are more prone to risky sexual behaviour and sharing of infected needles for injecting illegal drugs than whites, Asians, or Native Americans. But surveys of actual behaviour contradict this.

Clearly, HIV tests do not track a sexually transmitted agent. The prevalence of HIV is a marker of challenged health or actual illness in the sampled population, and the intensity of the body’s response to health challenges appears to be modified by genes associated with the immune system, which differ for different racial groups. According to the Perth Group, the prevalence of HIV reflects the oxidative stress resulting from an impending or actual illness. The tests that supposedly detect antibodies specific to HIV are actually detecting signs of nonspecific physiological stress. Finally, ‘HIV-positive’ is not necessarily a permanent condition, as shown by the fact that HIV is more prevalent among newborn babies than among older children. In short, ‘HIV’ is a reversible indicator of physiologic stress.


Africa: fact vs. fantasy

Whereas AIDS deaths have fallen in Europe and the USA and total around 250 a year in the UK, Africa is supposedly being ravaged by an AIDS epidemic running out of control, with tens of millions of cases. The media describe HIV/AIDS as ‘Africa’s big killer’. But there is a huge discrepancy between the figures being bandied about and hard facts. As Christine Maggiore puts it, ‘Unfounded estimates, rather than unprotected sex, are responsible for the alarming number of AIDS cases said to occur in Africa’ (2000, p. 20). Pregnant African women are routinely tested for syphilis at antenatal clinics, and some of the blood samples left behind are anonymously given a single Elisa HIV antibody test. The results are then extrapolated to the general population via computer simulations. However, pregnancy is a source of false positives, and a single Elisa test will also give an unacceptably high number of false positives.

One news report, based on UN estimates, claimed that ‘a Kenyan dies of AIDS every 3 minutes’. If that were true, 175,000 Kenyans would die of AIDS every year – yet the total number of diagnosed AIDS cases in that country since 1981 is less than half this figure (81,492) and many of these people remain alive and well. In 1987 the WHO estimated that there were one million cases of ‘HIV disease’ in Uganda. Yet 10 years later the cumulative number of AIDS cases actually reported was 55,000. ‘Nobody knew what had happened to the other 945,000,’ says James Hogan drily (2004, p. 322). In 1996 WHO statisticians multiplied reported AIDS cases in Africa by 12 to reach estimated totals; in 1997, by 17; and over an 18-month period in 1997/98, by 47!

An estimated one million people in Sub-Saharan Africa supposedly died from AIDS between 1980 and 2000. But during that period the total population grew at 2.6% per year – an increase of 274 million. So the unverified estimate for AIDS fatalities amounts to about a third of 1% of the change in population. A UNAIDS estimate of 250,000 AIDS deaths in South Africa has been shown to be at least four times greater than the actual number. One study claimed that young adults with HIV were 87 times more likely to die prematurely than their uninfected contemporaries. But newspaper reports forgot to mention that this was an extrapolation based on just 14 deaths and 5 actual AIDS diagnoses.

In reality, AIDS is not the terrible scourge it is portrayed to be by those who would lose out financially if the truth were told. 99.5% of Africans do not have AIDS, and 97% of Africans who test HIV-positive do not have AIDS. AIDS is not the leading cause of illness or death in any African nation. Several million cases of tuberculosis and malaria are reported each year in Africa while total AIDS cases on the continent for the entire AIDS epidemic hover just above half a million. Wildly inaccurate predictions of a rampaging AIDS epidemic have also been made about Brazil, India, Thailand, and other tropical places with endemic public health problems and poor health statistics.

Under the WHO’s Bangui definition, Africans are diagnosed with AIDS without an HIV test if they score at least 12 points based on a list of symptoms which includes: over 10% weight loss (4 points), protracted weakness (4), prolonged fevers for a month or more (3), prolonged diarrhea (3), thrush (4), persistent cutaneous herpes (4), shingles (4), persistent itching (4), and a cough (2). These same symptoms are caused by conditions that run rampant in Africa, such as malaria, tuberculosis, parasitic infections, malnutrition, and unsanitary drinking and bathing water. Since the longstanding underlying problems such as poverty and poor sanitation affect both sexes equally, AIDS in Africa also affects both sexes fairly equally.

Several large studies have found that among thousands of randomly selected Africans with standard AIDS diseases, fewer than half were HIV-positive. South Africa is the only sub-Saharan country in which an HIV antibody test is required before labelling an otherwise common disease or combination of diseases ‘AIDS’. But these results, too, are unreliable, because false positive results in HIV tests can be produced by exposure to malaria, tuberculosis, leprosy, parasitical infections, and other diseases that are widespread in Africa.

Based on the conventional view of HIV/AIDS, every African not known to be a homosexual or drug abuser is presumed to have acquired AIDS through heterosexual intercourse – thereby resurrecting the racist tendency to stereotype Africans as hyper-sexual. Lecturing people on their morals, distributing condoms, and poisoning African babies with ‘anti-AIDS’ drugs will do nothing to solve the root causes of Africa’s health problems.

More insidious, funds and resources are withdrawn from the support of low-cost but effective traditional clinics and the provision of basic nutrition, clean drinking water, and sanitation, and directed instead to ruinously expensive programs to contain a virus that exists for the most part in WHO statisticians’ computers. (Hogan, 2004, p. 323)

Many Africans participate in perpetuating the myth of an AIDS pandemic in Africa. The huge international funds poured into AIDS and HIV work means that politicians and health workers have a strong incentive to reclassify as AIDS old diseases that have always been endemic in tropical Africa. When African doctors are sent to AIDS conferences around the world, the daily allowance they receive is equal to what they earn in a whole year at home. It has become a joke in Uganda that you are not allowed to die of anything but AIDS. If someone is run over by a truck, doctors have been known to attribute it to AIDS-related suicide! The Ugandan government could afford to spend less than $1 a head on health care from its own funds, but in just one year it received $6 million for AIDS research and prevention from foreign agencies. As one commentator puts it, dysentery and malaria do not inspire headlines or fatten public health budgets; infectious ‘plagues’ do. What’s more, people in the developing world can obtain help from agencies if they have lost family members to ‘AIDS’ – but not if the deaths are attributed to other causes.

There is thus a vast overdiagnosis of AIDS and ‘HIV disease’ in Africa and other countries where malnutrition and grossly impoverished living conditions, and the associated infections, are the real killers. Neville Hodgkinson (2003) writes:

Perhaps ... it is easier on the West’s conscience to keep blaming an epidemic of a deadly new virus for an increase in immune deficiency in less-developed countries than it is to acknowledge the effects of worsening poverty consequent on economic restructuring, crippling debt, and the after-effects of decades of socially destructive policies towards black people such as occurred under apartheid. (p. 113)

There is no serious evidence to substantiate claims that ‘HIV’ originated in Africa as Simian Immunodeficiency Virus (SIV). SIV does not induce any of the 29 AIDS-defining illnesses. It induces only flu-like symptoms in monkeys kept in unnatural circumstances – i.e. laboratory animals with undeveloped immune systems who are injected with large quantities of SIV. Moreover, SIV causes illness within days of infection or not at all.


Poisoning the patients

The AIDS/HIV scare has been a tremendous boon for the pharmaceutical industry, which has reaped enormous profits by peddling highly toxic antiretroviral drugs. The main impact of these drugs, however, has not been to improve patients’ long-term health, but to boost the number of ‘AIDS deaths’!

AZT is a highly toxic chemical compound originally created for use as a cancer treatment. It is known as a nucleoside analogue drug, or DNA chain terminator, meaning that it stops DNA from replicating. It therefore destroys all growing cells, including new cells produced in bone marrow where the immune system is generated. In 1964, experiments with AZT on mice with cancer showed that it was so effective in destroying healthy growing cells that the mice died of extreme toxicity. As a result, the drug was shelved and no patent was ever filed.

20 years later the pharmaceutical company Burroughs Wellcome (now GlaxoSmithKline) launched a campaign to remarket AZT as an anti-HIV drug. The FDA gave its approval after abbreviated trials of less than six months sponsored by the drug’s manufacturer, who selected for publication only those trials with seemingly favourable outcomes. AZT is much more toxic than recreational drugs such as cocaine and heroin, and is now widely understood to have killed more patients than it has helped. No one has lived more than three years on AZT treatment. In 1994 the ability of AZT to delay the progression to AIDS was investigated by the British-French Concorde study, the largest, placebo-controlled study of its kind. It investigated 1749 HIV-positive subjects and found that AZT is unable to prevent AIDS and increases mortality by 25% (Duesberg et al., 2003). In addition to destroying T-cells, B-cells, and the red blood cells that carry oxygen throughout the body, AZT and similar drugs – e.g. Epivir (3TC), Zerit (D4T), Hivid (ddC), and Videx (ddI) – destroy the kidneys, liver, intestines, muscle tissue, and the central nervous system.


Laboratories receive AZT in bottles carrying this special label. The skull-and-crossbones on a bright orange background signifies an unusual chemical hazard. The label appears on bottles containing as little as 25 milligrams, a small fraction (1/20 to 1/60) of a patient’s daily prescribed dose of 500 to 1500 mg.


In 1996 a new class of antiviral drugs was introduced, known as protease inhibitors, which are used in combination with older chemotherapy compounds such as AZT and ddI. The mixture of these treatments is called a ‘combination cocktail’ or ‘highly active antiretroviral therapy’ (HAART). They were approved after the fastest and most lenient review process in FDA history, and as with AZT earlier, the media was full of hype about their ‘miraculous’ effects. When HAART produced immediate inflammation, opportunistic infections, liver damage, swollen glands, and the like, the drugs were not blamed because surrogate markers – CD4+ T-cell counts or viral load – seemed to improve. Instead, a new medical condition was invented, ‘immune restoration syndrome’, in which AIDS-like illnesses are said to be caused, in some mysterious manner, by the nascent recovery of the immune system. A large study published in 2006 confirmed that illness became worse even as surrogate markers improved (Bauer, 2007).

HIV-positive people who are very sick may initially experience some benefit after starting antiretroviral treatment. Later, however, the drugs tend to lose their effectiveness, which is currently taken to mean that the ‘AIDS virus’ becomes resistant. However, the temporary reprieve might not have anything to do with the drugs’ effect on any virus. For instance, ‘anti-HIV drugs have the unintended benefits of functioning as true “antibiotics”, because of their general toxicity to all living things. As such they will also reduce the load of opportunistic microbial diseases that affect most AIDS patients ...’ (Duesberg et al., 2003, p. 396). Another possible factor is hormesis: as with low doses of radiation, drug treatment may initially stimulate the immune system to fight harder. And finally there is the placebo effect: belief in the efficacy of a drug might for a time override its adverse effects.

In 2001 the US government reversed its policy of ‘hit hard, hit early’ for HIV-positive people; it now recommends delaying antiretroviral treatment as long as possible for those who have no symptoms of illness. Drug manufacturers were also ordered to tone down their upbeat ads for AIDS medications. The reason for this change of policy was the ‘unexpected toxicities’ of the drugs. Well-documented side effects include CMC retinitis (a viral infection often resulting in blindness), diabetes, liver failure, physical deformities, severe exhaustion, loss of appetite, pancreatitis, diarrhoea, nausea and vomiting, muscle and joint pain, neuropathy, sexual dysfunction, fever, chills, dizziness, abdominal pain, depression, sleep disorders, and sudden death. The drugs have a failure rate of 50%, and as many as 40% of participants drop out of protease inhibitor drug trials due to adverse effects.

Although the protease inhibitor ‘combo cocktails’ are often claimed to be behind the recent decline in AIDS, the decline began several years before these drugs became available for general use. A more likely explanation for decreased deaths is that since the 1993 revision of the AIDS definition, more than half of all newly diagnosed AIDS cases involve HIV-positive people with no symptoms of illness; by 1997 the figure stood at 65%. Another important factor is that dosages of nucleoside analogue drugs and protease inhibitors are much lower than the massive doses of AZT that were given in the late 1980s.


The CDC’s own data show that AIDS deaths began to decline at the end of 1995, before the release of new ‘wonder drugs’, and that AIDS cases began to decline before that. They would both have started to decline earlier if the CDC hadn’t expanded the definition of AIDS in 1993. Note that only 19% of HIV-positive people were actually on the new drugs by mid-1996. (http://hivinsite.ucsf.edu)


The immunosuppression supposedly caused by HIV is therefore being tackled with drugs that are themselves notoriously immunosuppressive, and cause AIDS-defining conditions such as diarrhoea, dementia, lymphoma (cancer), muscle wasting, and T-cell depletion. These medications amount to ‘AIDS by prescription’ – but patients are told they’re going to die anyway. This is the real tragedy of the HIV/AIDS scandal: hundreds of thousands of people – many of whom are initially perfectly healthy – have been and are still being poisoned with deadly, health-destroying drugs that have brought drug companies unprecedented profits. Patients are required to pop up to 30 pills a day and are warned that if they fail to adhere to the dosages and times, their virus will mutate into new drug-resistant strains. If patients don’t respond properly to a particular drug they are told they have failed the drug – not that the drug has failed them! And patients who quit the drugs due to the intolerable side effects are told that they are ‘in denial’ and depicted as a public health menace.

Even babies and infants are not spared. Expectant mothers who test HIV-positive are commonly advised to abort or take AZT. But the effects of AZT on expectant mothers include severe anaemia, nerve damage, liver damage, muscle wasting, lymphoma, acute nausea, diarrhoea, and dementia. One study found birth defects in 10% of babies born to women who took AZT during pregnancy. A major Italian survey showed that children born to mothers treated with AZT in pregnancy were more likely to get severely sick and die by the age of three than those whose mothers were left untreated.

Although HIV testing before 18 months of age does not yield conclusive results, several US states require mandatory HIV antibody testing for newborns in public hospitals. Healthy babies who test HIV-positive are usually treated with toxic antiretroviral drugs, sometimes against the wishes of parents; parents who refuse to cooperate have been threatened with prosecution for child neglect. Even on the standard view of HIV/AIDS, such treatment would be unwarranted as 50-75% of ‘HIV’ infection in newborns represents passive antibodies transferred from the mother. Moreover, 75% of HIV-positive babies revert to HIV-negative without medical intervention, and 90% of babies born to healthy HIV-positive mothers test negative without drug therapy. Mothering magazine has carried articles warning pregnant women not to use antiviral drugs during pregnancy and containing heartbreaking accounts of the clinical consequences for the babies, and of the pressures placed on mothers to administer toxic drugs to their babies.

Trials of ‘anti-AIDS’ drugs, from AZT onwards, have commonly been conducted without proper controls; ideally, a drug should be tested by giving half the subjects the real drug and the other half a fake drug (‘placebo’), and the trial should be double-blind, meaning that none of the subjects should know which group they are in – but this standard scientific practice has generally been discarded. Those who criticize such lax practices or question the safety and efficacy of the allegedly ‘life-saving’ drugs have been labelled ‘refuseniks’, ‘denialists’, and even ‘murderers’ by pharmaceutical representatives, AIDS activists, and lap-dog journalists. Christine Maggiore (2000, p. 43) writes: ‘Surprisingly, it is not considered a conflict of interest when AIDS researchers own stock in the companies whose products they test, or when they are hired to run the drug trials they publish in medical journals. It is common practice for drug companies to pay researchers to author favorable articles about their products.’ As former drug developer David Rasnick says, ‘The scientific-medical complex is a $2 trillion industry. You can buy a tremendous amount of consensus for that kind of money. ... Science has totally capitulated to corporate interests’ (Farber, 2006).

AIDS researchers claim that anti-HIV drug cocktails reduce morbidity and mortality, based on surveys that investigated how long clinically healthy HIV-positive people survived on various drugs. Yet none of the surveys included an untreated control group to see whether the healthy subjects would have survived anyway. The disclaimers enclosed by manufacturers with all anti-HIV medications indicate that none of them has been shown to prolong life, and that all of them cause debilitating side effects, some of which are indistinguishable from the symptoms of AIDS. In short, there are no clinical trials showing that people taking anti-HIV drugs live longer or at least better lives than HIV-positive people not taking the drugs. However, Duesberg et al. (2003) cite some 50 studies showing that HIV-positive people treated with antiretroviral medications experience AIDS-defining illnesses at a greater rate than untreated HIV-positive control subjects. A study of 36 German AIDS patients who volunteered to abstain from anti-HIV treatment began in 1985. Only 8% have since died, compared with 63% of German AIDS patients as a whole, most of whom were treated with antiretroviral drugs since 1987. The leading cause of death among medicated HIV-positives is no longer even an AIDS-defining disease at all, but liver failure, a well-documented adverse effect of protease inhibitors (Culshaw, 2007).

The WHO estimated that in 2000 there were 34.3 million HIV-positive people worldwide and 407,000 AIDS cases. Even if it were assumed that all AIDS cases were fatal in a given year, which is hardly likely, the corresponding mortality rate would be only 1.4%. By contrast, the mortality rate of HIV-positive people receiving antiretroviral medications in the US and Canada is between 6.7 and 8.8% (Duesberg et al., 2003). As Bauer (2007, p. 241) comments: ‘Something is very wrong if the worldwide mortality rate of largely untreated HIV-positive people in under-developed countries is only about one-fifth or one-sixth of the mortality of HIV-positive people being given the best available antiretroviral medications in the world’s most developed countries.’


Challenging the establishment

The massive injection of funds into HIV/AIDS has created an army of HIV-AIDS ‘experts’ – scientists, journalists, and activists – who cannot afford to question the direction of their crusade as it would threaten their livelihood.

In 2000 the South African President Thabo Mbeki attempted to start a dialogue between orthodox and dissident AIDS scientists in the run-up to the international AIDS conference in Durban. However, mainstream scientists refused to participate. Instead, 5000 scientists signed a declaration (published in Nature on 6 July 2000), proclaiming the ‘true gospel’ that there is only one AIDS and it is caused by HIV, and accusing dissenting scientists of threatening ‘countless lives’. A point-by-point refutation of the Durban Declaration has been published (Johnston et al., 2001), but has been ignored. Harvey Bialy, an opponent of official HIV/AIDS theory, recently challenged a prominent AIDS expert to a debate, but the latter replied by saying: ‘The science community does not “debate” with the AIDS denialists, it treats them with the utter contempt that they deserve and exposes them for the charlatans that they are’ (Culshaw, 2007, p. 68)!

It is certainly far easier for HIV=AIDS proponents to denounce their opponents than to engage in serious debate, given that the official paradigm has proved a colossal failure. James Hogan writes:

No believable mechanism has been put forward as to how HIV kills T-cells. And billions of dollars continue to be spent every year on trying to unravel the mysteries of how HIV can make you sick without being present, and how an antibody can neutralize the virus but not suppress the disease. Scientific principles that have stood well for a hundred years are arbitrarily discarded to enable what’s offered as logic to hang together at all, and the best that can be done at the end of it all is to prescribe a treatment that’s lethal even if the disease is not. Yet no looking into alternatives is permitted; all dissenting views are repressed. This is not the way of science, but of a fanatical religion putting down heresy. (2004, pp. 328-9)

Christine Maggiore is equally scathing:

Setting the focus of all AIDS efforts on HIV, a virus that strains the rules of biology, epidemiology and logic, has rendered humankind few, if any, beneficial results.
    The lives of over 400,000 Americans have been given to the notion that HIV is the only possible cause of AIDS, and that toxic drugs offer the only possible prevention, treatment, or hope for cure. Many more lives have been forever altered by a positive result on a non-standardized test for harmless antibodies that may or may not be associated with HIV.
    More than $50 billion in federal AIDS funding has provided no significant understanding of HIV, has produced no safe and effective therapies, and has not brought us any closer to ending AIDS. Instead, we have constructed a powerful AIDS establishment that regulates our news, limits our access to information, and demands an ever greater allocation of our resources and support. Rather than helping to resolve AIDS, we have funded the growth of multi-billion dollar industries, institutions and organizations that depend on AIDS and on our continued devotion to the narrow and unproductive HIV hypothesis. (2000, p. 61)

Maggiore quotes many other critical appraisals of the HIV/AIDS establishment, e.g.:

Beware the scientist who believes that mainstream research thinking on any public health issue is equivalent to truth. Or the scientist who bullies or ridicules other scientists because they oppose the prevailing view. This is a person who has become what I would call a propagandist and should not be trusted. ...
    In all the time I’ve worked as a journalist, I’ve never come across a nastier group of people to interview than those propagandists who work in HIV research. (Nicholas Regush, medical science reporter)

As a scientist who has studied AIDS for 16 years, I have determined that AIDS has little to do with science and is not even primarily a medical issue. AIDS is a sociological phenomenon held together by fear, creating a kind of medical McCarthyism that has transgressed and collapsed all the rules of science, and has imposed a brew of belief and pseudoscience on a vulnerable public. (David Rasnick, former pharmaceutical drug designer)

Kary Mullis states:

In the AIDS field, there is a widespread neurosis among scientists, but the frenzy with which people approach the HIV debate has slacked off, because there’s just so much slowly accumulating evidence against them. It’s really hard for them to deal with it. They made a really big mistake and they’re not ever going to fix it. They’re still poisoning people. (Farber, 2006)

As Mullis puts it: ‘We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake’ (Duesberg, 1996, p. xiv).

Blaming noninfectious diseases on infectious microbes has occurred many times before. For example, scurvy, pellagra, SMON, and beriberi were each in turn blamed on mysterious infectious agents, sometimes leading to control measures that only exacerbated these epidemics. But scurvy turned out to be caused by vitamin C deficiency, pellagra by niacin deficiency, and beriberi by vitamin B1 deficiency.

The SMON epidemic struck Japan in 1950s and 60s, and was eventually found to be caused by a drug called clioquinol – which doctors had prescribed to treat early symptoms of SMON itself (e.g. diarrhoea). SMON cases rose and fell with sales of clioquinol, and disappeared after it was banned. But by the time the virus-hunters realized their blunder, thousands had died and many victims were left blind or paralyzed. Nowadays, the virus-hunting establishment prefers to keep quiet about this embarrassing ‘incident’.

Peter Duesberg, a world authority on retroviruses and a leading AIDS dissident, says that while the war on SMON was a ‘molehill of misdirected science’, AIDS is ‘an unmovable mountain’. SMON and AIDS, he says, ‘have become episodes in a long series of miscalculations emanating from a single ongoing, self-propagating scientific program – microbe hunting’ (1996, p. 29). Virus hunting was nearly discredited by the failed war on cancer, but has now enjoyed a spectacular revival with the HIV=AIDS hypothesis. The truth is that infectious diseases only account for about 1% of all causes of death in the industrial world.

Many scientists have maintained that HIV alone is not sufficient to cause AIDS. Montagnier has repeatedly stated this, and even Gallo has hinted at it, though current orthodox opinion still resists this view. To explain how ‘HIV’ supposedly kills at least 10,000 times more T-cells than it actively infects, it is suggested that it acts in conjunction with various ‘cofactors’, which may include microbes, ulcers, stress, and diet. Robert Root-Bernstein calls AIDS a multi-factorial, synergistic syndrome to which HIV contributes, but probably no more than do several other viruses and noninfectious insults to the immune system.

Duesberg objects that since HIV is extremely rare and dormant in most antibody-positive AIDS patients, it is hard to imagine how it could contribute to the various AIDS ‘cofactors’. Claims that HIV depends on ‘clinical illness promotion factors’ or on a ‘preexisting immune abnormality’ are, he says, ‘euphemisms for saying that HIV cannot cause AIDS until something else does’ (1996, p. 551). Astonishingly, one factor that demonstrably causes immunosuppression – drug abuse – has been completely ignored by mainstream AIDS research. There has been no official funding for a single study on the long-term effects of recreational drug use.

Duesberg argues that, far from being the ferocious cell-killer portrayed by the media, HIV is a harmless ‘passenger virus’. Hallmarks of a passenger virus are that the time from infection to the onset of disease is unpredictable, and that the concentration and even presence of the virus are not consistently correlated with a specific disease – both are true of HIV/AIDS. Duesberg and others argue that the real causes of the destruction of the immune system are drug abuse, heavy exposure to blood and blood products, and toxic medical treatments directed against HIV. He considers immunosuppression through long-term intoxication to be analogous to the slow decline of liver cells in long-term alcoholics or of lung cells in long-term smokers.

For putting forward these views, beginning in 1987, Duesberg has been pilloried and ostracized by the scientific establishment. He has been labelled a scientific psychopath who should be imprisoned, and accused of having the blood of African AIDS babies on his hands! Federal support for his laboratory was cut off so that by the end of the 1980s he couldn’t afford a secretary. He had to fight for even routine pay increases from the University of California at Berkeley, where he still has tenure. Graduate students were advised to shun his classes or risk adverse consequences to their careers. To humiliate him further, he was placed in charge of his university’s annual picnic committee. He had previously received ongoing funding as a recipient of the NIH’s prestigious Outstanding Investigator Award, but since challenging the HIV hypothesis, he has had 25 research grant applications rejected. Publication in the mainstream scientific literature was denied, including the right of reply to personal attacks carried in Nature. He ceased to be invited to scientific conferences, and colleagues even declared they would refuse to attend any conference that included him. The claim is often made that Duesberg has been discredited, yet ‘there is no record of this “discrediting” anywhere in the scientific literature’ (Culshaw, 2007, p. 13).

Duesberg was once one of the most highly funded and prized scientists in the US. Following his fall from grace, he proceeded to formulate and test a theory that shifts the focus of cancer causation from the ‘mutant gene’ theory that has reigned for about three decades to a simpler explanation first proposed in the early 20th century – namely that cancer is caused by chromosomal malfunction (‘aneuploidy’). Normal human cells contain 23 pairs of chromosomes (46 in all), but cancerous cells may have between 60 and 90. Duesberg’s careful and compelling research has generated considerable scientific interest, and in this field at least, his star is in the ascendant again. It remains to be seen whether this will help his earlier work on HIV/AIDS to receive greater recognition.

While Duesberg believes that HIV is a genuine retrovirus, other scientists have challenged the very existence of HIV. The Perth Group believes that the existence of HIV is fatally undermined by the following facts:

(1) heroic attempts to isolate such a virus always fail, despite huge financial incentives and numerous attempts to do so by an enormous army of scientists dedicated to ‘HIV’ ...; (2) what is called HIV RNA and DNA comes in many sizes and varieties that always differ from each other (no two are alike, even when abstracted from the same patient), whereas viral RNA and DNA should be of uniform length and composition; (3) the lethargy that characterizes what is considered ‘HIV replication’ excludes the possibility that replicative mutation can explain the wide HIV genetic variation; and (4) no one has produced a whole ‘HIV RNA’ molecule or a complete ‘HIV DNA’ strip, offering instead as the ‘HIV genome’ cobbled together bits of genetic material. (Philpott, 1997)

When ‘HIV DNA’ shows up, it does so only in a tiny fraction of T-cells. For Duesberg, this means that HIV infects too few cells to cause any disease. But if HIV is so lethargic as to infect only a few cells, how can its amazing variability be explained? The Perth Group proposes that ‘HIV DNA’ originates from the rearrangement of normal cellular DNA sequences, and the fact that each one originates independently and separately in each cell where it is found explains why ‘HIV’ DNA strips are always of varying length and composition.

Pease (2005) says that the latest electron microscope work shows that particles previously presumed to be ‘HIV’ closely resemble cell-wall-deficient bacteria (such as mycoplasmas), both in shape and in variation of size. Such bacteria can transfer DNA from an outside source into someone’s own cells, and the altered cells might then attack normal cells, giving rise to autoimmune conditions such as rheumatoid arthritis and AIDS. The view that AIDS is essentially an autoimmune disease found currency in the early years of the epidemic but fell from favour after HIV was accepted as the cause of AIDS in 1984. Pease writes: ‘most mainstream investigators now recognize that AIDS is not a simple virus disease comparable with the great bacterial and viral epidemics of the past, but even so, research continues almost exclusively as if this were the case.’ One of the reasons is that there is ‘a considerable amount of pressure on research workers to direct and interpret their findings in a way that encourages the renewal of their grants’, and the present generation ‘has been taught that the cause of AIDS has been settled as a self-evident truth ... and that anyone who dares not accept it is mad, bad or both’ (p. 112).


Risk factors and survival

‘HIV’ raises more questions than it answers and does not help us to understand immunosuppression. ‘AIDS’ itself is a rather artificial construct as it does not appear to be caused by a single virus, AIDS-defining diseases all have their own causes and about a third do not even involve immune deficiency (e.g. dementia, wasting syndrome, and cancers). AIDS in Africa and perhaps the Caribbean differs in many ways from AIDS elsewhere. And due to changing definitions, 1980s AIDS in the US is not the same as post-1980s AIDS, and pre-1993 AIDS is not the same as post-1993 AIDS.

There are various health risk factors that can destroy the immune system. For instance, there is overwhelming evidence for a link between drugs and immune deficiency. Prolonged habitual consumption of drugs such as heroin, crack, speed, and cocaine, whether injected or taken orally, is well known to cause immune dysfunction. The immune systems of drug abusers are ruined by the damage opiates cause to T-cells, infections acquired from unsterile needles, insomnia, and malnutrition. The body seeks to resist the biochemical effects of drugs, and part of its response is to generate what are usually mistaken for components of ‘HIV antibodies’.

Recreational drug use is the common denominator for over 95% of all American and European AIDS patients, including male homosexuals. Although two-thirds of all AIDS cases in the developed world involve homosexuals, only a small percentage of homosexuals have fallen victim to AIDS, namely those leading the fast-track lifestyle (which emerged in the 1970s), characterized by widespread use of recreational drugs, high levels of promiscuity and venereal disease, and overuse of antibiotics.

Surveys have found that 93 to 100% of the gay men taking part used cocaine, crack cocaine, poppers, heroin, ecstasy, methamphetamines like speed and crystal, and/or Special K (an animal tranquillizer). At one time, 95% of gay men in major urban areas like Los Angeles, New York, and San Francisco used poppers – nitrite inhalants that dilate blood vessels and relax muscles (facilitating anal sex and heightening orgasm). Nitrite use correlates with Kaposi’s Sarcoma (KS) and non-Hodgkin’s lymphoma, two AIDS-defining cancers found almost exclusively in this risk group. KS is also documented in HIV-negative gay men who used poppers. By 1991 only a quarter of gays used poppers, and the proportion of AIDS cases with KS fell almost in unison, from 50% in 1981 to only 10% in 1991. Incredibly, KS – one of the defining AIDS diseases of the early 1980s – is no longer listed by the CDC as an HIV disease.

Injection drug users account for 35% of all diagnosed AIDS cases. Just 10% of Americans diagnosed with AIDS cite heterosexual contact as their only risk; nearly half of them (4%) mention sexual relations with users of injection drugs, but most later admit taking drugs themselves. Over 80% of the mothers of babies diagnosed with AIDS acknowledge using injection drugs during pregnancy, which almost always results in intrauterine malnutrition. The remaining cases may be due to medical treatments given in response to HIV-positive test results.

The key to the AIDS-drug hypothesis is that only long-term consumption causes irreversible AIDS-defining diseases, whereas occasional or short-term drug use causes reversible diseases or no diseases at all. And different drugs cause different infections. The long ‘latent period’ of HIV is a euphemism for the time needed to accumulate the drug dosage sufficient to severely damage the immune system. It takes 20 years of smoking to acquire irreversible lung cancer or emphysema, and 20 years of drinking to acquire irreversible liver cirrhosis. If it takes about 10 years of nitrites, heroin, amphetamines, or cocaine to develop AIDS, then AIDS is a consequence of the drug epidemic that started in America in the late 1960s during the Vietnam War. The much more toxic drug AZT can cause AIDS within a year. The virus hypothesis fails to explain why AIDS is linked to drugs or why the risk of AIDS depends on the lifetime dosage of drugs. The fact that 85% of AIDS-causing drugs are used by males, particularly sexually active homosexuals between 25 and 49 years of age, explains why about 80% of western AIDS patients are males.

Mainstream anti-AIDS campaigns focus on safe sex and clean needles while turning a blind eye to the well-documented health effects of long-term drug use. Duesberg (1996, p. 410) writes: ‘These strategies are based on the bias of the current medical establishment that recreational drugs are basically not toxic and that all diseases of drug addicts are caused by deadly viruses and microbes.’ They send out the perilous message that ‘drugs are safe but bugs are not’. Clean, sterile needles are better than dirty ones, but it is the contents of the syringe that are the main problem. Distributing sterile needles may even encourage further drug abuse, thereby promoting AIDS, and surveys show that HIV can be more prevalent among those who do not share needles than among those who do.

A positive HIV test gives rise to psychological risk factors: belief in the inevitability of AIDS creates chronic anxiety, stress, panic, and despair, which impair health. Innumerable ‘AIDS counsellors’ urge their clients to prepare for an early death as soon as they have tested HIV-positive! Furthermore, almost everyone with a positive HIV status consumes anti-HIV drugs that are highly toxic, destroy the immune and digestive systems, and cause 5 of the 29 official AIDS-defining illnesses. These drugs become harmful and even deadly when used on a daily basis. Duesberg argues that if toxic AIDS therapies were discontinued, thousands of lives could be saved virtually overnight. But the only way to reduce psychoactive drug consumption and win the war on drugs is to publicize the fact that drugs can cause ‘AIDS’ and other diseases.

As far as sexual practices are concerned, anal sex is hazardous because rectal tissues are easily torn, allowing semen to enter the bloodstream. This triggers immune suppression, as it is a general rule that exposure to other people’s cells triggers an immune response. However, semen alone, particularly in the minute quantities that could contact blood in anal intercourse, is unlikely to have an irreversible effect on the immune system. ‘Safe sex’ (the use of condoms) has value in that it can reduce the risk of contracting STDs in general, and can also protect people from AIDS caused by anti-HIV medication (rather than the ‘HIV virus’ itself), but condoms have a high breakdown rate in anal intercourse.

It is because the introduction of foreign protein into another person’s body disturbs the immune system that blood donors are matched as closely as possible to recipients, and recipients of organ transplants have to be given immunosuppressive drugs. Yet despite the matching of blood, blood transfusions still impair the immune system. Haemophiliacs and blood transfusion recipients make up 2% of adult AIDS cases in the US. Factor VIII (a blood-clotting agent used by haemophiliacs) and blood transfusions are immune suppressive and leave patients vulnerable to infection. Due to the serious conditions for which transfusions are necessary and the harmful effects they have on the immune system, half of all HIV-negative transfusion recipients die within a year of receiving a transfusion. So it is blood itself, not the ‘HIV’ it may contain, that undermines the immune system. Those who test HIV-positive are additionally subjected to immune-suppressive drug treatment.

In stark contrast to the US and Europe, AIDS cases in the developing world are found almost exclusively among non-drug-using heterosexuals. Mainstream AIDS experts can offer no plausible reason why AIDS would spread primarily through drug-free heterosexual contact only outside the US and Europe. Maggiore writes:

A coherent explanation for AIDS cases in developing areas of the world is the well-known health risks in these countries – widespread poverty and malnutrition; lack of clean water, a regular food supply, and sanitary living conditions; limited access to medical care; endemic diseases such as tuberculosis, malaria, and parasitic infections that manifest in conditions identical to AIDS; and the practice of diagnosing AIDS based on a nonspecific set of clinical symptoms.
    Although HIV tests are not required for AIDS diagnosis in many parts of world, widespread exposure to hepatitis, tuberculosis, leprosy, malaria and other conditions are more than sufficient to account for positive results on the nonspecific HIV antibody tests. (2000, pp. 58-9)

The money spent on antiretroviral drugs would be better spent on improving sanitation and access to safe drinking water, the absence of which kills 1.4 million children a year.

The way AIDS is now officially defined, no cure is possible: after testing positive for antibodies against HIV, people living in apparent good health a dozen years later remain classified as sufferers doomed to develop AIDS. With all other viruses, the presence of antibodies is taken to mean that the person concerned is at least potentially protected. And with all other diseases, long-term survival is taken as evidence of immunity or cure. Indeed, in contrast to what is alleged about the ‘AIDS virus’, no other fatal viral disease is known to cause death in nearly all infected people; virtually every microbe causes disease in only a minority of infected individuals, since the majority are usually healthy enough to mount a rapid immune response.

Contrary to mainstream mythology, AIDS diagnosis is not in fact an immutable death sentence. Thousands of HIV-positive men, women, and children throughout the world have remained free of AIDS for up to 20 years or more by quitting toxic AIDS medications, stopping or significantly reducing their use of recreational drugs, and pursuing health-enhancing practices such as proper nutrition, adequate rest, and regular exercise. Because these people are defying the HIV=AIDS=Death paradigm, they are ignored by orthodox AIDS researchers, and rarely mentioned in mainstream literature.

Christine Maggiore was diagnosed HIV-positive in 1992 and was given five to seven years to live, even though she had no symptoms of illness. At first she became an AIDS activist, but a series of conflicting HIV test results in 1993 inspired her to question official HIV/AIDS dogma and led her to become an AIDS dissident. She avoided antiretroviral therapy and remained healthy long after she was supposed to have died. In 1995 she founded Alive & Well AIDS Alternatives to support others like her. She died of pneumonia in 2008 (and not of AIDS, as her opponents claim).

First-hand accounts by many long-term survivors or ‘nonprogressors’ can be found in her book What If Everything You Thought You Knew About AIDS Was Wrong? This is what some of them have to say:

The decision to stop taking the drugs is a difficult one in the face of pressure from doctors, the propaganda from the pharmaceutical companies and the organizations funded by them, and all the media hype. You really have to believe in yourself and take responsibility for your own life out of their hands and into your own, and just let go. ... Once you take that leap of faith you realize there is life without the drugs. (p. 123)

I have taken responsibility for my own life and have not allowed someone in a white lab coat to do it for me. Had I chosen that path they offered me, I know I would be dead. I’m a survivor because someone had the guts to tell me the truth about the HIV=AIDS=Death lie. It’s bad science in the hands of bad government. (p. 111)

In 1996 I got married – five years after I was supposed to be dead! I’m very alive and healthy and wish people would listen to me and other people like me for a change. Fear and isolation is what really kills people who test HIV positive. I fully believe that the HIV=AIDS hypothesis is a violation of our rights to life and liberty, and that ignorance is the real epidemic. (p. 95)


Sources

Henry H. Bauer, ‘Demographic characteristics of HIV: I. How did HIV spread?’, Journal of Scientific Exploration, 19:4, 2005, pp. 567-603
-------------------- ‘Demographic characteristics of HIV: II. What determines the frequency of positive HIV tests?’, Journal of Scientific Exploration, 20:1, 2006a, pp. 69-94
-------------------- ‘Demographic characteristics of HIV: III. Why does HIV discriminate by race?’, Journal of Scientific Exploration, 20:2, 2006b, pp. 255-288

Henry H. Bauer, The Origin, Persistence and Failings of HIV/AIDS Theory, Jefferson, McFarland & Company, 2007

Harvey Bialy, Oncogenes, Aneuploidy and AIDS: A scientific life and times of Peter H. Duesberg, Cuernavaca, Mexico, Institute of Biotechnology, Autonomous National University of Mexico, 2004

Rebecca Culshaw, Science Sold Out: Does HIV really cause AIDS?, Berkeley, CA, North Atlantic Books, 2007

Peter H. Duesberg, Inventing the AIDS Virus, Washington, DC, Regnery, 1996

Etienne de Harven, MD, Problems with isolating HIV, address to the European Parliament, 2003

Etienne de Harven, MD, ‘Human endogenous retroviruses and AIDS research: confusion, consensus, or science?’, Journal of American Physicians and Surgeons, v. 15, 2010, pp. 69-74

Peter Duesberg, Claus Koehnlein and David Rasnick, ‘The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy and malnutrition’, Journal of Bioscience, v. 28, 2003, pp. 383-412, www.virusmyth.net/aids/data/pddrchemical.pdf

Celia Farber, ‘Out of control: AIDS and the corruption of medical science’, Harper’s Magazine, March 2006, www.harpers.org/OutOfControl.html

Neville Hodgkinson, ‘AIDS: scientific or viral catastrophe?’, Journal of Scientific Exploration, 17:1, 2003, pp. 87-120

Neville Hodgkinson, ‘Review essay on AIDS, Cancer and Arthritis: A new perspective by Phyllis Evelyn Pease’, Journal of Scientific Exploration, 23:3, 2007, pp. 595-605.

James P. Hogan, Kicking the Sacred Cow: Questioning the unquestionable and thinking the impermissible, Riverdale, NY, Baen, 2004

Robert Johnston, Matthew Irwin and David Crowe, ‘A rebuttal to the “Durban Declaration” published in Nature on July 6 2000’, 2001, www.healtoronto.com/durban

Christine Maggiore, What If Everything You Thought You Knew About AIDS Was Wrong?, Studio City, CA, American Foundation for AIDS Alternatives, 4th ed., 2000

Kary Mullis, Dancing Naked in the Mind Field, New York, Vintage, 1998

Eleni Papadopulos-Eleopulos, An analysis of evidence for the existence of HIV, evidence to the Supreme Court, Adelaide, 2006

Eleni Papadopulos-Eleopulos et al., The Perth Group revisits the existence of HIV, International Conference on HIV/AIDS, Ekaterinburg, Russia, 2008

Phyllis Evelyn Pease, AIDS, Cancer and Arthritis: A new perspective, Birmingham, Phyllis Evelyn Pease, 2005

Paul Philpott, ‘The isolation question’, Reappraising AIDS, June, July, August 1997, www.virusmyth.net/aids/data/ppisolation.htm

Janine Roberts, Fear of the Invisible: An investigation of viruses and vaccines, HIV and AIDS, Bristol, Impact Investigative Media Productions, 2nd ed., 2009

Websites:
theperthgroup.com
rethinkingaids.com
hivskeptic.wordpress.com (Henry Bauer)
Alberta Reappraising AIDS Society
Treatment Information Group
aliveandwell.org
healtoronto.com
duesberg.com
virusmyth.com
reviewingaids.com


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