Learning Lessons from an HIV Cure

[hanshan]

...

this is interesting & seems to have been overlooked


Learning Lessons from an HIV Cure

By Jason Bardi on June 16, 2011

For doctors confronting the AIDS epidemic, past ambitions always boiled down to two main goals: prevention, or finding ways to protect people not yet exposed to HIV, through vaccines, safe sex education or other means; and treatment, or discovering effective drugs and providing them to people with HIV/AIDS, helping them live longer.


Jay Levy, MD, professor of medicine and co-discoverer of HIV, has renewed hope for finding a cure for HIV/AIDS.
Now, thanks primarily to one test case, many doctors are beginning to think about a new possibility: finding a cure.

This case involved an American living in Germany, Timothy Brown, known popularly as the “Berlin patient,” whose infection appears to have been eradicated after two carefully planned bone marrow stem cell transplants in 2007 and 2008.

“There’s no evidence of HIV in my body after three years, even though dozens of tests have been done to look for it,” said Brown, now a San Francisco Bay area resident and a patient at UCSF and San Francisco General Hospital (SFGH). To this day, Brown is believed to be the only person ever cured of HIV.

While experts agree that the procedure used to cure Brown is not generally applicable to the tens of millions living with HIV worldwide, his story has changed the thinking of many scientists at the forefront of HIV/AIDS research.

Several UCSF-affiliated researchers interviewed for this story pointed to Brown’s experience as a seminal shift, giving them renewed hope for the possibility of developing a cure.

A Surprising New Hope
Halfway down a long corridor at UCSF Medical Center, Jay Levy, MD, a professor in UCSF’s Department of Medicine, and his colleagues in the Laboratory for Tumor and AIDS Virus Research, co-discovered HIV as the cause for AIDS in 1983.

Twenty-five years later, the news of the successful cure came as a surprise even to him. “I felt that a cure was not possible,” said Levy. “But the Berlin patient made me reevaluate that conclusion.”

30 Years of AIDS

30 Years of AIDS homepage
Learning Lessons from an HIV Cure
SFGH Grand Rounds Explores Disease That First Defined AIDS
UCSF Marks Three Decades of AIDS
SFGH's Ward 86: Pioneering HIV/AIDS Care for 30 Years
Treatment is Key to Prevention of HIV/AIDS, Doctors Say
AIDS Virus May Accelerate Aging, Scientists Say
First AIDS Research Conference in Uganda Focuses on Building Collaborations
Thirty Years of AIDS: A Timeline of the Epidemic
UCSF and AIDS: Facts and Firsts
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Levy was not the only one inspired by Brown’s story. According to UCSF immunologist Mike McCune, MD, PhD, the case has galvanized many researchers to think about how to extend, improve and repeat the achievement.

Even researchers already working on cure research have been influenced. Brown’s case is a vindication of their work – even if their approaches are fundamentally different.

For instance, scientists at the UCSF-affiliated Gladstone Institute of Virology and Immunology (GIVI) have begun to consider something short of a complete cure: the wholesale eradication of the virus from all tissues in the body. That would be a “functional cure,” where the virus is knocked down enough and the immune system enhanced to the point where the virus stays permanently in check.

“A functional cure might be a more reasonable goal,” said Warner C. Greene, MD, PhD, a UCSF professor and director of the GIVI.

“If you were to do this successfully, you might be able to remove therapy altogether,” said Eric Verdin, MD, a senior investigator at GIVI and a professor of medicine at UCSF.

At the same time, Greene warned, any eventual cures or functional cures could only realize the dream of ending the AIDS epidemic if they worked in the places hardest hit by the virus – regions like sub-Saharan Africa, home to about two-thirds of all people living with HIV/AIDS.

“We have to be constructing a therapy that is usable throughout the world,” said Greene, who also is the Nick and Sue Hellmann Distinguished Professor of Translational Medicine.

Failed Cures of the Past
For Steven Deeks, MD, a professor of medicine at UCSF and a clinician in the Positive Health Program at the UCSF-affiliated SFGH, the Berlin patient case raised as many questions as it answered.

What subtle biological processes were in play, and more importantly, how does this one case illuminate an expanded approach to curing HIV? Deeks and his team have now enrolled Brown in a series of ongoing UCSF-based studies and are overseeing a group of collaborators in the hope of addressing these and other questions.

In the last three years, Deeks has pondered these questions again and again. It was not the first time doctors had dreamed of curing someone with HIV – just the first time it actually worked.

Long-shot ambitions to cure HIV first ballooned into great hope in the mid-90s, as highly-active antiretroviral therapy (HAART) emerged as the standard care in treating AIDS. HAART is an umbrella term for numerous combinations of the two dozen or so FDA-approved antiretroviral drugs, which block HIV at various stages of the infection’s life cycle.

For Deeks, who started treating patients at SFGH in 1993, the impact of HAART on the lives of people with HIV is hard to overstate. He calls it one of the great milestones in HIV/AIDS – perhaps in all of medical history.

“It’s a different disease today,” Deeks said, “a chronic, manageable disease – there’s no comparison.”

According to Greene, almost any patient now can be treated to where he or she has no detectable levels of virus, and some of the newest drugs are less toxic than those used in the early days of treatment.

At the same time, HAART also provides a valuable lesson in failed cures.

When the earliest clinical trials using combinations of drugs appeared in the mid-1990s, they showed that HAART could drive down the virus to undetectable levels in the bloodstream. This led many scientists to wonder if the drugs might be able to actually cure people of the virus, allowing patients to stop taking their drugs.

After years of carefully designed trials, however, not a single person was ever cured of HIV. Moreover, one of the largest-ever clinical trials of HIV/AIDS patients showed that people who take the drugs continuously fare far better than those who go on and off their treatment.

Doctors now know that HIV can persist dormant in the body. When people stop taking the drugs, the virus rebounds – often in just a few weeks. And in the last 15 years, as the medical community came to realize that drugs alone would never be able to get rid of this hidden virus, the dreams of curing HIV through HAART quickly faded.

Then along came Brown. He had been on HAART since the 1990s, when he first was diagnosed with HIV. But he stopped the day of his first transplant operation in 2007 and has never taken the drugs again.

How the Berlin Cure Worked
The opportunity to cure Brown emerged when he was diagnosed with leukemia in 2006. A transplant of stem cells from the bone marrow of a donor was needed, giving his doctors the idea of choosing a donor resistant to HIV.

In operations like these, patients undergo chemotherapy and radiation to kill off the existing cells in their own bone marrow. Then they receive an infusion of new stem cells taken from a healthy donor who is “compatible” with the patient. Essentially, the transplant replaces the body’s source of T cells, the primary targets of HIV.

In Brown’s case, the donor’s cells were resistant to HIV thanks to a rare genetic mutation that left the donor with an altered form of a protein called CCR5 – the main co-receptor HIV uses to enter cells. This mutation causes the CCR5 protein to go missing from the surface of T cells, blocking HIV’s access.

A team led by Gero Hutter in Berlin in essence successfully transplanted into Brown an immune system resistant to HIV infection. While his leukemia reappeared the following year and he had to undergo a second stem cell transplant, the procedure appears to have wiped out all the HIV-infected cells in his body.

If asked five years ago, Levy said, many scientists would have been skeptical about the procedure, assuming HIV would simply shift to a second receptor – CXCR4. Why this didn’t happen is just one of the unexplained riddles that intrigues investigators.

A similar 1995 experiment at UCSF and SFGH also had fallen short of a cure. Jeff Getty, a Bay Area resident and AIDS activist, was given bone marrow-derived stem cells from a baboon, a species naturally resistant to HIV. While Getty may have experienced some transient benefit from the transplant, the baboon cells did not survive, and he was never cured of HIV. Getty died in 2006 due to oral cancer and complications of AIDS.

Moving Forward with Other Approaches
However much more promising Brown’s story may be, UCSF experts interviewed for this article all agreed the procedure that cured him could not easily be used on other patients.

The operation carries a significant risk of death, and it is prohibitively expensive, putting it out of reach for most people with HIV. But perhaps the greatest barrier of all would be locating compatible donors for all of those people. Finding a donor whose stem cells are matched to the recipient is difficult in any case. Finding one who also has the CCR5 mutation, only present in a small percentage people of northern European descent, would prove impossible in most cases.

A different approach, which Levy and his UCSF colleagues are pursuing, seeks to circumvent the problem of finding matched donors by using stem cells from the patient with HIV. The CCR5 receptor would be removed from the stem cells before they are infused back into the patient.

The technique has shown promise in mouse studies and in early human clinical trials. Levy, with UCSF professor Y. W. Kan and others, is working to improve the basic techniques for manipulating the stem cells and to find the funding needed to advance the studies toward the clinic.

Some, including Greene, are less enthusiastic about the stem cell approach because it would require immune-suppressing therapy and other procedures that must be performed in a sophisticated clinical setting with substantial laboratory support. While such resources are readily available in San Francisco and many other urban centers around the United States and Europe, they may be inaccessible in those parts of the world where the majority of people with HIV/AIDS live.

To really turn the tide of the pandemic, a cure would have to be accessible to millions, Greene said. Ideally, it would have to be non-toxic, available in a pill form, cheap to manufacture and not require refrigeration.

Toward that goal, Greene, Verdin and their colleagues at GIVI and UCSF are pursuing an approach they refer to as “shock and awe.”

The Shock and Awe Approach
Earlier attempts to cure HIV infections using HAART didn’t work because, while the drugs prevent the virus from replicating, they don’t kill the “latent” virus, which lies dormant and can persist for years in a small number of cells.

The idea of shock and awe is to use drugs to activate the virus, flushing it out in the open. Once the HIV is reactivated, the HAART drugs and the immune system could take care of the rest.

“The virus will come up but will have no place to go,” Verdin said.

While this concept has been demonstrated in cell culture, using latently infected cells from patients, many scientific issues remain to be resolved before shock and awe can be tested in people.

“We need to understand all of the places and types of cells where the virus can hide in the body, what the biological processes are that maintain HIV in its slumbering state and whether it is possible to rouse the virus without also activating its cellular host,” Greene said.

Other unanswered questions include what role inflammation plays in the disease. The virus induces a widespread inflammatory response that feeds forward during an infection. This seems to play a role in the disease progression and damages tissues.

McCune and Deeks are among those looking at the possibility that blocking inflammation may have played role in the Berlin Patient’s cure. Brown, like anyone undergoing a bone marrow transplant procedure, would have been given lots of anti-inflammatory drugs during the procedure. “That may have been important,” Deeks said.

Deeks and his colleagues are now looking at the effect of anti-inflammatory drugs on the persistence of the virus. They want to know whether controlling inflammation might help better control the infection.

Will Dreams of a Cure be Realized?
For his part, Brown is not satisfied with the mere fact that his HIV has been cured. He wants to see others to be cured as well and is exploring the possibility of starting a nonprofit foundation to raise awareness of and funding for HIV research into a cure.

“More money should be spent for cure research,” he said. “I’m just hoping that what I’ve gone through will be a catalyst for others and that more people will be cured of HIV.”

How likely is it that we will get there eventually?

“I wouldn’t be spending time on this if I didn’t think we could succeed,” McCune said. But, he added, getting there is going to require insights from fundamental laboratory research and from clinical studies with diverse populations of patients of different ages and gender and from different regions. McCune compares the effort to that behind a monumental shift in computer use as businesses and institutions switched from mainframes to desktop and laptop computers. This massive change was realized only with time, patience – and tremendous innovation.

Still, if the history of the AIDS epidemic proves anything, McCune added, it is that great advances are possible with a clear vision, dedication and hard work.

It’s not going to happen tomorrow, next week, or next year, added Greene, but every journey starts with a single step. Whether or not Brown’s cure turns out to be that first step, research in the field is off and marching – and gaining its stride.

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http://www.ucsf.edu/news/2011/06/10058/learning-lessons-hiv-cure

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[identity]

Stumbled across the following while looking up info on vitamin D. One is left with the impression that the best "cure" for those with a positive diagnosis is to maintain a healthy lifestyle and to simply refuse the antiretrovirals.

New film from award-winning team shows US and UK censorship alive and well
2017-03-16

The makers of the multi-award winning British HIV/AIDS documentary film Positive Hell, which was screened to acclaim last night at New York's 7th annual Queens World Film Festival (QWFF), have just released a new short film on YouTube, Censored. The first in a trilogy titled Positively wrong, Censored tells how in 2016 Positive Hell was suddenly barred from several confirmed screenings in London and New York after hefty and controversial lobbying. Two of the bans were from film festivals for which Positive Hell had already been selected and programmed.

The films' writer and narrator, Joan Shenton, said: "2016 for us was a year of censorship and removal of our right to free speech. On three separate occasions, at three unrelated events, Positive Hell was selected and programmed, then, at the last minute, banned after the organisers were lobbied and threatened with such activities as boycotts and mass demonstrations.

"Two organisers admitted the threats came from AIDS charities; the other one said the lobbyists described themselves as an "enraged community" but we believe they were also AIDS charities with vested interests in keeping the film suppressed. Why? Because HIV positive people interviewed in the film had the temerity to question the antiretroviral treatments offered to them and to ask whether the giant pharmaceutical companies who supply such treatments are always acting in the best interests of those diagnosed HIV positive."

"It seems to us that, behind closed doors, things were said about Positive Hell which are not true, and empty threats were made against it which were never going to materialise because there was no real-world objection to our film. It was made up by the lobbyists. This was all about fear being used to provoke censorship to protect corporate interests. They didn't like what we were saying.

"The point is that both the HIV test and the science behind an HIV positive diagnosis are flawed. An HIV positive diagnosis can be caused by many factors, from recreational drugs to pregnancy, yet can lead to a lifetime of fear and, effectively, drug dependency, not to mention serious side-effects for some. It is also at the centre of a multi-billion dollar global business.

"More and more HIV positives are questioning whether the big business approach is the right one for HIV/AIDS. Our film Positive Hell meets five of them and hears their personal side of the debate, a debate that is vital for the LGBTQ+ communities who are so affected by HIV/AIDS."

Positive Hell is a 30-minute documentary that follows the lives of five people, once diagnosed HIV positive, who refused a lifetime of antiretrovirals and lived on in defiance of standard medical prognoses. Both films are written and narrated by Joan Shenton and directed by Andi Reiss.

In the 1980s, Manoel, Pablo, Raquel, Jesus and Manuel, the last a practising MD, each had to confront difficult questions following their diagnoses as HIV positive and the bleak futures presented by their doctors. Though very different people, they had one thing in common: they all chose for varying reasons not to take the HIV treatments that were offered as, seemingly, their only hope. Almost three decades later, all five were living entirely normally, without the treatments, and Raquel had had children who themselves are now healthy adults and HIV negative.

Their stories explore burning questions which concern LGBTQ+ communities and also populations in the developing world with high rates of HIV/AIDS diagnoses: just how reliable are the regular tests and diagnoses for HIV and how essential is it for everyone found HIV positive to submit unquestioningly to a possible lifetime regime of antiretroviral drugs?

"It is all a business that is perfectly oiled and set up at world level."
—Quote from one of the interviewees in the film.

http://rethinkingaids.com/

[American Dream]

One is left with the impression that the best "cure" for those with a positive diagnosis is to maintain a healthy lifestyle and to simply refuse the antiretrovirals.

Sorry, I think that's extremely fucked up. Most of the people I know in and around the HIV positive community feel that retrovirals have changed the game and allow folks to live a relatively long and healthy life.

It doesn't seem right to be giving people health advice that could you know, kill them.

[Heaven Swan]

One is left with the impression that the best "cure" for those with a positive diagnosis is to maintain a healthy lifestyle and to simply refuse the antiretrovirals.

Sorry, I think that's extremely fucked up. Most of the people I know in and around the HIV positive community feel that retrovirals have changed the game and allow folks to live a relatively long and healthy life.

It doesn't seem right to be giving people health advice that could you know, kill them.

I don't see Identity's post as medical advice. Retroviral use is a personal choice and seems to work for many. But not all. Like my dear friend who died at age 45. The medication didn't work so well for him...although I know many others who it seems to be helping.

I think attempting to shut down discussion on the basis of giving deadly heath advice, on a forum that exists to question accepted narratives is "extremely fucked up."

[identity]

"I think attempting to shut down discussion on the basis of giving deadly heath advice, on a forum that exists to question accepted narratives is "extremely fucked up."

Well, Heaven Swan, we both might want to reflect for a moment upon Project Willow's words re: "what this board actually is rather than what some less agenda driven posters may perceive it is or could be."

[identity]

One is left with the impression that the best "cure" for those with a positive diagnosis is to maintain a healthy lifestyle and to simply refuse the antiretrovirals.

Sorry, I think that's extremely fucked up. Most of the people I know in and around the HIV positive community feel that retrovirals have changed the game and allow folks to live a relatively long and healthy life.

It doesn't seem right to be giving people health advice that could you know, kill them.

It doesn't seem like American Nightmare even watched the short docu. While I was not offering medical advice, the medical doctor interviewed in the film who has lived for over two decades after receiving an HIV positive diagnosis, without submitting to a toxic antiretroviral regime, perhaps was!

Anyway, it is no doubt felicitous that American Nightmare posted that nonsense, as it encourages me now to post a flood (in true American Nightmare-style) of AIDS/HIV mythbusting copypasta in this thread.

Oh, and since we still have the Ignore-function available, I'm now putting American Nightmare on ignore.

[identity]

FLOOD BEGINS!

HIV+ : alive and well without drugs

People with HIV and no symptoms have studied the flaws in the HIV=AIDS theory and stopped taking their medications—without any harmful effects. Health authorities recommend drug therapy from the first sign of HIV diagnosis, despite the unreliability of testing methods.

From NEXUS Magazine, vol. 23, no. 4, June–July 2016. HIV Positive without Treatment…and Healthy! by Pryska Ducoeurjoly, translated from french by Pol Dubart.

About the Author

Pryska Ducoeurjoly is an independent French journalist who writes about environmental and health subjects. She is the author of The Toxic Society (La Société Toxique, 2010, now freely available on her blog), where she explores the mass conditioning by media, food and drugs. She can be emailed at p.ducoeurjoly[a]gmail.com.

Why must people submit themselves to triple, highly active antiretroviral therapy (HAART) as soon as they are diagnosed HIV positive? This question goes against official recommendations but is at the core of the life experiences of many HIV positives who, after having enquired on the web and carefully considered the information they found, decided to abandon the « medicalisation of fear » and stop their treatment. And, surprisingly, their health has not deteriorated!

This little-studied phenomenon is qualified as extraordinarily rare by « HIV specialists ». Could those experts have got it wrong, pushing patients into unjustified and expensive medical care? This is what this investigation, dedicated to the diagnosis and medical follow-up of HIV positivity, reveals.

According to a 2014 UNAIDS report, 35 million people worldwide are estimated to be infected with HIV (human immunodeficiency virus). These figures are comparable to cancer prevalence. Every year, nearly US$20 billion is spent on research. The report also noted that in 2013 there were 1.5 million deaths related to AIDS (acquired immune deficiency syndrome)i.

Apparently, as the media remind us every year, it is a global disaster. However, such figures should be strongly questioned—and have been ever since epidemiologist James Chin, MD, former director of the World Health Organization (WHO) AIDS program and author of The AIDS Pandemic: The Collision of Epidemiology with Political Correctnessii, set the cat among the pigeons. In his book, Dr Chin demonstrates that the statistics concerning the prevalence of HIV infection have been exaggerated in order to maintain the fear of an explosion of the epidemic into the general population—an explosion which has been predicted often but never observed. However, Chin, who is by no means a dissident who would question the HIV=AIDS theory, wrote (p. vi): « HIV prevalence is low in most populations throughout the world and can be expected to remain low, not because of effective HIV prevention programs but simply because HIV infection rates can rise only to the level(s) permitted by the prevailing patterns and prevalence of HIV risk behaviors and the prevalence of facilitating and protective factors. The vast majority of the world’s populations do not have sufficient HIV risk behaviors to sustain significant epidemic HIV transmission ».iii

The HIV Testing Hoax

Officially, the USA now has around 1.2 million people living with HIV, with one in seven of these unaware that they have HIViv. In Australia, an estimated 27,150 people live with HIV. In 2014, 1,081 people were diagnosed with HIVv. In France each year, more than 6,000 people discover their HIV positivity by means of the ELISA and western blot tests, which is confirmed by their count of CD4 cells (T-cells) or viral load (the amount of virus in the blood).vi

With regard to the arguments brought by a large number of scientists (see Afterword, « What if everything you’ve learned about AIDS is wrong? »), the published counts of HIV-positive people should be taken with a grain of salt because screening tests are not reliable. Furthermore, many publications exist showing 70 conditions that can generate a false positivevii.

« This HIV test story is a huge hoax! » rages Williamviii, a 53-year-old HIV-positive Frenchman who was diagnosed in August 2014. After 11 months of triple therapy, this father finally stopped his treatment. He took this decision in November 2015 after having reviewed the medical literature.

Within William, the announcement of HIV positivity started a chain reaction which led him to discover « the incredible truth ». After the « enormous shock » of the diagnosis, he experienced sheer incomprehension: « I’ve always had a healthy sexual life. I am not on drugs. I do not smoke. I do sports; I have an athlete’s body. I was married for 20 years. I lived with a girlfriend for seven years. So when I did the test at the time of becoming involved in a new relationship, my first reaction was, ‘No, this can’t be possible!' »

After the incomprehension came the acceptance: « I underwent a lot of pressure as it is not possible to resist these doctors who kept telling me, ‘If you do not take the therapy for yourself, take it for your children’. Announcing my HIV status to my children was in itself a traumatising experience, and it took me a good month before resigning myself to taking the medicines. »

Not long after, William would follow his initial intuition: « Taking advantage of a professional break, I consumed considerable amounts of information until I realised that, finally, I was facing the biggest scam of the century. Then I passed the stage of questioning. The ‘viral load’ is nothing but absolute bullshit! And I am certainly not going to be a guinea pig for the AIDS industry. Rather than engage in arm-wrestling with the doctors, I am going to let them keep believing in their theory. What really matters to me is how I feel. And I feel great! »

The official line is that without triple-therapy « AIDS cocktails »—consisting of three drugs from at least two different classes—one cannot survive HIV infection. But in reality, William said that he is absolutely sure he will remain healthy, especially because of his very healthy lifestyle. He denounces a dehumanised medicine which defines the health status of so-called HIV-positive people solely on the basis of two controversial laboratory test results without any clinical observations.

The Viral Load: An Unsuitable Marker

Officially, the viral load describes the number of virus particles in the blood and is a marker of disease progression. « False! », argue the dissident scientists. The technique of PCR (polymerase chain reaction), used to identify and quantify HIV, the so-called « AIDS virus », is not only denounced by its very inventor, Dr Kary Mullis, who shared the 1993 Nobel Prize in Chemistry for this discovery, but also by a large number of specialists such as Professor Etienne de Harven, a pioneer of electron microscopy. Nevertheless, this test continues to be used with absolute confidence.

As Matt Irwin, MD, explains: « When [the viral load tests] are done on the serum of people considered HIV-negative, 3% to 10% of them commonly have positive viral loads, and the highest reported rate of false positive results is a remarkable 60% (HIV surrogate marker coll. group 2000). Although most cases reported have false viral loads of 10,000 or less, there have been reports of false positive viral loads as high as 100,000 copies per milliliter. In the United States, where the prevalence of HIV is about 1 in 250 people (0.4%), a false positive rate of only 2% would still mean that random screening of the population would result in 5 false positives for every true positive, and a false positive rate of 10% would result in 25 false positives for every true positive. The most likely explanation for this high false positive rate is that HIV-RNA assays commonly react with non-HIV RNA, such as that produced by normal human cells and other microbes. »ix

According to Roberto Giraldo, MD, an infectious diseases specialist as well as a board member of The Group for the Scientific Reappraisal of the HIV/AIDS Hypothesis (Rethinking AIDSx): « …Since the viral load results are given in copies per ml of plasma…AIDS researchers, health care professionals, and lay people may think that they represent copies or counts of the virus itself… However, the viral load test only makes copies of fragments of nucleic acids. It does not count HIV itself. A positive viral load test cannot be regarded as signifying the presence of the whole HIV genome, and therefore the test cannot be used to measure virus. »xi

Bertrand, a 34-year-old HIV-positive Frenchman who was diagnosed seven years ago, said: « When the doctor tells you that your viral load is measured in hundreds of thousands of copies, even in millions for some, that really freaks you out! » Although he already had a viral load of around 250,000 copies (against a maximum of 2,000 to avoid the combination therapy), he never wanted to take any treatment. Surprisingly, in spite of the unfavourable forecasts of the doctors, his viral load spontaneously fell to 11,500; in fact, it has never stabilised, oscillating randomly around 40,000 copies.

William, mentioned earlier, added to his testimony: « In a general way, I avoid following carefully the quarterly measurements as it remains a source of chronic stress that could undermine my immunity. » Doctors and researchers indeed underestimate the deleterious impact or « nocebo » effect of the announcement of poor results, which is capable of eliciting an immune drop (depression, stress) in some HIV-positive persons who are anxious or emotionally vulnerable to HIV medical discourse. William noted: « We have to be mentally very strong to resist the brainwashing and remain anchored in our convictions! »

The CD4/T-Cell Count Marker

The HIV=AIDS theory says that having a CD4 or T-cell count below 350 is also a sign of viral activity because this is the type of immune cell that HIV attacks and destroys. A count of 350 would then justify the initiation of treatment. A CD4 rate of less than 200 is considered to indicate an advanced stage of infection, and in the United States it is enough for a diagnosis of full-blown AIDS despite the absence of opportunistic infections. But here again, for HIV=AIDS dissidents, there is no scientific evidence proving that HIV preferentially destroys T-cells or has any toxic effect on these immune cells.

The counting method itself poses numerous reliability problems. Flow cytometry techniques (to determine the counts of every type of immune cell) require a sophisticated level of technical skill which is difficult to reproduce from one laboratory to another. Official notifications on Aidsmap.com concede that it’s best to monitor the trends in T-cell count over time. If possible, it’s also advisable for the T-cell count to be measured in the same clinic and at approximately the same time of day on each visit. It’s suggested that people suffering from an infection, such as flu or herpes, should delay the testing until they feel better.xii

Bertrand, mentioned above, who has been without treatment for seven years, noted: « Over the tests, I was able to notice significant variation in my count, without an apparent link to my health. It had already gone down to 220 CD4, and then it rose up naturally. On average, it would yo-yo around 350, without ever exceeding 500. » This example undermines the insidious argument of the health authorities which ensure that only treatment can bring CD4 counts back up or prevent a runaway viral load.

Pressure on Parents

Speaking of her experience, Sabine said: « When in 2004 I was informed of my HIV positivity during a routine exam, I saw myself dying. At that time, I knew nothing about the HIV=AIDS controversy. By educating myself on the Internet, I have gradually become convinced of the nonexistence of the virus. I have never taken any ARV [antiretroviral] treatment and my health has always remained good. »

Sabine’s story might have ended there, especially in Switzerland, a country of complementary medicines, except that a few years later Sabine gave birth at home to her second child, in agreement with her new companion who is aware of her HIV positivity. As happens to many children, her baby, then three months old, had to be admitted to hospital because of worrying symptoms. On this occasion, the doctors found Sabine’s medical record and discovered her HIV positivity. The child was immediately placed under triple therapy solely on the basis of the CD4 cell count and the viral load (without ELISA or western blot tests, which have been found to be unreliable in infants). This was the beginning of a two-month stay in intensive care at the hospital, where the child underwent a battery of tests resulting in all kinds of interventions:

« Following a scan, a small lump appeared on a lung, » said Sabine. « My baby underwent a bronchial lavage under general anaesthesia, following which they put a central line in his breast in order to administer all the medication. After a second general anaesthesia, some water was found on the lungs, which required intubation. After two months, they let us take him home with the obligation to give him the triple therapy. Quickly we decreased, then stopped the treatment. Our son got better and his CD4 and viral load tests were pretty good for the medical profession—until the day when they measured the dose of medication in the blood and found no trace of the treatment! Finally, I was reported by the hospital to the Child Protection Court. A few months later, I was sentenced by the court and my parental rights were restricted. From then on, we were controlled by a doctor. »

In the denunciation letter to the judge, the hospital wrote: « The child has been without any effective treatment for several months already. Right now, he is clinically healthy. Unfortunately, his blood tests are very disturbing, showing that the virus is very active and that the child has a very real risk of complications (progression to AIDS, or even death) that could occur soon. »

For six months, nurses came morning and evening to check that Sabine’s son was receiving treatment. Since the middle of 2014, the child has thus been under triple therapy. Meanwhile, Sabine was working on letting go. She turned to quantum medicine to mitigate the trauma: « I am hopeful because his treatment will be augmented by alternative practitioners. But his chemical treatment will last until my son reaches the age of majority, as long as his T-cell counts and viral load are not in the desirable range. The irony is that I am now waiting for results of an analysis that I don’t even believe in. »

In the boy’s medical record, which we were able to consult, the smugness of the doctors oozes from between the lines: « Parents whose interaction with their baby is extremely well adjusted and empathic, while expressing no sense of responsibility, or feelings of sadness, anxiety or anger with regard to the situation. The mother rationalises using a very solid and well-built model of thought. A very paradoxical situation, in connection with the parental functioning (denial of the consequences of the disease and risks of transmission). »

Yet the parents’ attitude is as rational as the scientific literature which questions these treatments. Sabine’s situation reveals the omnipotence of the current dogma which can quickly dish out punishment when its prescriptions are not respected.

But it is not just AIDS treatment which can deprive parents of their freedom of choice regarding health: this can also apply to vaccinations and cancer treatment, and maybe soon to autism and hyperactivity. Families had better watch out!

Escape from Abusive Treatments

The pressure is not less on adults. Here is the story of Etienne, who endured a heavy medical protocol continuously from 1993 (AZT, or azidothymidine, at first, then double therapy and then triple therapy) until 2013—in total, 20 years of antiretroviral therapy from which he only escaped thanks to the Internet!

« During all these years, I behaved like a good little soldier, » Etienne said. « I still do not know how I could bear all this medicine, especially since my fear of death encouraged me to use drugs. With my face of a zombie, I could not hide that I was HIV positive—until the day I came across a Facebook post. I went to the Rethinking AIDS association website. I read many books, in particular Peter Duesberg’s. There was nothing more wonderful to read! The hoax appeared to me so obvious that I did not doubt after five minutes. When I saw my doctor again and told him that I had stopped the treatment, he was speechless. Now that I don’t want him to measure my CD4 counts and viral load any more, I tell him, ‘I would rather you have a look at my level of vitamin D’! »

Another Look at HIV Controllers

Etienne is a survivor of both HIV and triple therapy— »proof » of the efficacy of triple therapy, his doctor will probably argue. But is it really proof, since triple therapy has never been tested against placebos (see below)? Is Etienne not an « HIV controller »xiii, that is to say a patient who naturally controls the progress of HIV? Officially, the answer is no! This is because Etienne does not fit the very narrow definition of this population, estimated at only 0.5% to 1.0% of all HIV-positive persons.

Indeed, to be considered an HIV controller, it is necessary to: (1) never have received any treatment (which is unusual in the Western world); and (2) have a viral load at baseline below 2,000 copies and eventually reduced to below 400 copies. These are very selective criteria. This is also why Bertrand cannot be considered an HIV controller in spite of a total absence of treatment for seven years: his laboratory results (profits) are not normal! And we cannot speak of Sabine as an HIV controller, despite her 10 years without treatment, because she never wanted her measurements to be taken. As for William, it has been only one year since he stopped taking medicine and his initial measurements disqualified him.

In reality, there are no reliable statistics on the number of healthy HIV-positive persons not taking triple therapy. We are therefore entitled to wonder if the « natural control of HIV » is not within the reach of the majority of HIV-positive people. On our part, it took only a day of research on social networks to find and interview four asymptomatic HIV-positive persons not taking treatment. But the medical profession simply cannot believe that this phenomenon exists on a large scale. As one of the specialists, Professor Olivier Lambotte, studying HIV controllers at ANRS (the French AIDS research agency) pointed out: « Those who have not progressed to AIDS, after stopping the treatment, are fewer than twenty. »xiv (Emphasis added.)

This specialist is referring to the ANRS VISCONTI (viro-immunological sustained control after treatment interruption) study which identified 14 patients in France who had a remission that, in certain cases, lasted 13 years after interruption of the antiretroviral treatments. But this study was only interested in patients who had started treatment within three months after the primary infection, which led his coordinator, Professor Christine Rouzioux, to claim: « Early treatment has probably limited the expansion of the viral reservoirs, and has protected their immune responses. This…allowed control of the infection after stopping treatment. »xv Translation: it is necessary, as soon as possible, to put all HIV-positive people under treatment! Not doing so would therefore be an infringement of medical ethics.

In fact, there are strong indications that the majority of patients, especially in populations that are not at risk, are improperly started on treatment.

This hypothesis is supported by David Crowe, President of Rethinking AIDS: « This is completely circular logic. Because they assumed that everyone was at risk, when they found out that this wasn’t true, and that everyone was on toxic drugs, they then said, ‘Well, maybe not everyone, but almost everyone’. Nobody knows how many HIV+ people would remain symptom free without drugs. In addition, it is estimated that there are millions of people worldwide who are HIV+ and don’t know it. Presumably many of these people have not sought medical assistance because they are symptom free. Furthermore, the average time from infection to ‘AIDS’ is estimated to be 10 years. It is unlikely that many HIV+ people who trust their doctors will be allowed to go medication free for 10 years, therefore there is no way of telling whether they are normal progressors or long-term non-progressors. »xvi

No Double-Blind Trials for Triple Therapy

Contrary to the requirements of good science, AIDS therapies enjoy the same exemption as vaccines.xvii Everyone is so sure of their benefits that antiretrovirals no longer have to comply with the basic rules of clinical trials for placing new drugs on the market.

As David Crowe said: « Only the early studies of AZT even claimed to use a placebo. Not only did those find very little benefit after any reasonable length of time, but it was seen that those taking AZT were much more likely to need blood transfusions. And the trials were corrupted, as evidenced by several articles by John Lauritsen, collected in his free online book Poison by Prescription.xviii The trials of cART, combination therapy, have two fundamental flaws. First, they can only show that cART is less toxic than the highly toxic AZT. Although many combinations used to include AZT, it was at a much lower dose (200 or 300 mg/day versus up to 1500 mg in the early trials of AZT). Secondly, they do not monitor for improved health, but just for improved CD4 counts and so-called viral load. »xix Thus, nothing is really proved!

Worse, triple therapy only changes the type of illnesses. We shall simply quote a 2005 study concerning patients under triple therapy arriving at hospital: « As the HAART era progressed, the holes in the HAART armor became more apparent. Although patients were not having as many opportunistic infections, there was still a relatively high incidence of certain HIV associated malignancies…deaths related to end stage liver disease [almost certainly caused by the drugs] were more common than deaths from opportunistic infections… Hospitalizations for lactic acidosis, reconstitution syndromes [which are opportunistic infections occurring shortly after starting AIDS drugs] and late stage complications related to HAART were becoming more apparent. Some authors also noted an increase in mortality and hospital admission rate as the HAART era progressed. »xx

Ignored Alternative Treatments

All around the world, there are alternative doctors who specialise in the field of AIDS and are especially active within organisations such as Alive and Wellxxi and Healxxii or are on a list published online on the Rethinking AIDS website. This is proof that all options for possible treatments are not given to patients. On the contrary, patients are intentionally diverted from them by coercion or, if necessary, by judicial power.

« These [alternative] treatments should be covered by health insurance or supported by national systems of health » is a statement written into the Declaration of Pont-du-Gard at a conference of dissidents in France in June 2012.xxiii This a great idea, but dreaming is useless in the current context where the financial stakes are so huge, especially as this is about treatments for life.

Changing approaches to immune deficiency treatment would dramatically reduce income for the industry. There would be indirect and difficult-to-estimate financial losses resulting from lower sales of drugs for opportunistic infections associated with either the disease or the side effects of triple therapy.

Treatment Costs to Make a Person Go Pale!

Triple therapy costs between 1,000 and 1,500 euros per month, the equivalent of a minimum income!xxiv With this sum, every patient could instead consult with world specialists in complementary medicine… But, « the global market for anti-AIDS treatments reached approximately [US]$13 billion in 2009. It increases by 13% per year, and should exceed $17 billion by 2018, just in Europe and the United States », the French newspaper Le Figaro reminds us.xxv

In 2015, globally, nearly 16 million HIV-positive people were under treatmentxxvi, compared to 9.7 million in late 2012!xxvii This huge increase is due to the efforts of global health authorities which now recommend treatment from the time of first awareness of HIV status, even without any clinical signs of diseases and independently of the results of laboratory analysis.xxviii

The WHO recommendations of June 2013 « include providing antiretroviral therapy—irrespective of their CD4 count—to all children with HIV under 5 years of age, all pregnant and breastfeeding women with HIV, and to all HIV-positive partners where one partner in the relationship is uninfected ». The stated objective is « ensuring that all 26 million people eligible for treatment have access—not one person less ».xxix

This medicalisation of fear continues to widen the indications for treatment—a common sales technique for laboratories, but not necessarily for the benefit of patients’ health.

Conflicts of Interest

David Crowe noted: « Government agencies should be independent, but there is a ‘revolving door’ at the top. This closely aligns the government agencies with the needs of the pharmaceutical companies. In addition, in the time of Ronald Reagan, the FDA [Food and Drug Administration] started to take fees from drug companies for drug approvals. This encourages swift approval of new drug applications which helps fund the FDA. Instead of being an independent agency, the FDA has become a rubber stamp for new drugs. The fact that quite a few drugs are pulled off the market after approval is an indication that the approval process has major problems. This rarely happens with AIDS drugs simply because people diagnosed with AIDS are believed to have a fatal condition so most drug side effects will be blamed on HIV, not the drugs. »xxx Circular logic…

The French AIDS agency, ANRS, is a good illustration of the problem of conflicts of interest: « All members of its committees are under multiple contracts with the firms that produce the drugs they have to evaluate, » says Professor Philippe Even in his latest book Corruptions and Credulity in Medicine.xxxi For example, for this article we looked for statements of conflicts of interest among the scientists who drafted the September 2015 report on the ANRS Pre-exposure Prophylaxis (PrEP).xxxii This report recommended more extensive use of Gilead’s Truvada®xxxiii, which was indeed announced by France’s Minister of Health in November 2015. But all the 23 experts except one have links, sometimes very close, with the antiretroviral industry, among which several ties are with Gilead laboratories. However, these links are minimised because they were only declared for « work on PrEP in the period since the referral by ANRS and CNS (April–July 2015) ».xxxiv

It would take a whole article to explain the extreme flaws in the ANRS recommendations. In any case, ANRS cannot be considered an independent agency since its experts flirt with industry! Besides, this recent ANRS report, favourable to the prescription of antiretrovirals for HIV-negative people considered to be at risk, is based on the Ipergay study, led by ANRS itself, which concludes that Gilead’s Truvada is effective—but the trial has created debate about ethical questions and conflicts of interest. This study cost the French public more than one million euros, all this being a saving for the lab!xxxv

« It is often said that ANRS is a unique institution in the world of research, due to both its mode of organisation and how it is financed, » boasts the agency’s director in the 2013–14 activity report.xxxvi This is actually the French health agency to which the most blank cheques are signed for its trials and where vigilance on conflict of interest is the least.

Afterword: 30 years of controversy…

The following statement was made in 1994 by Dr Kary Mullis, co-winner of the 1993 Nobel Prize in Chemistry, and two colleagues who are among 2,600 scientists and researchers from the « dissident » group Rethinking AIDS: « Although more than 75,000 scientific papers have been published on AIDS, no paper has seriously considered all relevant evidence and attempted to prove that HIV causes AIDS. Some papers respond to specific objections but begin by assuming that HIV causes AIDS, which is the very question at issue. If such a paper were possible to write, it would have been written, and been the most widely cited scientific publication of this century. Since such papers do not exist, it is impossible to refute or substantiate the arguments they might contain. »xxxvii

The Rethinking AIDS group was founded in 1991, inspired by Dr Peter Duesberg, Professor of Molecular Biology at the University of California at Berkeley, who in 1987 was the first to express doubt publicly about the HIV=AIDS hypothesis.xxxviii Among the prominent scientists who share the analysis of the Rethinking AIDS founding letterxxxix are Etienne de Harven, MD, a pathologist who pioneered research on retroviruses, and Gordon Stewart, MD, Emeritus Professor of Public Health at the University of Glasgow and a former WHO adviser on AIDSxl. These are internationally renowned experts who know what they’re talking about…

References at link: http://pryskaducoeurjoly.com/actu/2447/hiv-positive-without-treatmentand-healthy

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http://www.dailymail.co.uk/health/article-3837131/Rare-group-children-IMMUNE-AIDS-scientists-reveal-researchers-claim-cusp-cure-HIV.html

A rare group of children is immune to AIDS, scientists believe.

The 170 boys and girls in South Africa are known as 'non-progressors'.
They were all born with HIV, after being infected in the womb, and still have extremely high levels of the disease in their blood.
But they are completely healthy.
Most importantly, their infection has not made the natural progression to AIDS - and doctors believe it never will, even without antiretroviral (ART) drugs.

WHY ARE THESE KIDS RESISTANT TO AIDS?

Scientists have identified a group of 170 'non-progressors' in South Africa.
The children are all aged over five years old, and they were all born with HIV.
However, scientists say their disease will never develop into AIDS - even without antiretroviral therapy, the standard treatment for patients. These children have a uniquely weak immune system.
It means there are not enough immune cells for the HIV virus to infect and destroy to proliferate itself.
They also have lower levels of certain a receptor protein on cells.
Normally, the HIV virus accesses cells through this protein (which is called CCR5).
But without it, there are few - if any routes for the infection to take to proliferate.

The phenomenon, explained in a report by the University of Oxford on Thursday, could seem to defy logic.
HIV attacks a sufferer's immune system, leaving them open to infections, and causing their disease to develop into AIDS.
But these children, all over the age of five, have a uniquely weak immune system.
While that may seem to be dangerous, the report's lead researcher Dr Philip Goulder explains it is this biological quirk that means they have an almost zero per cent chance of contracting AIDS.
Essentially there are not enough immune cells for the virus to infect and destroy, which is the way it grows.
That is exactly what antiretroviral drugs are designed to do - suppress the immune system to deprive HIV of fuel.

'The critical factor was that they had very low levels of immune activation,' Professor Goulder said.
'We saw a failure of HIV to activate the immune system.
'It's difficult for the virus to get into [their immune cells], so they remain relatively unscathed.'

Professor Goulder and his colleagues have been monitoring blood samples of HIV patients for years, and found that just five per cent of children are non-progressors.
Their research shows these 'non-progressors' have lower levels of certain a receptor protein on cells.
Normally, the HIV virus accesses cells through this protein (which is called CCR5).
But without it, there are few - if any routes for the infection to take to proliferate.

Like all sufferers, these children will soon be put on ART, since the UN changed its guidelines to say all children with HIV need to take medication. But Professor Goulder explains that they don't need it.

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Letter from Neville Hodgkinson to Harper’s Magazine.

Sirs:
Celia Farber’s powerful article on AIDS, in particular her airing of the views of Professor Peter Duesberg, has been greeted with incomprehension by The Nation, the Columbia Journalism Review and others. They believe that questioning HIV as the cause of AIDS is a “crackpot theory”, “widely refuted for years”, as the CJR put it.

Unfortunately, these respected opinion-leaders have been misled. There has been a long and persistent unwillingness to think again on the part of those who, in good faith, brought the HIV theory into being. There has therefore been much denigration, but never any scientific refutation of Duesberg’s critique.

The reasons for this unwillingness are best understood from two very early responses to the critique.

On 28 April 1987, less than two months after publication of Duesberg’s first paper on the subject, a memo was sent from the office of the Secretary of Health and Human Services (HHS) headed MEDIA ALERT. Copies were addressed to the Secretary, Under Secretary, and Assistant Secretary of HHS, and to the “Assistant Secretary for Public Affairs”, the “Chief of Staff”, the Surgeon General, and “The White House”. The memo noted that:

This obviously has the potential to raise a lot of controversy (If this isn’t the virus, how do we know the blood supply is safe? How do we know anything about transmission? How could you all be so stupid and why should we ever believe you again?) and we need to be prepared to respond.

On November 17, 1988, John Maddox, the then editor of the influential science journal Nature, who rejected numerous submissions from Duesberg on HIV and AIDS, wrote to him:

I am glad you correctly infer from my letter that I am in many ways sympathetic to what you say. I did not ask you to revise the manuscript, however. The danger, as it seems to me, is that the dispute between you and what you call the HIV community will mislead and distress the public in the following way. You point to a number of ways in which the HIV hypothesis may be deficient. It would be a rash person who said that you are wrong, but…if we were to publish your paper, we would find ourselves asking people to believe that what has been said so far about the cause of AIDS is a pack of lies.

Concern for the public health, for the reputations of science and politicians, and good old-fashioned embarrassment, are all very human and understandable. Twenty years on, these same factors are still at work. In fact, they probably weigh even more heavily today on HIV’s “discoverers” and on those who took up the cause of fighting the virus that was said to constitute such a threat to humanity. But they do not constitute refutation of a leading scientist’s critique. Nor of the careful work contributed by many other scientists who have questioned the HIV orthodoxy, but whose views have been similarly kept out of the mainstream of scientific debate.

Thank you for publishing Farber’s article.

Yours faithfully

Neville Hodgkinson

Medical and Science Correspondent, The Sunday Times, London, 1985-89 and 1991-94; author, AIDS: The Failure of Contemporary Science (Fourth Estate, London, 1996)

(formatting edited for clarity)

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AIDS and the Corruption of Medical Science

By Celia Farber,
Harper's, March 2016

Joyce Ann Hafford was a single mother living alone with her thirteen-year-old son, Jermal, in Memphis, Tennessee, when she learned that she was pregnant with her second child. She worked as a customer service representative at a company called CMC Call Center; her son was a top student, an athlete and musician. In April 2003, Hafford, four months pregnant, was urged by her obstetrician to take an HIV test. She agreed, even though she was healthy and had no reason to think she might be HIV positive. The test result came up positive, though Hafford was tested only once, and she did not know that pregnancy itself can cause a false positive HIV test. Her first thought was of her unborn baby. Hafford was immediately referred to an HIV/AIDS specialist, Dr. Edwin Thorpe, who happened to be one of the principal investigators recruiting patients for a clinical trial at the University of Tennessee Medical Group that was sponsored by the Division of AIDS (DAIDS) — the chief branch of HIV/AIDS research within the National Institutes of Health.

The objective of the trial, PACTG 1022, was to compare the “treatment-limiting toxicities” of two anti-HIV drug regimens. The core drugs being compared were nelfinavir (trade name Viracept) and nevirapine (trade name Viramune). To that regimen, in each arm, two more drugs were added — zidovudine (AZT) and lamivudine (Epivir) in a branded combination called Combivir. PACTG 1022 was a “safety” trial as well as an efficacy trial, which means that pregnant women were being used as research subjects to investigate “safety” and yet the trial was probing the outer limits of bearable toxicity. Given the reigning beliefs about HIV’s pathogenicity, such trials are fairly commonplace, especially in the post-1994 era, when AZT was hailed for cutting transmission rates from mother to child.

The goal of PACTG 1022 was to recruit at least 440 pregnant women across the nation, of which 15 were to be enrolled in the University of Tennessee Medical Group. The plan was to assign the study’s participants to one of two groups, with each receiving three HIV drugs, starting as early as ten weeks of gestation. Of the four drugs in this study, three belong to the FDA’s category “C,” which means that safety to either mother or fetus has not been adequately established.

Joyce Ann Hafford was thirty-three years old and had always been healthy. She showed no signs of any of the clinical markers associated with AIDS — her CD4 counts, which measure the lymphocytes that are used to indicate how strong a person’s immune system is, and which HIV is believed to slowly corrode, were in the normal range, and she felt fine. In early June 2003, she was enrolled in the trial and on June 18 took her first doses of the drugs. “She felt very sick right away,” recalls her older sister, Rubbie King. “Within seventy-two hours, she had a very bad rash, welts all over her face, hands, and arms. That was the first sign that there was a problem. I told her to call her doctor and she did, but they just told her to put hydrocortisone cream on it. I later learned that a rash is a very bad sign, but they didn’t seem alarmed at all.”

Hafford was on the drug regimen for thirty-eight days. “Her health started to deteriorate from the moment she went on the drugs,” says King. “She was always in pain, constantly throwing up, and finally she got to the point where all she could do was lie down.” The sisters kept the news of Hafford’s HIV test and of the trial itself from their mother, and Hafford herself attributed her sickness and nausea to being pregnant. She was a cheerful person, a non-complainer, and was convinced that she was lucky to have gotten into this trial. “She said to me, ‘Nell’ — that’s what she called me — ‘I have got to get through this. I can’t let my baby get this virus.’ I said, ‘Well, I understand that, but you’re awful sick.’ But she never expressed any fear because she thought this was going to keep her baby from being HIV positive. She didn’t even know she was in trouble.”

On July 16, at her scheduled exam, Hafford’s doctor took note of the rash, which was “pruritic and macular-papular,” and also noted that she was suffering hyperpigmentation, as well as ongoing nausea, pain, and vomiting. By this time all she could keep down were cans of Ensure. Her blood was drawn for lab tests, but she was not taken off the study drugs, according to legal documents and internal NIH memos.

Eight days later, Hafford went to the Regional Medical Center “fully symptomatic,” with what legal documents characterize as including: “yellow eyes, thirst, darkening of her arms, tiredness, and nausea without vomiting.” She also had a rapid heartbeat and difficulty breathing. Labs were drawn, and she was sent home, still on the drugs. The next day, July 25, Hafford was summoned back to the hospital after her lab reports from nine days earlier were finally reviewed. She was admitted to the hospital’s ICU with “acute and sub-acute necrosis of the liver, secondary to drug toxicity, acute renal failure, anemia, septicemia, premature separation of the placenta,” and threatened “premature labor.” She was finally taken off the drugs but was already losing consciousness. Hafford’s baby, Sterling, was delivered by C-section on July 29, and she remained conscious long enough not to hold him but at least to see him and learn that she’d had a boy. “We joked about it a little, when she was still coming in and out of consciousness in ICU,” Rubbie recalls. “I said to her, ‘You talked about me so much when you were pregnant that that baby looks just like me.’” Hafford’s last words were a request to be put on a breathing tube. “She said she thought a breathing tube might help her,” says Rubbie. “That was the last conversation I had with my sister.” In the early morning hours of August 1, Rubbie and her mother got a call to come to the hospital, because doctors had lost Hafford’s pulse. Jermal was sleeping, and Rubbie woke her own daughter and instructed her not to tell Jermal anything yet. They went to the hospital, and had been there about ten minutes when Joyce Ann died.

###

Rubbie recalls that the hospital staff said they would clean her up and then let them sit with her. She also remembered a doctor who asked for their home phone numbers and muttered, “You got a lawsuit.” (That person has not resurfaced.) They hadn’t been sitting with Hafford’s body long when a hospital official came in and asked the family whether they wanted an autopsy performed. “We said yes, we sure do,” she says. The hospital official said it would have to be at their expense — at a cost of $3,000. “We said, ‘We don’t have $3,000.’ My sister didn’t have any life insurance or anything,” says Rubbie. “She had state health care coverage, and we were already worried about how to get the money together to bury her.” Consequently, no autopsy was done. There was a liver biopsy, however, which revealed, according to internal communiqués of DAIDS staff, that Hafford had died of liver failure brought on by nevirapine toxicity.

And what was the family told about the cause of Hafford’s death?

“How did they put it?” Rubbie answers, carefully. “They told us how safe the drug was, they never attributed her death to the drug itself, at all. They said that her disease, AIDS, must have progressed rapidly.” But Joyce Ann Hafford never had AIDS, or anything even on the diagnostic scale of AIDS. “I told my mom when we were walking out of there that morning,” Rubbie recalls, “I said, ‘Something is wrong.’ She said, ‘What do you mean?’ I said, ‘On the one hand they’re telling us this drug is so safe, on the other hand they’re telling us they’re going to monitor the other patients more closely. If her disease was progressing, they could have changed the medication.’ I knew something was wrong with their story, but I just could not put my finger on what it was.”

When they got home that morning, they broke the news to Jermal. “I think he cried the whole day when we told him,” Rubbie recalls. “My mom had tried to prepare him. She said, ‘You know, Jermal, my mom died when I was very young,’ but he was just devastated. They were like two peas in a pod those two. You could never separate them.” Later on, Jermal became consumed with worry about how they would bury his mother, for which they had no funds and no insurance. The community pitched in, and Hafford was buried. “I haven’t even been able to go back to her grave since she passed,” says Rubbie.

###

Rubbie King is haunted by many questions, including whether her sister was really infected with HIV, [1] and also what the long-term damage might be to Sterling, whom Rubbie is now raising, along with Jermal and her own child. Sterling, in addition to the drugs he was exposed to in the womb, was also on an eight-week AZT regimen after birth. One of the reasons the family suspects Hafford may have been a false positive is that St. Jude’s Children’s Research Hospital has not released Sterling’s medical records, and although they have been told that he is now HIV negative, they never had any evidence that he was even born positive. (All babies born to an HIV-positive mother are born positive, but most become negative within eighteen months.)

Hafford’s family was never told that she died of nevirapine toxicity. “They never said that. We never knew what she had died of until we got the call from [AP reporter] John Solomon, and he sent us the report,” says Rubbie King. “It was easier to accept that she died of a lethal disease. That was easier to handle.” The family has filed a $10 million lawsuit against the doctors who treated Hafford, the Tennessee Medical Group, St. Jude’s Children’s Research Hospital, and Boehringer Ingelheim, the drug’s manufacturer. [2]

Rubbie King made a final, disturbing discovery when she was going through Hafford’s medical records: In addition to discovering that her sister had only ever been given a single HIV test, she also came across the fifteen-page consent form, which was unsigned.

###

On August 8, 2003, Jonathan Fishbein, who had recently taken a job as the director of the Office for Policy in Clinical Research Operations at DAIDS, wrote an email to his boss, DAIDS director Ed Tramont, alerting him that “there was a fulminant liver failure resulting in death” in a DAIDS trial and that it looked like “nevirapine was the likely culprit.” He said that the FDA was being informed. He was referring to Joyce Ann Hafford. Tramont emailed him back, “Ouch. Not much wwe can do about dumd docs!”

This email exchange came to light in December 2004, when AP reporter John Solomon broke the story that Fishbein was seeking whistle-blower protection, in part because he had refused to sign off on the reprimand of an NIH officer who had sent the FDA a safety report concerning the DAIDS trial that launched the worldwide use of nevirapine for pregnant women. The study was called HIVNET 012, and it began in Uganda in 1997.

The internal communiqués from DAIDS around the time of Hafford’s death made it clear that doctors knew she had died of nevirapine toxicity. Tramont’s reply to Fishbein suggests that he thought blame could be placed squarely with Hafford’s doctors, but it was the NIH itself that had conceived of the study as one that tested the “treatment-limiting toxicities” of HIV drugs in pregnant women.

The conclusion of the PACTG 1022 study team was published in the journal JAIDS in July of 2004. “The study was suspended,” the authors reported, “because of greater than expected toxicity and changes in nevirapine prescribing information.” They reported that within the nevirapine group, “one subject developed fulminant hepatic liver failure and died, and another developed Stevens-Johnson syndrome.” Stevens-Johnson syndrome is skin necrolysis — a severe toxic reaction that is similar to internal third-degree burns, in which the skin detaches from the body. Another paper, entitled “Toxicity with Continuous Nevirapine in Pregnancy: Results from PACTG 1022,” puts the results in charts, with artful graphics. A small illustration of Hafford’s liver floats in a box, with what looks like a jagged gash running through it. Four of the women in the nevirapine group developed hepatic toxicity.

###

As Terri Schiavo lay in her fourteenth year of a persistent vegetative state, and the nation erupted into a classically American moral opera over the sanctity of life, Joyce Ann Hafford’s story made only a fleeting appearance — accompanied by a photo of her holding a red rose in an article that was also written by the AP’s John Solomon. But soon a chorus of condemnation was turned against those who were sensationalizing Hafford’s death and the growing HIVNET controversy to condemn nevirapine, which had been branded by the AIDS industry as a “life-saving” drug and a “very important tool” to combat HIV in the Third World.

So-called community AIDS activists were sprung like cuckoo birds from grandfather clocks at the appointed hour to affirm the unwavering AIDS cathechism: AIDS drugs save lives. To suggest otherwise is to endanger millions of African babies. Front and center were organizations like the Elizabeth Glaser Pediatric AIDS Foundation, which extolled the importance of nevirapine. Elizabeth Glaser’s nevirapine defenders apparently didn’t encounter a single media professional who knew, or cared, that the organization had received $1 million from nevirapine’s maker, Boehringer Ingelheim, in 2000. [3] This was no scandal but simply part of a landscape. Pharmaceutical companies fund AIDS organizations, which in turn are quoted uncritically in the media about how many lives their drugs save. This time the AIDS organizations were joined by none other than the White House, which was in the midst of promoting a major program to make nevirapine available across Africa. [4]

America is a place where people rarely say: Stop. Extreme and unnatural things happen all the time, and nobody seems to know how to hit the brakes. In this muscular, can-do era, we are particularly prone to the seductions of the pharmaceutical industry, which has successfully marketed its ever growing arsenal of drugs as the latest American right. The buzzword is “access,” which has the advantage of short-circuiting the question of whether the drugs actually work, and of utterly obviating the question of whether they are even remotely safe. This situation has had particularly tragic ramifications on the border between the class of Americans with good health insurance, who are essentially consumers of pharmaceutical goods, and those without insurance, some of whom get drugs “free” but with a significant caveat attached: They agree to be experimented on. These people, known in the industry as “recruits,” are pulled in via doctors straight from clinics and even recruited on the Internet into the pharmaceutical industry and the government’s web of clinical trials, thousands of which have popped up in recent years across the nation and around the world. Such studies help maintain the industry’s carefully cultivated image of benign concern, of charity and progress, while at the same time feeding the experimental factories from which new blockbuster drugs emerge. “I call them what they are: human experiments,” says Vera Hassner Sharav, of the Alliance for Human Research Protection in New York City. “What’s happened over the last ten to fifteen years is that profits in medicine shifted from patient care to clinical trials, which is a huge industry now. Everybody involved, except the subject, makes money on it, like a food chain. At the center of it is the NIH, which quietly, while people weren’t looking, wound up becoming the partner of industry.”

By June 2004, the National Institutes of Health had registered 10,906 clinical trials in ninety countries. The size of these trials, which range from the hundreds to more than 10,000 people for a single study, creates a huge market for trial participants, who are motivated by different factors in different societies but generally by some combination of the promise of better health care, prenatal care, free “access” to drugs, and often — especially in the United States — cash payments. Participating doctors, whose patient-care profits have been dwindling in recent years because of insurance-company restrictions, beef up their incomes by recruiting patients.

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Dr. Jonathan Fishbein is hardly a rabble-rouser. But he is a passionate advocate of “good clinical practice,” or GCP, a set of international standards that were adopted in 1996, as clinical-trial research boomed. The GCP handbook states: “Compliance with this standard provides public assurance that the rights, safety, and well-being of trial subjects are protected, consistent with the principles that have their origin in the Declaration of Helsinki, and that the clinical trial data are credible.” During the decade prior to his arrival at DAIDS, Fishbein had overseen and consulted on hundreds of clinical trials for just about every pharmaceutical company. Fishbein knew, before he took his job as director of the Office for Policy in Clinical Research Operations at DAIDS, that there was a troubled study haunting the whole division. Nobody was supposed to talk about it, but it hung heavily in the air. “Something about Uganda, that’s all I knew,” he says. There was a trial staged there, a big one, that had been plagued with “problems,” and there was also a lot of talk about one particular employee connected to this trial who would need to be disciplined. Soon he discovered just how bad the situation was. “The HIVNET thing,” he recalls, “it hit me like a fire hose when I walked in there.”

Fishbein’s position was new. “It sounded like a very important position,” he says. “I was to oversee the policies governing all the clinical-research operations, both here and abroad.” He was told he would have “go‒no go” authority over individual trials. It wasn’t long before Fishbein realized that he was, in effect, taking a job that was the equivalent of piloting an already airborne plane. “They had all these trials going on, and hundreds of millions of dollars flowing in every year, but there was apparently no one in a senior position there who really had clinical expertise — who knew all the nuances, rules, and regulations in the day-to-day running of clinical trials.” DAIDS, when Fishbein came to work there in 2003, was running about 400 experimental trials both in the United States and abroad.

A DAIDS project officer close to the HIVNET study closed the door when she had her first meeting with Fishbein. She had also crossed over from the private sector, and so she and Fishbein shared a disillusionment over how much shoddier and more chaotic the research culture was within the government, compared with industry. “I’m really frightened about the stuff that goes on here,” she told him. “We really need somebody.” This project officer, who for her own protection cannot be named, told Fishbein that the division’s flagship study in Africa — HIVNET 012 — had been wracked with problems and completely lacking in regulatory standards. She told Fishbein that the trial investigators were “out of control,” and that there was no oversight of them, and nobody with either the inclination or the authority to make them adhere to safety standards. What Fishbein subsequently learned entangled him in a story with eerie echoes of John Le Carré’s Constant Gardener.

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For our purposes, the story of nevirapine begins in 1996, when the German pharmaceutical giant Boehringer Ingelheim applied for approval of the drug in Canada. The drug had been in development since the early 1990s, which was a boom time for new HIV drugs. Canada rejected nevirapine twice, once in 1996 and again in 1998, after the drug showed no effect on so-called surrogate markers (HIV viral load and CD4 counts) and was alarmingly toxic. In 1996, in the United States, the FDA nonetheless gave the drug conditional approval so that it could be used in combination with other HIV drugs. [5]

By this time, Johns Hopkins AIDS researcher Brooks Jackson had already generated major funding from the NIH to stage a large trial for nevirapine in Kampala, Uganda, where the benevolent dictator Yoweri Museveni had opened his country to the lucrative promise of AIDS drug research, as well as other kinds of pharmaceutically funded medical research. HIVNET 012, according to its original 1997 protocol, was intended to be a four-arm, Phase III, randomized, placebo-controlled trial. [6] Its sole sponsor was listed as the National Institute of Allergy and Infectious Diseases (NIAID), though one of the investigators was a Boehringer employee. The “sample size” was to be 1,500 HIV-1 infected Ugandan women more than thirty-two weeks pregnant. The four arms they would be divided into were (1) A single dose of 200 mg nevirapine at onset of labor and a single 2 mg dose to the infant forty-eight to seventy-two hours post-delivery, and (2) a corresponding placebo group; (3) 600 mg of AZT at onset of labor and 300 mg until delivery, with a 4 mg AZT dose for the infant lasting seven days after birth, and (4) a corresponding placebo group. There were to be 500 women in each “active agent” arm and 250 in each placebo arm. The study was to last eighteen months, and its “primary endpoints” were to see how these two regimens would affect rates of HIV transmission from mother to child, and to examine the “proportion of infants who are alive and free of HIV at 18 months of age.” Another primary objective was to test the “safety/tolerance” of nevirapine and AZT. HIVNET’s architects estimated that more than 4,200 HIV-positive pregnant women would deliver at Mulago hospital each year, allowing them to enroll eighty to eighty-five women per month. Consent forms were to be signed by either the mother or a guardian, by signature or “mark.” One of the exclusion criteria was “participation during current pregnancy in any other therapeutic or vaccine perinatal trial.”

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Although HIVNET was designed to be a randomized, placebo-controlled, double-blind, Phase III trial of 1,500 mother/infant pairs, it wound up being a no-placebo, neither double- nor even single-blind Phase II trial of 626 mother/infant pairs. Virtually all of the parameters outlined for HIVNET 012 were eventually shifted, amended, or done away with altogether, beginning with perhaps the most important — the placebo controls. By a “Letter of Amendment” dated March 9, 1998, the placebo-control arms of HIVNET were eliminated. The study as reconstituted thus amounted to a simple comparison of AZT and nevirapine.

On September 4, 1999, The Lancet published HIVNET’s preliminary results, reporting that “Nevirapine lowered the risk of HIV-I transmission during the first 14‒16 weeks of life by nearly 50 percent.” The report concluded that “the two regimens were well-tolerated and adverse events were similar in the two groups.” The article also reported that thirty-eight babies had died, sixteen in the nevirapine group and twenty-two in the AZT group. The rate of HIV transmission in the AZT arm was 25 percent, while in the nevirapine group it was only 13 percent. As Hopkins Medical News later reported, the study was received rapturously. “The data proved stunning. It showed that nevirapine was 47 percent more effective than AZT and had reduced the number of infected infants from 25 to 13 percent. Best of all, nevirapine was inexpensive — just $4 for both doses. If implemented widely, the drug could prevent HIV transmission in more than 300,000 newborns a year.”

With the results of the study now published in The Lancet, Boehringer, which previously had shown little interest in HIVNET, now pressed for FDA approval to have nevirapine licensed for use in preventing the transmission of HIV in pregnancy.

###

There were complications, however. On December 6, 2000, a research letter in The Journal of the American Medical Association warned against using nevirapine for post-exposure treatment after two cases of life-threatening liver toxicity were reported among health-care workers who’d taken the drug for only a few days. (One of them required a liver transplant.) The January 5, 2001, issue of the CDC’s Morbidity and Mortality Weekly Report (MMWR) contained an FDA review of MedWatch — an informal reporting system of drug reactions — that highlighted an additional twenty cases of “serious adverse events” resulting from fairly brief nevirapine post-exposure prophylaxis. “Serious adverse events” were defined as anything “life-threatening, permanently disabling,” or requiring “prolonged hospitalization, or [...] intervention to prevent permanent impairment or damage.” The MMWR stressed that there probably were more unreported cases, since the reporting by doctors to MedWatch is “voluntary” and “passive.”

But NIAID was on another track altogether, either oblivious of or undeterred by the toxicity controversy. In 2001, Boehringer Ingelheim submitted its supplemental licensing request to the FDA. The request was submitted based entirely on the results of HIVNET, as published in The Lancet. Around the same time, the South African Medicines Control Counsel (MCC) conditionally approved nevirapine for experimental use in mother-to-child transmission treatment. To its credit, however, the FDA decided to go to Kampala, inspect the site, and review the data itself.

Since Boehringer had not originally intended to use this study for licensing purposes, it decided to perform its own inspection before the FDA arrived. Boehringer’s team arrived in Kampala and did a sample audit. They were the first to discover what a shambles the study was. According to Boehringer’s preinspection report, “serious non-compliance with FDA Regulations was found” in the specific requirements of reporting serious adverse events. Problems also were found in the management of the trial drug and in informed-consent procedures. DAIDS then hired a private contractor, a company named Westat, to go to Uganda and do another preinspection. This time the findings were even more alarming. One of the main problems was a “loss of critical records.” One of two master logs that included follow-up data on adverse events, including deaths, was said to be missing as the result of a flood. The records failed to make clear which mothers had gotten which drug, when they’d gotten it, or even whether they were still alive at various follow-up points after the study. Drugs were given to the wrong babies, documents were altered, and there was infrequent follow-up, even though one third of the mothers were marked “abnormal” in their charts at discharge. The infants that did receive follow-up care were in many cases small and underweight for their age. “It was thought to be likely that some, perhaps many, of these infants had serious health problems.” The Westat auditors looked at a sample of forty-three such infants, and all forty-three had “adverse events” at twelve months. Of these, only eleven were said to be HIV positive. The HIVNET team had essentially downgraded all serious adverse events several notches on a scale it had created to adapt to “local” standards. That downgrade meant, among other things, that even seemingly “life-threatening” events were logged as not serious. Deaths, unless they occurred within a certain time frame at the beginning of the study, were not reported or were listed as “serious adverse events” rather than deaths. In one case, “a still birth was reported as a Grade 3 adverse event for the mother.”

As a defense, the HIVNET team often cited ignorance. They told the Westat monitors that they were unaware of safety-reporting regulations, that they’d had no training in Good Clinical Practice, and that they had “never attempted a Phase III trial.” The principal investigators and sub-investigators “all acknowledged the findings [of the audit] as generally correct,” the Westat report said. “Dr. Guay and Dr. Jackson noted that many (‘thousands’) of unreported AE’s and SAE’s occurred... They acknowledged their use of their own interpretation of ‘serious’ and of severity.” “All agreed” that the principal and subinvestigators “had generally not seen the trial patients,” and “all agreed” that in evaluating adverse and serious adverse events “they had relied almost entirely on second or third hand summaries...without attempting to verify accuracy.” Westat also discovered that half the HIV-positive infants were also enrolled in a vitamin A trial, which effectively invalidates any data associated with them.

###

In light of the Westat report, DAIDS and Boehringer asked the FDA for a postponement of its inspection visit. The FDA responded by demanding to see the report immediately. On March 14, 2002, the FDA called a meeting with DAIDS, Boehringer, and the trial investigators. “They reprimanded the whole gang,” says Fishbein. Then they said to Boehringer: Withdraw your application for extended approval, if you want to avoid a public rejection.” Boehringer complied with the FDA’s demand, though statements put out by NIAID made it sound as if the company had withdrawn the application for FDA approval in a spirit of profound concern for protocol. In South Africa, a few months later, the news focused on the angry chorus of AIDS experts and activists, speaking as one. The South African MCC was reconsidering its approval of nevirapine for pregnant women because of Boehringer’s withdrawal and the growing HIVNET controversy. The Associated Press reported that “activists fear the government, notorious for its sluggish response to the AIDS crisis, is pressuring the council to reject nevirapine, and that it could misrepresent the current discussions as proof the drug is toxic. Studies show nevirapine given to HIV-pregnant women during labor and to their newborn babies can reduce HIV transmission by up to 50 percent.” The problem with such statements, of course, is that the study in question was precisely the one that established the claim that nevirapine cut HIV transmission.

###

Two inspections had now declared HIVNET to be a complete mess: Boehringer’s own and Westat’s, which had been performed in conjunction with DAIDS. But the ways in which the various players were tethered together made it impossible for DAIDS to condemn the study without condemning itself. [7] But DAIDS was well aware of what had transpired.

According to DAIDS’s public version of events, which was dutifully echoed in the AIDS press, the trouble with HIVNET was that it was unfairly assailed by pedantic saboteurs who could not grasp the necessary difference between U.S. safety standards and the more lenient standards that a country like Uganda deserved. Two weeks after the fifty-seven-page Westat report was delivered, the deputy director of NIAID, Dr. John LaMontagne, had set the tone by stating publicly: “There is no question about the validity [of the HIVNET results]...the problems are in the rather arcane requirements in record keeping.” DAIDS was so dismissive of the Westat report that Westat’s lawyers eventually put officials on notice that they were impugning Westat’s reputation.

Meanwhile, as the investigations continued, nevirapine had long since been recommended by the World Health Organization and registered in at least fifty-three countries, and Boehringer had begun shipping boxes of the drug to maternity wards across the developing world. In 2002, President Bush announced a $500 million program to prevent maternal transmission of HIV in which nevirapine therapy would play a major role — despite the fact that the drug has never received FDA approval for this purpose.

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In 2003, when Jonathan Fishbein was drawn into the HIVNET saga, the cover-up (for that, ultimately, is what the NIH response had become) was ongoing. In response to the massive failures documented by Boehringer and Westat, DAIDS embarked on a “re-monitoring review” in an attempt to validate the study’s results. Ordinarily, an outside contractor would be retained for such a complex project, but Tramont made the decision to keep the remonitoring in-house. Drafting the review was a massive undertaking that took months of research, lengthy interviews with the investigators, and painstaking analysis of poorly organized documentation, as the DAIDS team attempted to learn what had actually taken place in Kampala. Even so, Tramont wanted the HIVNET site reopened in time for President Bush’s visit to Uganda. In March 2003, Tramont and his staff gathered together the different sections and substantially rewrote the report, especially the safety section, minimizing the toxicities, deaths, and record-keeping problems. The rewritten report concluded that nevirapine was safe and effective for the treatment of mother-to-child transmission of HIV, thus saving HIVNET 012 from the scrapheap of failed scientific studies.

While preparing the safety review section, however, an NIH medical officer named Betsy Smith noticed a pattern of elevated liver counts among some of the babies in the AZT arm. Following FDA regulations, she drafted a safety report documenting this finding and gave it to Mary Anne Luzar, a DAIDS regulatory affairs branch chief. Luzar forwarded the safety report to the FDA. The HIVNET investigators were furious; Tramont, who had previously signed off on the safety report, ordered a new version to be drafted, essentially retracting the previous one, and sent it to the FDA. [8] The political stakes were very high: nevirapine was now a major element in the Administration’s new $15 billion African AIDS program — on July 11, President Bush even toured the HIVNET site in Kampala, which DAIDS had reopened for the occasion over Fishbein’s objections.

By late June 2003, Jonathan Kagan, the deputy director of DAIDS, asked Fishbein to sign off on a reprimand of Luzar for insubordination. Fishbein reviewed the HIVNET documentation and concluded that Luzar had done nothing wrong, that she had simply followed protocol. Fishbein’s refusal to go along with Luzar’s reprimand amounted to a refusal to participate in the HIVNET cover-up. In July, Tramont sent an email to all DAIDS staff instructing them not to speak about HIVNET at all. “HIVNET 012 has been reviewed, re-monitored, debated and scrutinized. To do any more would be beyond reason. It is time to put it behind us and move on. Henceforth, all questions, issues and inquiries regarding HIVNET 012 is [sic] to be referred to the Director, DAIDS.” [9]

What followed, as internal emails and memorandums clearly show, was a vicious and personal campaign on the part of Kagan and Tramont to terminate Fishbein’s employment. DAIDS officials wrote emails in which they worried about how to fire him without creating repercussions for NIAID director Anthony Fauci, who had given Fishbein a commendation for his work. The communiqués took on conspiratorial tones as Tramont led the operation and mapped out its challenges. On February 23, 2004, Tramont emailed Kagan: “Jon, Let’s start working on this — Tony [Fauci] will not want anything to come back on us, so we are going to have to have ironclad documentation, no sense of harassment or unfairness and, like other personnel actions, this is going to take some work. In Clauswitzian style, we must overwhelm with ‘force.’ We will prepare our paper work, then...go from there.” The web now included several more NIH/NIAID employees, who weighed in with suggestions about how best to expel Fishbein without leaving damning legal fingerprints on the proceedings.

Fishbein spent months trying to get a fair hearing, petitioning everyone from Elias Zerhouni, the director of the NIH, to Secretary of Health Tommy Thompson. It was around this time that Fishbein became a “ghost.” Nobody addressed him in the corridors, in the elevators, in the cafeteria. “There was an active campaign to humiliate me,” he says. “It was as if I had AIDS in the early days. I was like Tom Hanks in Philadelphia. Nobody would come near me.”

In March 2004, Fishbein began seeking whistle-blower protection. He met with congressional staff and attracted enough attention on Capitol Hill to force the NIH to agree to a study by the National Academy’s Institute of Medicine (IOM). The terms of that inquiry were skewed from the outset, however, and the nine-member panel decreed that it would not deal with any questions of misconduct. The panel ignored Fishbein’s evidence that DAIDS had covered up the study’s failures and relied on testimony from the HIVNET investigators and NIH officials. Not surprisingly, it found that HIVNET’s conclusions were valid. Six of the nine members on the panel were NIH grant recipients, with yearly grants ranging from $120,000 to almost $2 million. [10]

Fishbein dismissed the IOM report as a whitewash. Indeed, the report’s conclusions are hard to credit, given the overwhelming evidence uncovered by the Westat investigation and documentation such as the following email, which was sent by Jonathan Kagan to Ed Tramont on June 19, 2003. Tramont was considering HIVNET researchers Jackson and Guay for an award:


Ed — I’ve been meaning to respond on this — the bit about the award. I think that’s a bit over the top. I think that before we start heaping praise on them we should wait to see if the lessons stick. We cannot lose sight of the fact that they screwed up big time. And you bailed their asses out. I’m all for forgiveness, etc. I’m not for punishing them. But it would be “over the top” to me, to be proclaiming them as heroes. Something to think about before pushing this award thing...

NIAID has issued a total ban against any employee speaking to the press about Fishbein’s allegations. Instead, they have posted “Questions and Answers” about the matter on their website. The first question is: “Is single-dose nevirapine a safe and effective drug for the prevention of mother-to-infant transmission of HIV?” Fishbein has said that due to the spectacular failures of the HIVNET trial, the answer to this is not known, and not knowable. Fishbein believes that ultimately the HIVNET affair is not “about” nevirapine or even AIDS, but about the conduct of the federal government, which has been entrusted to do research on human beings and to uphold basic standards of clinical safety and accuracy.

NIAID answers its first question mechanically and predictably: “Single-dose nevirapine is a safe and effective drug for preventing mother-to-infant transmission of HIV. This has been proven by multiple studies, including the HIVNET 012 study conducted in Uganda.” The phrase “safe and effective” has been baked into both the question and the answer, rendering both blank and devoid of meaning. The “multiple studies” line is a familiar tactic, designed to deflect from the study that is actually being addressed, and that is HIVNET 012.

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A short letter published in the March 10, 2005, issue of Nature quietly unpegged the core claim of NIAID and its satellite organizations in the AIDS industry regarding nevirapine’s “effectiveness.” Written by Dr. Valendar Turner, a surgeon at the Department of Health in Perth, Australia, the letter read:


Sir — While raising concerns about “standards of record keeping” in the HIVNET 012 trial in Uganda, in your News story, “Activists and Researchers rally behind AIDS drug for mothers,” you overlook a greater flaw. None of the available evidence for nevirapine comes from a trial in which it was tested against a placebo. Yet, as the study’s senior author has said, a placebo is the only way a scientist can assess a drug’s effectiveness with scientific certainty.
The HIVNET 012 trial abandoned its placebo group in early 1998 after only 19 of the 645 mothers randomized had been treated, under pressure of complaints that the use of a placebo was unethical.
The HIV transmission rate reported for nevirapine in the HIVNET 012 study was 13.1%. However, without antiviral treatments, mother-to-child transmission rates vary from 12% to 48%. The HIVNET 012 outcome is higher than the 12% transmission rate reported in a prospective study of 561 African women given no antiretroviral treatment.

The letter concluded by asking: “On what basis can it be claimed that ‘there’s nothing that has in any way invalidated the conclusion that single-dose nevirapine is effective for reducing mother-to-child transmission’? Without supporting evidence from a placebo-controlled randomized trial, such statements seem unwarranted.” HIVNET claimed to reduce HIV transmission by “nearly 50 percent” by comparing a nevirapine arm to an AZT arm. Turner’s letter points out that 561 African women taking no antivirals transmitted HIV at a rate of 12 percent. Had nevirapine been asked to compete with that placebo group, it would have lost. As it was, there was no placebo group, so HIVNET’s results are a statistical trick, a shadow play, in which success is measured against another drug and not against a placebo group — the gold standard of clinical trials. The question should not be, Is nevirapine better than AZT? but, Is nevirapine better than nothing?

Independent evidence suggests that it is not.

A 1994 study, for example, that gave vitamin A to pregnant HIV-positive mothers in Malawi reported that those with the highest levels of Vitamin A transmitted HIV at a rate of only 7.2 percent. This is consistent with a vast body of research linking nutritional status to sero-conversion, as well as to general health. Another study on the efficacy of nevirapine in mother-to-child transmission was performed by researchers from Ghent University (Belgium) in Kenya and published in 2004.

Dr. Ann Quaghebeur, who led the Ghent study, was reached at her home near London. I asked her what she thought of the reaction to HIVNET 012. She replied in a very quiet voice, almost a whisper. “Our results showed that nevirapine had little effect. I actually felt it was a waste of resources. HIVNET was just one study, but usually before you apply it in a field setting there should be a few more studies to see if it works in real life. What I think they should have done is wait for more studies before they launched this in all those countries.” When I asked her how she explained this, she replied, “Well, I want to be careful, there seems to be an industry now.”

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The failure of the HIVNET researchers to properly control their study with a placebo group is not as unusual as one might think. In fact, this failure is perhaps the outstanding characteristic of AIDS research in general. The 1986 Phase II trial that preceded the FDA’s unprecedented rapid approval of AZT was presented as a double-blind, placebo-controlled study, though it was anything but that. As became clear afterward through the efforts of a few journalists, as well as the testimony of participants, the trial was “unblinded” almost immediately because of the severe toxicity of the drug. Members of the control group began to acquire AZT independently or from other study participants, and eventually the study was aborted and everyone was put on the drug. As in the case of HIVNET, documents obtained by journalist John Lauritsen under the Freedom of Information Act subsequently suggested that data-tampering was widespread. Documents were altered, causes of death were unverified, and the researchers tended to assume what they wished to prove, i.e., that placebo-group diseases were AIDS-related but that those in the AZT group were not. So serious were the deviations from experimental protocol at one Boston hospital that an FDA inspector attempted to exclude data from that center. In the end, however, all the data were included in the results, and the FDA approved the drug in 1987. [11]

AZT was approved in record time, but that record didn’t stand for long. In 1991, the FDA approved another DNA chain terminator, ddI, without even the pretense of a controlled study. Anti-HIV drugs such as Crixivan were approved in as little as six weeks, and cast as a triumph of AIDS activism. This pattern of jettisoning standard experimental controls has continued up to the present, as the HIVNET affair amply demonstrates, and has characterized not only research into new drugs designed to exterminate HIV but the more fundamental questions at the root of AIDS research.

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The HIVNET cover-up can only be understood within the larger political context of AIDS. The emergence of this syndrome in the 1980s sparked a medical state of emergency in which scientific controls, the rules that are supposed to bracket the emotions and desires of individual researchers, were frequently compromised or removed entirely. AIDS helped turn disease into politics, and politics, at least in the United States, is all about turning power into money.

No one has been more persistent in calling attention to the failings of AIDS research than Peter Duesberg, a virologist and cancer specialist at the University of California at Berkeley. If Duesberg’s name sounds familiar, it’s because he has been quite effectively branded in the international media as the virologist who is wrong about HIV. His name entered the popular culture in the late 1980s pre-stamped with wrongness. You knew he was wrong before you knew what he had said in the first place.

In 1987, Duesberg published a paper in the journal Cancer Research entitled “Retroviruses as Carcinogens and Pathogens: Expectations and Reality.” He was, at the time, at the top of the field of retrovirology, having mapped the genetic structure of retroviruses and defined the first cancer gene in the 1970s. He was the youngest member, at age fifty, ever elected into the National Academy of Sciences. In this paper, which in the words of his scientific biographer, Harvey Bialy, “sealed his scientific fate for a dozen years,” Duesberg argued that retroviruses don’t cause cancer and concluded by detailing how and why the retrovirus HIV cannot cause AIDS.

As AIDS grew in the 1980s into a global, multibillion-dollar juggernaut of diagnostics, drugs, and activist organizations, whose sole target in the fight against AIDS was HIV, condemning Duesberg became part of the moral crusade. Prior to that 1987 paper, Duesberg was one of a handful of the most highly funded and prized scientists in the country. Subsequently, his NIH funding was terminated and he has received not one single federal research dollar since his pre-1987 Outstanding Investigator Grant ran out. Duesberg lost his lab facilities and had to move twice within a few years to smaller labs on the Berkeley campus, where he spent much of his time writing futile research grant proposals asking to test his hypothesis that AIDS is a chemical syndrome, caused by accumulated toxins from heavy drug use. He lost his graduate students, who were warned that to emerge from his lab would blight their careers. He was denied and had to fight for routine pay increases by his employers at UC Berkeley, where he has tenure and still teaches. He was “dis-invited” from scientific conferences, and colleagues even declared that they would refuse to attend any conference that included him. Duesberg also was banished from publishing in scientific journals that previously had welcomed his contributions, most theatrically by the editor of Nature, Sir John Maddox, who wrote a bizarre editorial declaring that Duesberg would be denied the standard scientific “right of reply” in response to personal attacks that were frequently published in that journal. Prior to 1987, Peter Duesberg never had a single grant proposal rejected by the NIH. Since 1991 he has written a total of twenty-five research proposals, every single one of which has been rejected. “They took him out, just took him right out,” says Richard Strohman, an emeritus professor of biology at UC Berkeley.

And what was it, exactly, that Peter Duesberg had done? He simply pointed out that no one had yet proven that HIV is capable of causing a single disease, much less the twenty-five diseases that are now part of the clinical definition of AIDS. [12] He pointed to a number of paradoxes regarding HIV and argued that far from being evidence that HIV is “mysterious” or “enigmatic,” these paradoxes were evidence that HIV is a passenger virus.

The classical tests of whether or not a microorganism is the cause of infectious disease are known as Koch’s postulates. They state: (1) the microorganism must be found in all cases of the disease; (2) it must be isolated from the host and grown in pure culture; (3) it must reproduce the original disease when introduced into a susceptible host; and (4) it must be found present in the experimental host so infected. Although claims to the contrary have been made, Duesberg maintains that it has never been demonstrated that HIV satisfies all of Koch’s postulates. His exhaustive analysis of the peer-reviewed scientific literature has revealed more than 4,000 documented AIDS cases in which there is no trace of HIV or HIV antibodies. This number is significant, because there are strong institutional forces deterring such descriptions and because the vast majority of AIDS cases are never described in formal scientific papers. In fact, most AIDS patients have no active HIV in their systems, because the virus has been neutralized by antibodies. (With all other viral diseases, by the way, the presence of antibodies signals immunity from the disease. Why this is not the case with HIV has never been demonstrated.) Generally speaking, HIV can be isolated only by “reactivating” latent copies of the virus, and then only with extraordinary difficulty. Viral load, one of the clinical markers for HIV, is not a measurement of actual, live virus in the body but the amplified fragments of DNA left over from an infection that has been suppressed by antibodies. Another embarrassment for the HIV hypothesis is the extraordinary latency period between infection and the onset of disease, despite the fact that HIV is biochemically most active within weeks of initial infection. This latency period, which apparently grows with every passing year, enables proponents of the theory to evade Koch’s third and fourth postulates.

The foregoing is merely a sketch of the central mystery presented by the HIV theory of AIDS. There are many more, which Duesberg has laid out very carefully in his scientific papers and in a trade book published ten years ago, but they all boil down to the central point that when it comes to AIDS, basic scientific standards seem no longer to apply. [13] AIDS is a “syndrome” defined by twenty-five diseases, all of which exist independently of HIV. No one has ever demonstrated the cell-killing mechanism by which HIV is supposed to cause all these different diseases, and no one has ever demonstrated how a sexually transmitted virus can manage to restrict itself overwhelmingly to gay men and other AIDS risk groups instead of spreading randomly through the population, as do all other infectious diseases. The “overwhelming” character of the evidence for HIV’s causation has always been epidemiological; which is to say, a correlation, a coincidence. Whenever we have AIDS, researchers say, we also have HIV. But this correlation is a result of the official definition of AIDS, which states that a disease counts as AIDS only if it corresponds with HIV antibodies. (“AIDS without HIV” has been given a singularly unmemorable name: idiopathic CD4 lymphocytopenia.)

Given that the evidence for HIV is coincidental, a number of research avenues suggest themselves, yet orthodox AIDS researchers have failed to demonstrate, using large-scale controlled studies, that the incidence of AIDS-defining diseases is higher among individuals infected with HIV than among the general uninfected population. Consequently, it could very well be the case that HIV is a harmless passenger virus that infects a small percentage of the population and is spread primarily from mother to child, though at a relatively low rate. (This hypothesis would tend to explain the fact that the estimated number of HIV-positive Americans has remained constant at about 1 million since 1985.) Nor have large-scale controlled studies been carried out to directly test the AIDS-drug hypothesis, which holds that many cases of AIDS are the consequence of heavy drug use, both recreational (poppers, cocaine, methamphetamines, etc.) and medical (AZT, etc.) [14] Nor have controlled studies been carried out to prove that hemophiliacs infected with HIV die sooner than those who are not infected. Such studies might be expensive and tedious, but expense has never been a serious objection to AIDS researchers, who have spent many billions of dollars in the last twenty years on HIV research and practically nothing on alternative causes or even co-factors. (Even Luc Montagnier, the discoverer of HIV, has stated repeatedly that the virus cannot cause AIDS without contributing causes.)

Attempts to rigorously test the ruling medical hypothesis of the age are met not with reasoned debate but with the rhetoric of moral blackmail: Peter Duesberg has the blood of African AIDS babies on his hands. Duesberg is evil, a scientific psychopath. He should be imprisoned. Those who wish to engage the AIDS research establishment in the sort of causality debate that is carried on in most other branches of scientific endeavor are tarred as AIDS “denialists,” as if skepticism about the pathogenicity of a retrovirus were the moral equivalent of denying that the Nazis slaughtered 6 million Jews. Moral zeal rather than scientific skepticism defines the field. It has been decided in advance that HIV causes AIDS; consequently all research and all funding must proceed from that assumption. Similarly, it was known in advance that AZT was a “magic bullet” against HIV; the word was out that it was a “life-saving drug” before anyone could possibly verify this, and so scientific controls were compromised. Journalists (myself included) who reported at the time that the drug apparently was killing patients were labeled “AZT refuseniks” and even “murderers.”

The nevirapine debate follows the same histrionic, antiscientific pattern. Because of his concerns about the toxicity of this and other antiretroviral drugs, President Thabo Mbeki of South Africa was pilloried in the international press as pharmaceutical companies and their well-funded “activist” ambassadors repeated their mantra about “life-saving drugs.” So, too, was Jonathan Fishbein, who never questioned the premise that HIV causes AIDS, tarred and feathered for pointing out that the NIH flagship study on nevirapine was a complete disaster. Fishbein’s failure to fall into line, his failure to understand in advance of experimental proof that nevirapine was too important to fail, meant that the AIDS bureaucracy’s neutralizing antibodies had to be activated to destroy them.

In the end, the NIH failed to silence Fishbein. In late December 2005, he won his case and was retroactively reinstated at the agency, though he won’t be returning to DAIDS. He is unable to discuss the terms of his settlement, but he has promised to continue his commitment to research integrity and the protection of human research subjects. Peter Duesberg has been less successful, though there are signs of rehabilitation.

Regardless of whether Duesberg is right about HIV, his case, like Fishbein’s, lays bare the political machinery of American science, and reveals its reflexive hostility to ideas that challenge the dominant paradigm. Such hostility is not unusual in the history of science, [15] but the contemporary situation is dramatically different from those faced by maverick scientists in the past. Today’s scientists are almost wholly dependent upon the goodwill of government researchers and powerful peer-review boards, who control a financial network binding together the National Institutes of Health, academia, and the biotech and pharmaceutical industries. Many scientists live in fear of losing their funding. “Nobody is safe,” one NIH-funded researcher told me. “The scientific-medical complex is a $2 trillion industry,” says former drug developer Dr. David Rasnick, who now works on nutrition-based AIDS programs in Pretoria, South Africa. “You can buy a tremendous amount of consensus for that kind of money.”

“You have to write a grant a year almost. And you have to write four to get one, if you’re any good. I got out just in time. Everybody who’s still in there says the same thing,” says Berkeley’s Strohman. “Before the biotech boom, we never had this incessant urging to produce something useful, meaning profitable. Everybody is caught up in it. Grants, millions of dollars flowing into laboratories, careers and stars being made. The only way to be a successful scientist today is to follow consensus. If you’re going to produce something and put it on the market you don’t want any goddamn surprises. You’ve got the next quarter to report and you don’t want any bad news. It’s all about the short term now. Science has totally capitulated to corporate interests. Given their power and money, it’s going to be very hard to work our way out of this.”

Duesberg has never been afraid to challenge consensus, but contrary to what many in the AIDS establishment would have us believe, he is very far from being a scientific psychopath. [16] In 1997, on the brink of scientific demise in the U.S., Duesberg was quietly invited back to his native Germany to resume his cancer research. During this time, commuting biannually between Mannheim and Berkeley, Duesberg formulated and tested 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 that revives an abandoned thread of research from early in the twentieth century, which posited that cancer is caused by chromosomal malfunction, now known as “aneuploidy.”

Harvey Bialy, the founding scientific editor of Nature Biotechnology, a sister journal to Nature, recently spent four years writing a scientific biography of Duesberg entitled Oncogenes, Aneuploidy, and AIDS. The book is a history of the papers, review articles, and letters that Duesberg published between 1983 and 2003, and the responses they generated. I asked him why he wrote the book. “I am persuaded that aneuploidy is the initiating event in carcinogenesis,” Bialy said. “Peter has found the genetic basis for cancer. The most immediate application of it will be early diagnosis.”

“When aneuploidy, or genetic instability, or whatever linguistic term you want to use, gets reincarnated as the dominant theoretical explanation for the genesis of cancer, Peter Duesberg will be recognized as a major contributor to that,” Bialy said. “I wanted to make sure that his contributions were not swept aside or ignored.” I asked him about the AIDS controversy. “AIDS is a political thing, and Peter’s stuck in it. There’s nothing to discuss anymore on that.” Bialy made a critical point: Science is amoral and should be. There is no right and wrong, only correct and incorrect. “Duesberg,” Bialy said, “is a classical molecular biologist. All he is interested in is rigorously testing dueling hypotheses. The twin pillars, AIDS and oncogenes, both are crumbling because of the questions Peter Duesberg put into motion.”

“The basis of speciation is changing the content and the number of chromosomes,” says Duesberg. “Cancer is essentially a failed speciation. It’s not mutation. Cancer is a species. A really bad breast, lung, or prostate cancer has seventy, eighty, or more chromosomes. Those are the real bad guys — they’re way outside our species. But it’s a rare kind of species that as a parasite is more successful in its host than the normal host cell is.”

There has been considerable international interest in Duesberg’s new research. [17] In January 2004, he hosted a conference on aneuploidy and invited fifty cancer researchers from around the world who also have been working on the connections between aneuploidy and cancer. Seventy showed up, including such luminaries as Thomas Ried, the National Cancer Institute’s head of cancer genomics, Gert Auer from the Karolinska Institute in Stockholm, and Walter Giaretti, who heads the equivalent of the NCI in Italy. And on May 31 of last year, amid considerable tension, Duesberg was invited by the National Cancer Institute to give a talk at the NIH. The auditorium crackled with nervous tension as people filed in and took their seats. His talk was succinct and laced with his characteristic irony, but the questions afterward were civilized, with no tangible hostility. All was not forgiven, however. After the talk, while Duesberg remained at the podium talking to a group of people from the audience, I noticed a very angry-looking NIH publicist standing at the back of the room admonishing a colleague, a scientist, who’d posed a question that somehow connected aneuploidy to HIV. “You opened it up,” she scolded. “We got through it okay, but you opened it up.” As the questioner tried to defend himself, a thickset man who’d been standing in the circle said loudly, as though intending to broadcast it across the room: “Well, at least if he’s wrong about this he won’t be killing millions of people.”

Nobel laureate Kary Mullis, who discovered the revolutionary DNA technique called the polymerase chain reaction, has long been a supporter of Duesberg, but he has grown weary of the AIDS wars and the political attacks on contrarian scientists. “Look, there’s no sociological mystery here,” he told me. “It’s just people’s income and position being threatened by the things Peter Duesberg is saying. That’s why they’re so nasty. 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.”

Duesberg thinks that up to 75 percent of AIDS cases in the West can be attributed to drug toxicity. If toxic AIDS therapies were discontinued, he says, thousands of lives could be saved virtually overnight. And when it comes to Africa, he agrees with those who argue that AIDS in Africa is best understood as an umbrella term for a number of old diseases, formerly known by other names, that currently do not command high rates of international aid. The money spent on antiretroviral drugs would be better spent on sanitation and improving access to safe drinking water (the absence of which kills 1.4 million children a year).

It’s too late to save people like Joyce Ann Hafford, but it is possible that an open and honest debate about the risks of current AIDS treatments and the scientific questions concerning HIV could save others.

References at link: http://aidswiki.net/index.php?title=Document:Out_of_Control

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PERTH GROUP COMMENTARY ON THE RETHINKING AIDS RESPONSE TO THE GALLO ET AL CRITICISM OF CELIA FARBER IN HARPERS

In the view of the "HIV" experts there are two groups of "dissidents": " Mullis,
Giraldo, De Harven etc have all made statements that build upon the "logic" of
Duesberg and the Perth Group. Nothing original". (N Bennett: Re:Re:Re:
Analysis: the properness of the HIV hypothesis is a media hype, 21 March 2005
http://www.rethinking.org/bmj/response_101072.html). The "HIV" experts as
well as the "dissidents" are fully aware there are significant differences between
Peter Duesberg and our "logic". The aim of Celia Faber's article in Harpers
seems two-fold: exposure of the unethical behaviour in some scientific circles
and the promotion of the "dissidents" view. We were surprised to see that the
only "dissident" view presented was that of Peter Duesberg. We were even
more surprised to see that the 56 "items" meant to respond to the Robert Gallo
et al criticism of Celia Faber's article are also based on Peter Duesberg's
"logic". Nonetheless, we would like to make some comments in regard to
some.

Items 1, 4, 5, 12, 13
The statements "False Positive HIV Tests" in pregnancy, "HIV Antibodies in
Babies”, “Problems with HIV Tests”, "Are HIV Tests Widely based in Africa", and
"Tropical Diseases and False Positive HIV Tests" assume the existence of a
unique human retrovirus, "HIV" as well as antibodies specific to it in same group
or individuals. No such evidence exists.1-12 In 1996 when Peter Duesberg
claimed the Continuum prize, he also claimed that the existence of the "HIV
infectious molecular clone" is the proof that HIV exists. However, he was never
able to present any evidence for the existence of the "HIV" molecular clone. At
the same time he also wrote "...particles and proteins could reflect non-viral
material altogether". Now he claims some recently published electron
micrograph of particles found in cultures, which have never been shown to be
retroviral particles, are proof for the existence of HIV.
http://www.theperthgroup.com/REJECTED/S ... tterPG.pdf

In the BMJ on-line debate, Brian Foley, the "custodian" of the "HIV" genome at
the Los Alamos Laboratories used Peter Duesberg's 1996 argument as
evidence for the existence of HIV. Yet like Peter Duesberg he too was never
able to present any evidence for the existence of the "HIV infectious molecular
clone".

Item 11 - Does AIDS in Africa Differ from Malnutrition, Malaria, Parasitic
Infections and other Common Tropical Illnesses?
A thorough and original analysis of item 11 can be found in our papers AIDS in
Africa Distinguishing Fact and Fiction;13 Deconstructing AIDS, Reconstructing
AIDS;13-15 a letter to the South African, Sunday Independent newspaper,
http://www.theperthgroup.com/SOUTHAFRICA/NEWSPSA1.pdf;
our Mother to Child Transmission Monograph10 and the BMJ on-line debate.11

Item 18, Did HIVNET 006 Lower Viral Load?; Item 20, HIVNET 012 Protocol
Changes; Item 21, HIVNET 012: Phase II or Phase III?; Item 22, HIVNET
012 Not Placebo Controlled; Item 28, Maternal Nevirapine Proven in
'Multiple Studies'; Item 29, Valendar Turner, Nevirapine and Placebo
The most thorough and original analysis of these items can be found in Part IV
of our Mother to Child Transmission Monograph,10 our letter to Nature16 and
PowerPoint presentation
http://www.theperthgroup.com/PRESENTATIONS/nevppsn1.ppt

Item 30, Nevirapine Study with 561 People
Neither in the letter to Nature by one of us (Val Turner), nor in Gallo's critic, is
there any mention of "Nevirapine study with 561 people". To the contrary. In
the 1998 Rwanda study of 561 "people" where the transmission rate was
reported to be 12%, no antiretroviral drugs were used.17

Item 31, Vitamin A and HIV Transmission Rates
An analysis of "Vitamin A and HIV Transmission Rates" is found in part V of our
Mother to Child monograph.10

Item 38, How Does AZT Work?
According to Peter Duesberg, AZT is triphosphorylated extracellularly. The
triphosphorylated AZT enters the cells and attaches to the DNA and stops its
synthesis - AZT is a DNA chain terminator and by doing so becomes toxic to the
cells.18 However, the enzymes which triphosphorylate AZT are found only
intracellularly which means that AZT cannot be triphosphorylated extracellularly.
In addition, the cell membrane is impermeable to the phosphorylated
nucleotides.19 Furthermore, all the presently available data show there is no
significant triphosphorylation of AZT even intracellularly.20 Since for
triphosphorylation of AZT reducing equivalents are necessary, and since AZT is
an oxidising agent by which property it induces its toxicity, this is not
surprising.20

Item 39, Does HIV Cause Any Diseases?
An answer to this question presumes the existence of HIV. No such evidence
exists.21 (See previous).

Item 40, Does HIV Fulfil Koch's Postulates for AIDS?
If one accepts that "HIV" and "HIV" antibodies exist, then one has no choice but
to also accept that Koch's postulates have been fulfilled which means that HIV
is the cause of AIDS.

Item 42, Is HIV Active In The Bodies of AIDS Patients?; Item 43, Can HIV
be Isolated Without 'Reactivating' Latent Copies?
These questions imply that "HIV" exists in the bodies of patients in an inactive
form and that it can be isolated by "Reactivating Latent Copies". If "HIV" exists
in an inactive form in AIDS patients and those at risk then, given that AIDS
patients and those at risk are exposed to numerous agents which activate
retroviruses, it would also be present in an active form as well. In fact "HIV" has
never been isolated even in vitro without the use of a plethora of activating
agents. By "isolation" the "HIV" experts including Montagnier mean detection of
reverse transcriptase (RT) activity. Nowadays the non-specificity of RT is
known even to the general public in the form of magazine reports evaluating the
investment potential of biotechnology stocks.22

Item 44, Antibodies Mean Immunity...Except for HIV?
Only a minority of people (Peter Duesberg among them) believe that
"Antibodies Mean Immunity". Many "HIV" experts including Gallo et al in their
critique repeatedly presented evidence which disproves the claim that
"Antibodies Mean Immunity". Yet, Peter Duesberg still insists that "Antibodies
Mean Immunity". Antibodies do not mean immunity as was shown as long ago
as 1935 by no less an authority than Albert Sabin.23-25

Item 45, Does 'Viral Load' Measure Live Virus?
By the nature of the test, viral load cannot measure either "Live" or not "Live"
virus. It can only measure the “viral” RNA. Since there is no evidence that
proves the existence of a unique human retrovirus, "HIV" either "Live" or not
"Live" and thus "HIV" RNA, it is not possible to claim that the "viral load"
measures any of them.

Item 47, Does HIV Spread Randomly? Should it?
Before one asks "Does HIV spread randomly", one must first have evidence
which proves that:

(i) "HIV" exists
(ii) "HIV" spreads by any means.

No such evidence exists.10, 13-15, 21, 26

Item 50, Does HIV Kill T-Cells?
A most comprehensive answer to the question "Does HIV kill T-cells?" can be
found in our Genetica paper27 and in the BMJ Online debate.28

Item 52, Non-HIV Causes for AIDS
Before "HIV" was accepted as a cause of AIDS we were the first to propose a
non-infectious theory of AIDS which encompassed all the AIDS risk groups (gay
men, haemophiliacs, drug users) and included a mechanism of pathogenesis.
In our non-infectious theory of AIDS, drugs both recreational and prescribed
were considered to play a significant role. The discovery and acceptance of
"HIV" as a causative agent of AIDS led us to critically analyse the evidence
which was claimed to prove the existence of "HIV" as well as its role in AIDS. It
was concluded that (a) neither Montagnier's et al nor Gallo's et al evidence
proved the existence of a unique human retrovirus, LAV/HTLV-III (HIV) even in
vitro, much less in AIDS patients and those at risk; (b) AIDS and the
phenomena which were claimed to prove the existence of HIV were the result of
the many oxidative agents such as recreational and prescribed drugs (including
factor VIII infusions), to which the AIDS patients and those at risk were
exposed. The conclusions were incorporated in a paper sent to Nature entitled:
Reappraisal of AIDS: Is the oxidation induced by the risk factors the primary
cause? The paper was rejected. The 10th of July 1986 letter of re-submission
to Nature was accompanied by a response to the reasons given by the Journal
for rejection. The response ended with the following: "If my paper does nothing
other than draw attention to the oxidative nature of the risk factors and its
biological importance, then it offers what is so far the only hope of treatment
which will arrest and reverse the otherwise invariable fatal course of the
disease. This alone would more than justify it's publication". The paper was
again rejected and was eventually published in Medical Hypotheses in 1988.2
In the same year the paper was sent to Peter Duesberg.

In a paper29 in which Peter Duesberg accepted that the "hallmark" of AIDS "is a
defect in T-cells" and that the existence of "HIV" has been proven, he put
forward a number of arguments against the "HIV" hypothesis of AIDS. He did
not give an alternative explanation for AIDS. In 1989 paper Peter Duesberg
wrote: "What Are the Causes of AIDS? I propose that AIDS is not a contagious
syndrome caused by one conventional virus or microbe...Since AIDS is defined
by new combinations of conventional diseases, it may be caused by new
combinations of conventional pathogenic factors. The habitual administration of
factor VIII or blood transfusions or of drugs, chronic promiscuous male
homosexual activity that is associated with drugs, numerous acute parasitic
infections, and chronic malnutrition, each for an average of 8 yearsare
factors that appear to provide biochemically more tangible and plausible basis
for AIDS than an idle retrovirus".30

In a 1990 paper he wrote "The risk-AIDS hypothesis suggest that AIDS is
caused primarily by non-infectious agents. These include psychoactive drugs,
over-medication with antibiotics and above all AZT, a chain terminator of DNA
synthesis administered to treat HIV infection since 1987".31 Subsequently Peter
Duesberg published numerous papers and a book32 in which he argued against
the "HIV" theory of AIDS and claimed that "HIV" is an "innocent", "passenger"
virus and that "antibodies to HIV" are one of the "most specific markers" for
AIDS.30

Unlike Peter Duesberg, from the beginning of the "HIV" era we claimed there
was no evidence which proves the existence of "HIV" proteins or antibodies.
Our claims were vindicated in 1997.12, 33-35

According to Montagnier, "analysis of the proteins of the virus demands mass
production and purification" of the viral particles. In 1983 Montagnier and his
colleagues claimed to have purified "HIV". In their "purified" virus they found
three proteins, p80, p45 (now known as p41) and p24 that reacted with
antibodies in their patient’s serum. They made no comments regarding p80 and
the reacting antibodies, claiming that p41 was the cellular protein actin, and p24
to be the "HIV" specific protein and the antibodies which reacted with "HIV"
antibodies. In 1997 Montagnier admitted that in their "purified" virus they did
not have even particles with "the morphology typical of retroviruses" much less
a specific retrovirus, "HIV".35, 36

The minimum absolutely necessary but not sufficient condition to claim that
what are called "HIV" proteins are viral and not cellular is to show that the
sucrose density fraction said to represent "purified" virus contains proteins
which are not present in the same fraction obtained from non-infected cells,
what Bess et al referred to a "mock" virus. In 1997 Bess et al showed this is not
the case. The only difference one can see in their SDS-polyacrylamide gel
electrophoresis strips of "purified" virus and "mock" virus is quantitative, not
qualitative. Bess et al left the strip from the "mock" virus unlabelled. The
proteins of molecular weight 30,000 and above were labelled as cellular
proteins. Although Bess et al did not determine the identity of the p24, p13,
p6/7 proteins, they were labelled "HIV" proteins " when one of the reviewers
asked for them".

Thus according to the presently available evidence the ultimate origin of all the
"HIV" proteins including the most famous, p24, are cellular proteins.

The question is what are the antibodies present in the patient sera which react
with these proteins? Many researchers, including Montagnier, have shown that
AIDS patients and those at risk have high levels of auto-antibodies such as anti-
cardiolipin, anti-nuclear factor, anti-cellular, anti-platelet, anti-red cell, anti-actin,
anti-DNA, anti-tubulin, anti-albumin, anti-myosin and anti-thymosin antibodies. 6,
37, 38
Anti-lymphocyte auto-antibodies have been found in 87% of HIV
seropositive patients and their levels correlate with clinical status.39, 40 It is also
known that serum IgG levels are higher in African-American blood donors than
in Caucasians.41 Furthermore, AIDS patients and those at risk are exposed to
many infectious agents, whose antibodies may cross-react with the "HIV"
proteins.

The presently available data shows that among the risk groups in North
America, Europe and Australia a positive test confers upon an individual a
propensity to develop and die of diseases defined as AIDS. This should be
expected. Healthy individuals do not develop high levels of antibodies which
persist for a long time. The fact that individuals belonging to the high risk
groups have high levels of antibodies means that something is amiss in the
body but it does not reveal exactly what is the problem.

The explanation of how a positive antibody test may predict early deaths is far
less curious than the predictions engendered by an increased erythrocyte
sedimentation rate (ESR). The ESR is simply the rate at which red blood cells
fall to the bottom of a test tube of blood. It was discovered by John Hunter in
the late 1700s as an “indicator of inflammatory conditions”42 and rediscovered in
1918 by Fahraeus while seeking an early test for pregnancy. It is a commonly
used but non-specific test which, when elevated, "is a measure of the presence
and intensity of morbid processes within the body".43 Like a positive "HIV"
antibody test an elevated ESR also has the capacity to predict "a likelihood of
death within the next several years far above" a normal ESR. A common cause
of elevated ESR is infection and "Elevated ESRs are also seen with pregnancy,
malignancy, collagen vascular diseases, rheumatic heart disease, and other
chronic disease states, including human immunodeficiency virus infection".
Even asymptomatic, non-anaemic HIV positive individuals may have an
increased ESR44 and the test may be predictive for disease progression.45 In
HIV positive children a correlation exists between seropositivity,
hypergammaglobulinaemia and an elevated ESR.46 As far back as 1988
researchers from the Institut de Transfusion Sanguine, Paris, France, found
that: "An increased ESR in HIV-seropositive subjects seems to constitute a
predictive marker of progression towards AIDS before the decrease of the CD4
count".47 In other words the ESR is a superior predictive marker for the
development of the clinical AID syndrome than is a decrease in the CD4 cell
count, although the latter is said to be the cause of the syndrome. One
important factor which affects the ESR is the size of the red cells, especially
rouleaux formation where the red blood cells clump together. Rouleaux
formation may result from changes in the negative charge of red cells, caused
by "the dielectric effect of proteins in the surrounding plasma", especially by
"fibrinogen, immunoglobulins, and other acute-phase reaction proteins",43 and
their increased levels in some disease states. Diseases such as tuberculosis
and AIDS are not caused by red blood cell clumping induced by "the dielectric
effect of proteins" but the fact this can be demonstrated and measured in vitro is
of great diagnostic and prognostic utility in clinical practice.

Given that the evidence that "HIV" proteins are existing or newly induced
cellular proteins, and that individuals who test positive have high levels of auto-
antibodies and/or antibodies to many "non-HIV" antigens, all or some of which
may cross-react with cellular proteins, "HIV" seropositivity, like the ESR,
represent nothing more than a non-specific indicator, serendipitiously
discovered in 1983/84, of altered homeostasis connoting a propensity to
develop particular diseases. Whether or not a positive test is predictive of such
diseases outside the risk groups, remains to be proven. As long as the present
interpretation of a positive test is accepted this may never be ascertained
because knowledge of seropositivity by both patient and physician attracts
multiple confounding factors virtually impossible to eliminate. 10

The fact that “HIV” antibodies do predict illness from AIDS indicator diseases
without proof of their being caused by a retrovirus appears to be a stumbling
block for some scientists. It should not be. Every mother of every baby knows
that if her baby appears unwell she can measure his temperature. If this
measurement shows he has a fever she knows something is amiss. She will
expect other symptoms and signs to develop over the ensuing days. When
they do she may gauge resolution of the illness by noting the fever abates.
However, she does not imagine for a moment that her baby’s temperature is
diagnostic of one of the several dozen common diseases of childhood. Mothers
would have no problem understanding our argument in regard to “HIV”
antibodies and the propensity to illness.

Peter Duesberg, claims that the "Antibody to HIV is a Marker for American AIDS
Risk" but "HIV is a harmless passenger". He claims that it is easy to prove that
HIV is only a passenger virus because if a study is done one will discover that
“HIV” positive and "HIV" negative individuals from the risk groups will develop
AIDS and die from it with the same frequencies. (See the Duesberg
Phenomenon.48 Duesberg and Critics Agree: Haemophilia Is the Best Test.49
Although we as well as others have pointed out the ample evidence to the
contrary, he still insists this is the case. Some of the best evidence is published
by the MultiCenter AIDS Cohort and similar studies.50, 51 In Celia Farber's
article one reads: "Given that the evidence for HIV is coincidental, a number of
research avenues suggest themselves, yet orthodox AIDS researchers have
failed to demonstrate, using large-scale controlled studies, that the incidence of
AIDS-defining diseases is higher among individuals infected with HIV than
among the general uninfected population. Consequently, it could very well be
the case that HIV is a harmless passenger virus...no controlled studies have
been carried out to prove that hemophiliacs infected with HIV die sooner than
those who are not infected".

Gallo et al presented well documented evidence that a positive test signifies an
increased probability of having or developing AIDS. It is amazing that this
response by Gallo was not addressed in the 56 items considered for response
to Gallo et al. Since this item relates to the “crucial” experiments proposed by
Peter Duesberg, does it mean that Peter Duesberg is in agreement with the
"HIV" experts? Or would he agree with us that a positive antibody test in the
AIDS risk groups predicates an increased probability of having or developing
AIDS but is not proof for the presence in humans of a unique retrovirus "HIV"?
If the former is the case he may find himself in disagreement with the discoverer
of "HIV", Luc Montagnier who appears to have become an apologist of our
oxidative theory of AIDS.

In 1997, that is more than a decade after we proposed an oxidative theory of
AIDS and "HIV" and fully aware of it, Montagnier and his associates wrote: "in
AIDS pathogenesis, oxidative stress is proposed as a metabolic alteration that
favours disease progression by inducing both viral replication and apoptotic
death".52 A speech which Montagnier gave in 2003 to the European parliament
can be summarised as follows:

(i) the cause of the clinical syndrome, that is of the diseases and thus death
of the patients is acquired immune deficiency (AID) whose main
determinant is T4 cell decrease.
(ii) T4 Cell death is due to apoptosis.
(iii) The cause of apoptosis is oxidation.
(iv) The cause of oxidation is African is malnutrition.

Thus, according to the discoverer of "HIV" the cause of AIDS is OXIDATION.

References at: http://rebuttal.rethinkers.net/OtherOpinions/PerthGroup.pdf

All thanks to American Nightmare for flood inspiration!

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Final version of the Gallo Document to which the Perth Group responds above:

http://rebuttal.rethinkers.net/GalloScreed-20060325.html

Rethinking AIDS Responds to the Gallo Screed:

http://rebuttal.rethinkers.net/overview.html

[identity]

A CRITIQUE OF THE EVIDENCE FOR THE ISOLATION OF HIV
A Summary of the Views of Papadopulos et. al. ("The Perth Group")

The proposal that AIDS is caused by a unique, infectious retrovirus requires proof for the existence of such a retrovirus. Since the announcement of the discovery of certain laboratory phenomena claimed as proof of the existence of HIV we have critically analysed the data and have always maintained that no such proof exists [1-11].

A virus is a microscopic particle of particular size and shape (morphology) which contains particular constituents (biochemical properties) and which is able to replicate only at the behest of living protoplasm, that is, a virus is an obligatory intracellular parasite. Replication of a virus-like particle is the property which defines the particle as being infectious, that is, virus-like particle + replication = virus. These defining data determine that the only way to prove the existence of a novel (new) virus is to (i) isolate viral-like particles, that is, first obtain the particles separate from everything else; (ii) determine their morphological characteristics; (iii) analyse their constituents (nucleic acid and proteins) demonstrating that such properties are those of retroviruses and are unique; (iv) prove that the particles are infectious, that is, when pure particles are introduced into non-infected cell cultures, new but identical particles appear. Only then can the viral-like particles be deemed to a virus. In the case of retroviruses, the steps in this procedure were developed over the half century that preceded the AIDS era and are described in Toplin and Sinoussi. [12,13]. These steps are:

1. Culture of putatively infected cells demonstrating that such cultures contain retroviral-like particles, that is, particles virtually spherical in shape with a diameter of 100-120nM and with "condensed inner bodies (cores)" and surfaces "studded with projections (knobs)" [14].

2. Purification of a sample by ultracentrifugation through a sucrose density gradient. A test tube containing a solution of sucrose, ordinary table sugar, is prepared light at the top but gradually becoming heavier towards the bottom. A drop of supernatant (decanted) cell culture fluid is gently placed on top of the sucrose column and the test-tube is centrifuged for several hours at extremely high speeds. This generates tremendous forces forcing any particles present through the sugar solution until they reach a point where their buoyancy prevents further penetration. For retroviral particles this occurs where the density of the sucrose solution reaches 1.16 gm/ml. At this the point the particles concentrate or, to use virological terminology, this is where the particles band. The 1.1 band is then selectively extracted for further analysis.

3. Using the electron microscope (EM), photograph the 1.16 band proving there are particles of the correct morphology and no other material.

4. Disrupt and analyse the constituents of such particles.

5. Introduce pure particles into a virgin culture and, by repeating the above steps, prove that identical particles are produced.

To date, many electron micrographs of particles claimed to be retrovirus-like have been published. However, not one of these micrographs demonstrates particles satisfying both main morphological features of retroviral particles, that is, a diameter of 100-120nM and a surface studded with knobs. (HIV researchers are unanimous that the knobs contain a protein, gp120, which is essential for the first step in infection and replication, that is, for the particle to fuse with the membrane of an uninfected cell in order that the HIV particle with its 'HIV RNA" gains access to the interior of the cell [15].

To prove the existence of HIV, both Montagnier's group in 1983 and Gallo's group in 1984 banded supernatant in sucrose density gradients. However, until March 1997, for unknown reasons, neither these groups nor anyone else had ever published an electron micrograph of the banded (purified) material to show which if any of the many different variety of particles seen in gross cell cultures [20] are present at 1.16 gm/ml. Indeed, until March this year it was not possible to know whether any structured material whatsoever was present at the density which defines retroviral particles. Nonetheless, from the time of the Montagnier and Gallo studies [16,17], the material from culture supernatants banding at 1.16 gm/ml has been regarded as pure HIV particles. Acting on this premis, the proteins which are present in this band and which react with antibodies present in the sera of AIDS patients are claimed to be the HIV proteins and the antibodies reacting with such proteins the HIV antibodies. Similarly, a particular portion of the RNA banding at 1.16 gm/ml is claimed to be the HIV genome. All these conclusions were drawn without ever proving that the proteins and RNA are structural elements of a particle, viral-like, retroviral-like or any other particle of any other kind, that is, without any scientific basis.

New Data

This March, two papers [18,19] were published with electron micrographs of sucrose density gradient banded material. In one of these papers the authors confirmed that:

"Virus to be used for biochemical and serological [using "viral" proteins to test for antibodies in patients] analyses or as an immunogen [to produce antibodies in animals and test patients for "viral" proteins] is frequently prepared by centrifugation through sucrose density gradients. The fractions containing viral antigen [proteins] and/or infectivity are considered to contain a population of relatively pure viral particles" [19] (italics ours).

However, to the contrary, the data in these papers support our claim that the existence of HIV is unproven:

1. The authors of both papers concede that the particles which are present in the banded material and which are said to be HIV represent only a very small fraction of the total material. Gelderblom et al. state that the material contains "an excess of [cellular] vesicles with a size range 50-500nm, as opposed to a minor population of virus particles...cellular vesicles appear...to be a major contaminant of HIV preparations enriched by sucrose gradient centrifugation".

2. For the small number of particles deemed to be "HIV" no evidence is given that they are even a retrovirus-like particle. Indeed, to the contrary:
(a) the particles do not appear to have surface spikes (knobs), although the possibility that such projections may be present cannot be excluded. (However, in other papers published by many researchers including Gelderblom and his associates such projections are noted to be absent [14,20];
(b) the particles referred to as "HIV" are not spherical and have diameters exceeding 100-120 nM. In the EM in Gluschankof et al. [19] there are arrows pointing to five "HIV" particles devoid of surface projections whose dimensions are 121 X 145; 121 X 169; 121 X 145, 121 X 145 and 133 X 145 nM respectively. In Bess et al. [18] there are a total of six "HIV particles" also devoid of surface projections whose dimensions are 160 X 240; 200 X 240; 280 X 280; 208 X 250; 167 X 250 and 250 X 292 and nM respectively.

Thus, by definition, the particles cannot be retroviral-like particles and even less, a unique retrovirus, HIV. Furthermore, the particles noted by Gluschankof et al. and Bess et al. cannot be the same particle. Indeed, the method adopted by all HIV researchers for proving the existence of HIV, that is, excluding proof based on purification of particles with retroviral morphology shown capable of faithful replication but rather by detection of antibody/protein reactions, does not satisfy any scientific principle and defies common sense.

Eleni Papadopulos-Eleopulos
Department of Medical Physics
Royal Perth Hospital
Perth, Western Australia
August 1997

References at link: http://www.virusmyth.com/aids/hiv/epsummary.htm

[identity]

WHAT IS THE EVIDENCE FOR THE EXISTENCE OF HIV?
By Valendar Turner

Department of Emergency Medicine, Royal Perth
Hospital, Perth, Western Australia

The real purpose of scientific method is to make sure Nature hasn't misled you into thinking something you don't actually know... One logical slip and an entire scientific edifice comes tumbling down. One false deduction about the machine and you can get hung up indefinitely.
Robert Pirsig, Zen and the Art of Motorcycle Maintenance


Does the currently available evidence prove beyond reasonable doubt that a unique, exogenously acquired retrovirus has been isolated from the tissues of AIDS patients? Perhaps. Perhaps not. This is what I invite you to judge. And in case you are inclined to be assaulted by the opinions of overwhelming majorities, you may take comfort from a most venerated, international scientist who said, "In Science the authority embodied in the opinion of thousands is not worth a spark of reason in one man." I shall reward you with his identity at the end of this talk.

A virus is two things. Number one: It's a microscopic particle of certain size and form. Number two, such particles generate identical progeny by parasitising chemical constituents and energy from a living cell. This is what is actually meant by the term infectious. It is this attribute which justifies a particle being called a virus. This is the property which prevents our calling every particle we see a virus. By definition, a retroviral particle is spherical in shape and has a diameter of 100-120 Nm. On the outside is a shell studded with outwardly projecting knobs, knobs obligatory to latch on to and infect new cells. On the inside there is a core containing RNA as well as some proteins, one of which is an enzyme called reverse transcriptase. The latter gives retroviruses their name and its function is to catalyse the transcription of viral RNA into DNA, that is, to copy information contained in RNA in a direction opposite the customary direction, DNA to RNA. According to virologists, it is the DNA copy of the RNA blueprint, not the original RNA, which hibernates inside the cell nucleus awaiting an opportune time to orchestrate the production of new viruses.

To analyse their constituents and to prove they are truly viruses, retroviral-like particles must first be purified. This is done by a process called density gradient ultracentrifugation, something that may sound complicated but which isn't. A test tube containing a solution of sucrose, ordinary table sugar, is prepared light at the top, but gradually becoming heavier towards the bottom. A drop of fluid from a cell culture is gently placed on top and the test-tube is centrifuged for several hours at extremely high speeds. This generates forces many thousands of times that of gravity and any tiny particles present are gradually forced through the sugar solution until they reach a point where their buoyancy prevents them penetrating further. For retroviral particles, this occurs where the density reaches 1.16 gm/ml, the point where the particles concentrate or, to use virological jargon, band. The 1.16 band can then be selectively extracted and photographed with an electron microscope. So, to prove the existence of a retrovirus one is obliged to:

1. Culture putatively infected cells.

2. Purify a sample in a sucrose density gradient.

3. Photograph the 1.16 band proving there are particles of the right size and form, and there is no other material.

4. Extract and analyse the constituents of the particles and prove they contain reverse transcriptase by showing they can make DNA from RNA.

5. Culture purified particles with virgin cells demonstrating that a new set of particles appears with the same morphology and constituents as the originals.

Now I am going to discuss some of the data from four papers published in Science in May 1984 by Dr. Robert Gallo and his colleagues from the US National Cancer Institute. These papers do not describe the original discovery of what the overwhelming majority regard as HIV, that distinction falls a year earlier to Professor Luc Montagnier and his colleagues from the Pasteur Institute from where, it is important to say, samples were sent to the Gallo laboratory and which later caused Gallo and his colleagues, as well as the US government, quite a number of problems. Neither are the Gallo papers the last word on HIV isolation but there is no doubt they are most important because it was they that led to the famous Washington press conference of April the 23rd 1984, two weeks prior to publication, at which an anxious, waiting world was told that the cause of AIDS had been identified. In fact, as one scrutinises the vast AIDS literature, it is fair to say that of all the papers published on HIV isolation, including the very latest, the Gallo papers are the most rigorous by far. The problem is, are they rigorous enough?

The first paper begins with cultures made of T-lymphocyte cells from AIDS patients. These cells were chosen because, included amongst their numbers, are the putatively infected cells, a subgroup known as T4 lymphocytes. It is these that are often diminished in AIDS, the hypothesis being that the yet to be discovered retrovirus was infecting and killing them. After an unspecified time, concentrated fluids from these T-cell cultures were subcultured with cells of a stock, leukaemic T-cell line known as HT. In these secondary cultures the Gallo team reported particles in electron microscopic examination of gross, unrefined culture fluids and measured reverse transcriptase activity in both these and banded specimens but without evidence that retroviral- like particles or indeed any particles were present at 1.16 gm/ml. They also reported reactions were seen between culture proteins and some antibodies present in human and animal sera. From these data, the Gallo team claimed to have isolated a new retrovirus, HIV, as well as inducing it to grow in the HT cell line in large enough quantities for use in analysis and diagnosis. In a subsequent third paper, from banded culture fluids obtained from a disrupted HT cell clone, two proteins, and for no other reason than they reacted with antibodies present in human AIDS sera, were deemed to be the HIV proteins. Subsequent papers, published after the Gallo four, using the same logic, increased the number of such proteins to about ten.

Reading these data it is obvious that Gallo and his colleagues had abandoned the traditional method of retrovirus isolation. This is enigmatic when one realises that, in 1976, Gallo himself had stressed that the detection of particles and reverse transcriptase, even reverse transcriptase inside particles, are not proof of the existence of retrovirus because, no matter how remarkably such particles may resemble retrovirus, many such particles are not viruses because they totally lack the ability to replicate (Gallo et al., 1976). You must appreciate the magnitude of the particle problem. Cell cultures contain many and many kinds of particles, some viral-like and some not. The viral-like include retroviral-like. In the 1970s, retroviral-like particles were frequently observed in human leukaemia tissues (Gallo et al., 1976), cultures of embryonic tissues, and "in the majority, if not all, human placentas." (Panem, 1979) One genus of retroviral-like particles, the type-C particle and the one into which Gallo classified his newly discovered retrovirus HIV, is found in "fish, snakes, worms, pheasant, quail, partridge, turkey, tree mouse and agouti" (Grafe, 1991) as well as in "tapeworms, insects...and mammals." (Frank, 1987) This being the case, there seems to be no way of avoiding the rules developed over the decades of research into animal retroviruses, rules that enabled a scientists to sort out this clutter. And there are two more complicating factors. The first is that reverse transcription is not only a property of retroviruses. Normal cells contain enzymes which reverse transcribe RNA and so does hepatitis B virus, a virus that infects T-cells as well as liver cells and is present in a considerable number of AIDS patients. The second is the choice of the HT cell line. It was long known that leukaemic cells theselves can reverse transcribe and, strange as it may seem, although Dr. Gallo was about to look for reverse transcription as a sign of a new retrovirus, the HT cell line originated from a patient who, according to Dr. Gallo, had a disease caused by a retrovirus he discovered called HTLV-I. In fact, in 1983, Gallo reported that the HT parental cell line contained HTLV-I genetic sequences. On this basis alone one would expect to find evidence of reverse transcription in the HT cell line. Given all these data, one would imagine it was impossible for the Gallo team to abandon the need to follow the traditional method and isolate and characterise infectious particles, but abandon it they did. By what reasoning then did the Gallo team claim to have proven the existence of a new retrovirus from AIDS patients?

For their 1984 papers, they reiterated the limitations of particles and reverse transcriptase and made three assumptions which, taken together, constitute a precept known as specific reactivity. (Gallo et al., 1986) The first assumption was that AIDS patients are infected with a replicating retroviral particle, a virus which could be grown in cell cultures to yield unique, virus-specific proteins. Second, being foreign, the virus would stimulate the production of a number of distinctive antibodies directed against the viral proteins. Third, the proteins and the antibodies react specifically, that is, only with each other and with no other agent. Let us take a very careful look at this paradigm. First, when the Gallo team began their experiments, the existence of specific viral proteins as constituents of a replicating viral particle which could infect humans was entirely hypothesis, not fact. Second, antibodies and proteins are not monogamous, even the purest of each take on other partners. Third, even if they were monogamous, we know that AIDS patients contain antibodies to many different agents, many with which they are infected, for example hepatitis B and cytomegalic inclusion viruses, mycoplasma, fungi and mycobacteria. Unless Gallo further hypothesised that all these agents or parts of them, or their respective antibodies, disappear from cultures or sera, when blood from an AIDS patient is mixed with cell cultures of the same or another AIDS patient, how can anyone tell what is reacting with what, let alone define precisely where each of the reactants originated? As far as the reactions are concerned, it's no different from mixing up milk from six species of animals, adding a mixture of a dozen different acids and claiming to know which acid is curdling which milk. So, although the term specific HIV proteins conjures up visions of proteins being extracted from retroviral-like particles proven to be a unique virus, this is not how it was done. It was done by breaking up cells of the HT cell line, not a virus particle, and observing unknown proteins reacting with unknown antibodies. From these data both the proteins and the antibodies were deemed viral, and not just any virus, but HIV. That's all. Logic or magic? And as an aside, similar to the proteins, the origin of what is called the HIV genome, the HIV RNA, is also based on circumstance, not on purification and dissection of particles proven to be infectious. The Gallo team may have claimed isolation of a new retrovirus but what they actually did was weave a nexus between reverse transcriptase, particles, and certain proteins under the dubious imprimatur of specific reactivity. Is this virus isolation? Is this even virus detection?

There are also a number of unsolved mysteries in the Gallo papers.

Mystery number one:

Reading the first paper one gets the impression that the HT cell line was cultured with individual AIDS patient cultures. However, the National Institutes of Health enquiry instigated after allegations of misappropriation of the French specimens found that the HT cell line was cultured with concentrated fluids pooled initially from individual cultures of three patients and ultimately from the individual cultures of ten patients. (Maddox, 1992) In evidence given to the enquiry, the reason given was because none of the individual cultures "was producing high concentrations of reverse transcriptase." That means not enough to convince the Gallo team of scientists or anybody else there actually was a virus in any of the individual specimens in the first place. The fact that pooled specimens produced reverse transcription is not proof of a retrovirus. The conditions may have merely changed in favour of the action of one of the cellular enzymes that performs the same trick. Or it could have been due to the HT cell line, unaided or at the behest of its HTLV-I retrovirus. The Gallo investigation found the pooling of specimens "of dubious scientific rigor." One scientist described the procedure as "really crazy." In essence, it is no different from investigating an outbreak of pneumonia by having all patients spit in separate pots and, when nothing turns up, getting them all to spit in the same pot.

Mystery number two:

The method of specific reactivity required a source of antibodies to the putative viral proteins. The logical place to obtain these was from AIDS patients -- after all, that is what the hypothesis required. The antibodies reported in the first paper appeared from two sources, a haemophiliac patient known as E.T. who had pre-AIDS and rabbits. Yes, rabbits. What precisely constituted E.T's pre-AIDS we are not told, but pre-AIDS is often generalised enlargement of the lymph nodes, a condition not invariably followed by AIDS and which is not AIDS. Thus, according to the paradigm of specific reactivity, we cannot be sure that E.T. actually had the right kind of antibodies. Rabbits do not develop AIDS and if specific antibodies to a retrovirus were to exist, they could only be produced by immunising rabbits with pure virus or, as the first Gallo group paper reported, from rabbits infected repeatedly with disrupted HIV. I hope you are beginning to see the problem. To make antibodies just to HIV, one has to inject rabbits with pure HIV. Pure virus means isolated virus and if rabbits were injected with pure virus, why should it be necessary to produce antibodies to define the isolation of virus that had already been isolated?

Mystery number three:

In the second paper, the Gallo team attempted what they called HIV isolation from 72 AIDS patients. Again, they cultured cells and detected particles and reverse transcriptase in unrefined culture fluids, and observed some protein/antibody reactions, but also added a fourth category, transmission, by which was meant finding particles or reverse transcriptase in bone marrow and other cells cultured with fluids, but not purified banded, photographed fluids, from one of the 72 starting cultures. What is enigmatic about the second paper is that HIV isolation was defined merely as detecting at least two of any of these four phenomena. The same criticism applies as in the first paper. Nothing was isolated and detection of unspecific phenomena is not surrogate isolation of a retrovirus. Even it were, this peculiar definition leads to some rather bizarre possibilities, for example, instances of virus isolation without the need to see particles or measure reverse transcriptase, for a retrovirus about as convincing as trying to sell a car without a body and an engine. Even so, loose as these criteria were, isolation was successful in only 26 of the 72 patients, that is, in only 36%. And, in case you think things have improved, there is a recent, international cooperative study reported by the World Health Organisation. In this study, by HIV isolation was meant detection of a single protein, p24, in culture fluids using a single antibody. Not only is p24 not specific for HIV (Agbalika et al., 1992; Mortimer et al., 1992), but from 224 HIV positive individuals, the success rate was a mere 37%, not significantly better than Gallo's figures a decade earlier. (WHO, 1994)

Even if the Gallo team had proved the existence of a new retrovirus, on what basis did they claim it was the cause of AIDS? Even if virus had been isolated from all patients and all patients had antibodies, which they didn't because in the fourth paper, the data showed only 88% of AIDS patients had antibodies (and on a single ELISA test which no one now regards as specific), is this sufficient proof that HIV causes AIDS? If the bank manager and his constant, faithful offsider are present at the bank robbery, is this proof that the manager robbed the bank? The Gallo papers provide no evidence whatsoever that HIV kills T4-cells or that low numbers of T4-cells is necessary and sufficient for the development of the AIDS infections and cancers and, I might add, there is still no such evidence. (Papadopulos-Eleopulos et al., 1994)

Let me finish by summarising the problem. The method of retrovirus isolation presented at the beginning flows logically from the definition of a virus. It is model of intelligibility, it is the only method, and was used for decades of research into animal retroviruses. (Sinoussi et al., 1973; Toplin, 1973) The problem is that, to date, nobody in the world has reported use of this method in AIDS patients. Without it, for example, how can one resolve the dilemma imposed by the numerous particles of stunning morphological variability present in cell cultures of AIDS patients? Even so, although some particles are the right diameter, there are no particles with the right diameter AND the projecting knobs, both integral to the definition of a retroviral particle and the latter essential to infect new cells. (Gelderblom et al., 1988; Layne et al., 1992; Levy, 1996) Yet, as I speak, there is still not even one published electron micrograph from a density gradient to tell us which, if any constituents of this zoo of particles, presents itself to be proved an infectious retrovirus. Perhaps, if someone were to look, there might not be any. Reading the literature, it is obvious that scientists everywhere have abandoned the traditional method of isolation and, under the assumed aegis of specific reactivity, claimed that two unknowns, antibodies and proteins, interact in specific pairs simultaneously betraying each other's genesis from a virus. In other words, what is the guts of what is called HIV isolation is actually no more than a chemical reaction, an antibody test, and from an antibody test, one cannot claim proof of isolation of anything. If an antibody test is isolation of a virus then the pregnancy test, which uses an antibody to detect the placental hormone beta HCG, must be regarded as placental isolation. Of course, there may be instances of specific reactivity involving viral proteins and antibodies, but the only way to prove this is to compare reactions in the test-tube with the virus of interest. Nature would then reveal specific reactivity by the fact that reactions, the virological equivalent of curdling milk, show up only when there is virus and never if there is no virus. This is crux of the matter and where the evidence for the existence of HIV begins to fall apart. To prove specific reactivity, one must first isolate the virus for use as a gold standard for comparison. One cannot adopt specific reactivity as a premise to prove the existence of a virus if one must first isolate the virus to prove the premise upon which isolation is contingent. Try as you will but the cart does not go before the horse and the Gallo argument is reductio ad absurdum.

This leaves us in a perilous quandary. What are these unknown antibodies to unknown proteins which we call being HIV positive? They could represent a virus, but that remains to be proven by isolating a retroviral-like particle and proving it is a retrovirus. It is certainly not cogent to argue that the conjunction of a number of unspecific phenomena makes one possibility a definite outcome any more than claiming that ten men, all dressed in white, hitting a ball around a paddock, must be playing cricket. They might just as well be Ku Klux Klaners playing baseball. If not a virus, then what? If someone tests positive, is this proof that a virus has been transmitted? Or is it something altogether different? Whatever these reactions mean, they do seem to be a marker for AIDS in the high risk groups, but are they just as significant in those at low or at no risk? Does just knowing you're HIV positive affect your health? Does your doctor knowing you're positive lead to treatments for a virus you may not have? Could such treatments themselves cause harm? We now know that antibodies to the germs that cause the diseases present in 90% of AIDS patients also react with the so called HIV proteins. (Muller et al., 1991; Kashala et al., 1994) Are we being fooled by antibodies that have nothing to do with a retrovirus? Are we seeing curdle from a different milk? Why, in one study, did 10% of 1300 individuals at low risk for AIDS including blood donors have antibodies to a sufficient number of HIV proteins to deem them HIV infected by the most stringent United States criteria? (Lundberg, 1988) Why do 30% of individuals transfused with HIV negative blood develop antibodies to the same p24 protein nearly every HIV researcher uses to "isolate" HIV? (Genesca et al., 1989) Why do 50% of dogs have antibodies to one or more of these same proteins? (Strandstrom et al., 1990) How come healthy, non-HIV-infected mice injected with blood from similar mice, or mice injected with extracts of a common human bowel bacterium, develop some of the same antibodies? Why does transfusion of one's own, irradiated blood produce the same antibodies? (Kozhemiakin & Bondarenko, 1992) If these data do not mean that HIV antibodies are non-specific, then there must be some completely unknown as well as very peculiar ways for men, dogs, and mice to acquire HIV infection. On the other hand, if some humans, injected with their own or someone else's blood, or mice injected with foreign cells and foreign proteins develop "HIV antibodies" but are not infected with HIV, why should gay men, IV drug users, and haemophiliacs, who are all exposed to foreign cells and/or foreign proteins, not also develop "HIV antibodies" and not be infected with HIV? Is it possible that we been misled by non-retroviral phenomena altogether? This would not be the first time. Over the mid- to late-1970s, Gallo and his colleagues claimed to have isolated the first human retrovirus, HL23V, from patients with various types of leukaemia and their evidence included a picture from a density gradient. (Gallagher & Gallo, 1975; Gallo et al., 1976) Soon enough antibodies to the HL23V proteins were found to be widespread, even amongst normal people and there was great excitement that a cause of leukaemic was at last in the offing. However, two groups of researchers then found that the antibodies were in reality directed against a wide range of naturally occurring substances, thus destroying that particular notion of specific reactivity. (Barbacid et al., 1980; Snyder & Fleissner, 1980) Overnight, HL23V vanished from the scientific literature, so much so that Gallo now never mentions it. Does a similar fate await HIV? Neville Hodgkinson (Hodgkinson, 1996), the former science and medical correspondent for the London Sunday Times, has suggested that HIV is the greatest scientific blunder of the twentieth century. If so, there are alternative theories and therapies for AIDS we would do well to consider.

Now, are you ready for that scientist? His name is Galileo Galilei, a man no stranger to heresy. Perhaps we should heed his counsel and begin to trust our own sparks. I say the sooner the better. *

References at link: http://www.virusmyth.com/aids/hiv/vtevidence.htm

[identity]

A PARADIGM UNDER PRESSURE
HIV-AIDS model owes popularity to wide-spread censorship
By Gordon Stewart

Index on Censorship (UK) Issue 3, 1999

AIDS entered the medical domain quietly in 1981 with a report in Los Angeles of five cases of severe pneumonia caused by a parasite, Pneumocystis carinii, common in animals but uncommon in humans. All five were young homosexual men who engaged in anal intercourse very frequently, with multiple changes of partners; had histories of previous attacks of gonorrhea and other sexually-transmissible diseases (STDs); and used mind-altering drugs regularly. They became fatally ill with uncontrollable diarrhea, weakness, and wasting. Also in 1981, a series of cases of an unusual form of skin cancer, Kaposi's sarcoma, was reported in New York City in young homosexual men with similar histories, many of whom also had the same kind of pneumonia together with opportunistic infections in the mouth, gullet, intestine, and skin, with enlargement of lymph glands.

Within a few months, many similar cases attracted attention in Los Angeles, San Francisco, and New York City because they were all homosexual men in their twenties who used drugs freely, either by inhaling volatile nitrites from 'popping' capsules or by injecting or ingesting heroin, amphetamines, and other illicit drugs. Although usually previously healthy except for attacks of STDs, they succumbed rapidly to debilitating illness as described above, with the same unusual pneumonia, yeasty white saliva, uncontrollable diarrhea, and other infections to which they seemed to have no immunity. They lacked energy, lost weight, and suffered pitifully before early death. This condition was described in the official publication of the US Centers for Disease Control at first as a gay-related wasting syndrome and then, after further investigation of immune status, as Gay-Related Immune Deficiency (GRID). A similar disease was noted in non-homosexual drug addicts who shared needles for heroin injection, and a similar loss of immunity -- already well recognized in patients who were rejecting skin and other surgical grafts -- was described in hemophiliac patients who began about this time to receive transfusions of the corrective Factor VIII, prepared from pooled donations of blood plasma. GRID was then renamed the Acquired Immune Deficiency Syndrome (AIDS).

Thus defined, AIDS spread rapidly in the USA in promiscuous homosexual men and drug addicts, and then in conurbations in Europe and Australia. There were no reports in females, older persons, or children until similar cases were detected in much smaller numbers in women or girls who used drugs or were partners of bisexual males. In late 1983, Science magazine published a report from the Pasteur Institute in Paris claiming discovery of a new retrovirus in a culture from an enlarged lymph gland in an otherwise asymptomatic homosexual man. Workers at the US National Cancer Institute in Washington then claimed that the new retrovirus in this culture was one which they had already isolated from many homosexual men with AIDS in the USA. The virus presumed to be present in these cultures was pronounced in 1984 by the US Secretary of Health to be the sole cause of AIDS and after some argument about priorities and patents,. named the Human Immune Deficiency Virus (HIV).

In this way, AIDS entered the public domain in headlines as a plague already causing thousands of cases in North America as the start of a lethal, global pandemic. This pronouncement -- without confirmation by isolation of the original retrovirus -- was accepted instantly by responsible medical scientists and hence by health authorities worldwide because antibodies, allegedly specific for indirect detection of HIV, were found in the blood of patients with AIDS. Wider testing supported the belief that HIV had spread beyond the risk groups defined above to the general population by heterosexual transmission. This became a dogma accepted without further question by an international consensus. Up to this point, the origins and causation of AIDS had been investigated openly and without prejudice. However, with the "discovery" of HIV as the putative, universally infectious retrovirus and the conversion of this hypothesis into a dogma by the consensus, all dissent began to be suppressed by anonymous censorship, which became absolute, amazingly pervasive, and apparently immune from disclosure of conflicts of interests.

While all this was happening, I was acting as a consultant to the World Health Organization (WHO) on social and behavioral aspects of communicable diseases. Although I accepted HIV as a possible participant in the complex pathogenesis of AIDS, I was impressed by the overriding fact that, in all countries with reliable registration procedures, full-blown AIDS was confined to the original risk groups of homosexual men and drug users, and to those -- like female partners of bisexual men and their infants -- who were passively exposed to the same risks. This trend was so invariable by 1987 that predictions based on appropriate mathematical formulae were accurate in numbers and distribution, year by year. There was no evidence whatsoever in 1987 that AIDS was being transmitted heterosexually in general populations except in headline propaganda about the scare of AIDS internationally. But I found then that, although the data and opinions that I offered to the WHO received attention internally, they were barred from publication. Meanwhile, medical literature exploded, with worldwide coverage in all media, to accommodate the consensus view that AIDS was becoming a global pandemic. Alarming figures accepted at face value by WHO from some third world countries were used to support this assertion.

In 1987, Professor Peter Duesberg, a pioneer in retrovirology at the University of California in Berkeley, suggested instead that HIV was a latent virus incapable of causing AIDS which was due, in his view, either to suppression of immunity by toxic drugs or to a recrudescence of other diseases. A fuller statement of his view, published by the prestigious US National Academy of Sciences in 1989, caused a furor. Duesberg's arguments were not debated. He was almost universally demonized but not silenced. Indeed, his dilemma became the focus of all doubts about AIDS, from whatever source. This did not help his courageous effort to promote rational debate because, by attracting irresponsible support, it enabled the consensus to discredit responsible doubts.

In 1989 also, the Royal Society organized a learned symposium on epidemiology. With few caveats, this endorsed earlier predictions of tens of thousands of cases in the UK by 1992. When I suggested that this was exactly what was not happening, the editor of the Society's Transactions generously invited me to submit my data and analysis of the problem. A four-year correspondence ensued, of questions by numerous peer-reviewers and answers by myself, which ended in 1994 when my paper was finally rejected. Among the two-inch file of correspondence amassed in that time were such comments as "Why should I read a paper by someone who believes the earth is flat?", and "the alternative proposed by the author provides no coherent criticism of the accepted position, for reasons that were well articulated in the national press following the notorious Duesberg Channel 4 program." The first comment says more, I think, about the reviewer, than about my paper, while the latter defies belief. That peer reviewers selected for their specialist knowledge should take a cue from the popular press is somewhat unusual, to say the least.

Meanwhile, the passage of time showed that my predictions made in 1989 were accurate to within 10 percent of actual registrations of AIDS, whereas those published in the symposium, official projections, and other expert quarters were exaggerated, often by orders of magnitude. It seemed that I was right for the wrong reasons whereas they were wrong for the right reasons -- a not impossible contingency, which should have provoked debate.

Instead, since 1990, Nature, Science , the New England Journal of Medicine , the British Medical Journal and other mainstream, peer-reviewed journals have preferred to reject papers by others besides my colleagues and me containing verifiable data that throw doubt on the claim that AIDS is capable of causing epidemics in general populations of developed countries by heterosexual transmission of HIV, and also falsify the hypothesis that HIV is the sole cause of AIDS. The Lancet has published some short letters but has consistently refused to publish fuller reasons for dissent. This is interesting in a journal which, since 1945, has regularly accepted papers from me on other subjects, and often invited me to draft editorials and assist with reviews. Twice I have been invited by the Royal Statistical Society to present my views and then turned down peremptorily. On many occasions, I have been asked by the BBC and other networks to talk about AIDS only to find, at the last minute, that my appearance was canceled. This happened also when a program with several distinguished experts participating made by Meditel Productions for Channel 4 was unaccountably stopped.

Secretive censorship like this is familiar to everyone who has dared to question orthodox views on AIDS. The result is that essential questions are never debated openly except in a few lesser journals, or in well-informed non-medical magazines like Reappraising AIDS and Continuum . The barrier to discussion at a UN Global AIDS Conference was breached for the first time by the (Swiss) International Forum for Access to Science in Geneva in 1998 in a marginalized session. Otherwise, the censorship maintained by the international consensus of experts in the main research councils, learned societies, official committees, and WHO is unyielding; so also are the main channels in radio, television, and the press. This censorship is not unique, but in my 57 years as a professional, I have never encountered anything like it nor did I ever think that I would in the world of medical science where, as in all other science, difference of opinion is the sine qua non of all advance.
There are many reasons for the censorship I have encountered. Different reasons for different people -- scientists profess scientific explanations for rejecting articles, editors profess editorial reasons, such as, "it's no longer news." In all, however, colleagues and I attempting to publish have met an unholy alliance intent on rejecting any papers that offer serious criticisms of the orthodoxy. There are, naturally, vested interests involved; many bodies and individuals receive high rewards for their work within orthodox AIDS science. Underlying much of this, the pharmaceutical companies have their own obvious agenda.

The mainstream journals and media to which I refer pride themselves on their independence and support for open debat, but whenever they are presented with reasonable doubts about AIDS, they close ranks like regimented clams.

Gordon Stewart M.D. serves as emeritus professor of public health at the University of Glasgow, a consultant in epidemiology and preventive medicine.