Everyone expected to rubber-stamp this. After all, this was Burroughs Wellcome. Their drug applications were always clean and thorough--no discrepancies or anomalies. By the time a drug had overcome all the regulatory hurdles to reach this stage of the approval process--and only 20% do--it was usually ready to be marketed. Itzak Brook, who chaired the FDA panel, had even alerted the agency's public-affairs officer to prepare a press release.

Brook, a spare man with delicate features, is a professor of pediatrics and surgery at the Uniformed Services University of the Health Sciences in nearby Bethesda. He had chaired the FDA's Anti-Infective Drug Advisory Committee for two years. But he had never seen anything quite like this. There wasn't an empty seat in the large room. AIDS activists were patrolling the grounds and buttonholing panelists whey they went to the bathroom, pressuring them to approve the drug. Brook and the 10 other members of the approval panel felt a tremendous burden of responsibility to do the right thing.

But as the morning wore on, Brook became increasingly uneasy. According to the testimony given that day, more patients in the AZT group had died since the study was halted. And the many blood transfusions given to patients on AZT could have accounted for the difference in survival rates.

The FDA's anti-viral chief, Ellen Cooper, a cool professional, was sharply critical of the study during her testimony. She had little more than a month to review the data--normally FDA medical officers have several months to digest this information and do a meaningful analysis--but what she found was troubling. The study had been unblinded, leaving open the possibility of biases in patient management. It alarmed her that long-term toxicity studies on animals weren't completed, so there was no telling what the consequences of AZT would be in humans over time. "Will efficacy last? Will toxicity accumulate to intolerable levels with longer exposure? Prolonged administration of an anti-retroviral agent, such as AZT, may be of more harm than benefit, she concluded. To approve this drug would represent a "significant and potentially dangerous departure from our normal toxicology requirements.

Perhaps the initial results were a statistical fluke, Brook thought. Perhaps the study was stopped prematurely. At the lunch break, he discovered other panelists shared his misgivings, agreeing that they needed more data. After lunch, Brook recalls, the FDA brought in the heavy artillery.

It was such a shocking incident that it seemed to unfold in slow motion. Researcher Peter Mansell, normally cerebral and brooding, was almost jovial as he reeled off figures from a nationwide test of ribavirin, a drug to combat AIDS. A ripple of excitement swept through the capacity crowd gathered in an unremarkable meeting room in the Washington Hilton hotel for the third International Conference on AIDS in June, 1987.

Mansell's presentation of dull scientific data didn't obscure his underlying message: ribavirin worked. HIV patients who took the drug were less likely to develop AIDS than those who didn't. "Dr. Mansell, a man shouted from the back of the room. "Do you or any of the other researchers have a financial interest in the approval of this drug of the company that makes it?

The audience erupted. Mansell, a veteran cancer researcher at M.D. Anderson Hospital in Houston, had a spotless reputation. The implication that he, or any of the scientists conducting the study, had acted unethically was outrageous.

Suddenly, another man jumped up on the podium and grabbed the microphone, a larger-than-life blur in the blinding dress whites of the U.S. Public Health Service. "Frank Young, FDA, he said, identifying himself as the commissioner of the Food and Drug Administration. Young told the stunned crowd that the FDA thought the ribavirin study was biased, perhaps even fraudulent, and that the Securities and Exchange Commission suspected ICN Pharmaceuticals, the Costa Mesa, Calif., company that made the drug, had used bogus test results to artificially inflate the price of its stock.

"It was like God coming down, recalls Peter Heseltine, who tested ribavirin at USC. He could not remember ever witnessing a government official publicly humiliating a respected researcher.

Subsequently, the FDA and the SEC launched separate investigations, raiding researchers' offices and confiscating file cabinets full of documents. Months later, they issued similar verdicts. Everyone was exonerated: The test data was deemed accurate, and no stock manipulation had occurred.

The affair still pains Heseltine, now director of the HIV clinic at Los Angeles County-USC Medical Center, where one-third of the county's AIDS patients are treated. "The humiliation fades, he says. "But the guys who literally gave their lives to do these studies and test ribavirin, the fact that their sacrifice was wasted, that's sticks with me. This was a potentially useful drug, but it was never given a chance.

n Mexico, oral ribavirin has been available since the 1980s as an over-the-counter drug ("ribavirina," ICN pharmaceuticals Spanish tradename Vilona), for treating influenza. In this form it was occasionally brought into the U.S. for HIV/AIDS patients. However, ribavirin has proven to have little if any clinical usefulness against HIV, and it can greatly increase blood levels and also toxicity of the HIV antiviral didanosine (ddI, Videx). Other interactions with nucleoside antivirals for HIV should be considered when HIV/AIDS patients use ribavirin to treat hepatitis C (see "aidsinfo" external link).

A scant six months before the conference, scientists at the National Institutes of Health and officials at the FDA had lined up behind another drug, zidovudine, nicknamed AZT for its chemical components. AZT was a chemotherapy that had been sitting in an NIH shelf for 20 years because it was expensive and toxic to produce and didn't do much against cancer. But it had a rich producer with influential friends--Burroughs Wellcome, one of the pharmaceutical giants--and the enthusiastic backing of Dr. Samuel Broder, then associate director of the National Cancer Institute, one the behemoth research facilities that compose the NIH.

As with any war on disease, there is only so much money, only so many scientists. But in the mid-80's, AIDS activists were bringing intense pressure against the political and medical establishment, including candlelight vigils on the White House lawn and sit-down strikes at NIH headquarters. The medical community, desperate for something that would alleviate patients' suffering, began to focus almost all its resources on AZT. Nothing else, aside from two similarly designed chemotherapies, ddI and ddC, has been approved for use in combatting HIV since AZT was sanctioned by the FDA in 1987. Only today, six years later, is ribavirin--along with a few other AIDS drugs--finally being tested on humans.

Until 1991, of the more than $420 million that has poured into the NIH's AIDS Clinical Trials Group, which conducts tests of experimental AIDS drugs in humans, 80% went toward studies on AZT. "We've lost many valuable years because of the sole preoccupation with AZT and its close relatives, ddC and ddI, says Michael Lange, an FDA adviser and assistant chief of infectious diseases at St. Luke's-Roosevelt Hospital in New York.

Now a new European study, the Concorde, casts doubts about whether AZT, which is used by 180,000 people worldwide and whose sales topped $385 million in 1992, should be taken by HIV-positive people who aren't yet ill. Some critics contend the drug may actually hasten the deterioration of the immune system associated with AIDS. In the post-mortems on AZT, some AIDS activists now admit that in their haste to get the drug approved, caution was swept aside.

With AIDS, an epidemic that blindsided the biomedical establishment, all these endemic problems were magnified. Scientists, desperate to conquer the disease that was sucking the life out of so many, jumped on the hypothesis that HIV was the lone AIDS assassin; they embraced AZT because it seemed to work by destroying some HIV when nothing else even came close. And because this disease hit a vocal and extraordinarily well-organized population, the scrutiny and political pressures have been intense.

But science is not always predictable. Scientific knowledge moves forward incrementally, with each new discovery built upon the bricks of the last. Many of the greatest breakthroughs--such as Alexander Fleming discovering the bacteria-fighting ability of penicillin after he saw mold forming in a petri dish in 1928--have been serendipitous. The likelihood of these fortuitous accidents increases if research is proceeding down many paths rather than intractably sticking to one road--which could be a dead end.

"I think we made a terrible mistake when we narrowed our focus, says Joseph Sonnabend, head of the Community Research Initiative on AIDS in New York, which conducts community-based tests of AIDS drugs. "Because if the role (of other factors besides HIV) had been worked out, then we might have come up with (other treatment) that could have helped people.

Many dedicated AIDS researchers, however, have wearied of all this criticism from the sidelines. "There's a fascinating phenomenon here--there's a couple hundred people who are doing the studies and generating data, and a few thousand commentators, says Douglas Richman, a top AIDS researcher and a professor of pathology and medicine at UC San Diego. "These 'experts' all say the same thing--AZT was done too quickly, and drug development is going too slowly. We can't win. Still, progress has been incredibly fast. This virus was discovered less than 10 years ago, and we have three drugs approved and a whole bunch more that look promising.

"We're very proud of the speed with which we developed AZT, says Burroughs Wellcome spokesperson Kathy S. Bartlett. "Since 1985, we've supported more than 30 million clinical trials with AZT involving more than 20,000 patients. It's the most thoroughly studied antiretroviral medication there is. People need to remember a little bit what it was like back in 1985 and '86--how hard people worked to find a treatment for this disease. AZT certainly has its limitations, but it has made a big difference in people's lives.

Nonetheless, there is a consensus that politics shackled AIDS drug development. In the competitive world of AIDS research, dissent has often been stifled, and scientists who have challenged the twin pillars of AIDS research--that HIV is the sole cause of AIDS and that AZT is its only effective combatant--find it difficult to get grants. "It's a bit like the war on cancer in Nixon's time, observes Gunther Stend, former chairman of the molecular and cell biology department at UC Berkeley. "In some instances, people who couldn't hack it in other fields moved to AIDS, where they could get funding, and forced out the good scientists.

In the early '80's, Burroughs Wellcome resynthesized AZT from a public-domain formula, saw that it prevented HIV from making an enzyme critical to its reproduction, and decided to throw its weight behind the drug. It was perhaps inevitable that AZT would become a pharmaceutical front-runner, but no one expected it to go unchallenged for so long. Some observers claim that most of the major pharmaceutical companies weren't initially interested in AIDS because the patient populations were too small to justify the research expense. Plus, viruses are wily foes--witness science's inability to conquer the common cold.

"AZT was seen as a temporary stopgap, says John James, editor of AIDS Treatment News. "Ideally, we should have gone on to fundamentally better drugs--which we have not done.

IN 1985, AFTER AZT SHOWED THAT IT was able to thwart HIV in test tubes, Burroughs Wellcome, with the blessing of the FDA, moved quickly to test the drug in people with AIDS. From the start, the tests were problematic. Patients were already desperately ill, and the drug seemed to make them even sicker. To be admitted to the tests, they had to have had pneumocystic carinii pneumonia, the No. 1 killer of people with AIDS, and their T-cell counts--the number of immune cells--had to have dropped below 200.

The study began in early 1986 with 282 patients at 12 medical sites around the country. The first step in this process was to hire principal investigators, or PI's--researchers at leading medical schools and hospitals who designed the AZT trial as a double-blind, placebo-controlled trial: Give half the patients the drug, the other half a placebo, and see which group fares best. Not even the doctors know who gets the real thing.

But the AZT trials in which 145 people with AIDS were on AZT and 137 on a placebo, were unblinded almost immediately. Patients knew right away who was getting what. The AZT pills tasted bitter, and the side effects tore up the gastrointestinal tract, causing nausea, vomiting and a loss of appetite; a severe atrophy made their muscles feel like wet spaghetti. Not to mention acne, pounding migraines, impotence and high fevers.

The People With AIDS Coalition in New York set up a hotline to analyze patients' pills. If patients weren't receiving AZT, they often bought the drug on the black market. According to Michael Callen, one of the founders of the PWA, some patients shared their pills with those on placebos out of a sense of solidarity.

Within a month, doctors also knew who was on what. According to FDA reports, nearly half the people taking AZT developed such severe anemia that they needed blood transfusions, so patient care was hardly identical. The AZT was devouring their bone marrow, which produces the immune-system cells that HIV attacks, so it was accelerating the very process it was supposed to stop. Some patients were so weak they couldn't get out of bed. Twenty-seven were taken off the drug temporarily, another 21 altogether.

The NIAID reports that, "In the mid-1980s, clinical trials enrolling patients with AIDS found that AZT given as single-drug therapy conferred a modest survival advantage compared to placebo. Among HIV-infected patients who had not yet developed AIDS, placebo-controlled trials found that AZT given as single-drug therapy delayed, for a year or two, the onset of AIDS-related illnesses. Significantly, long-term follow-up of these trials did not show a prolonged benefit of AZT, but also did not indicate that the drug increased disease progression or mortality. The lack of excess AIDS cases and death in the AZT arms of these placebo-controlled trials effectively counters the argument that AZT causes AIDS. Subsequent clinical trials found that patients receiving two-drug combinations had up to 50 percent improvements in time to progression to AIDS and in survival when compared to people receiving single-drug therapy. In more recent years, three-drug combination therapies have produced another 50 to 80 percent improvement in progression to AIDS and in survival when compared to two-drug regimens in clinical trials."[53] "Use of potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, an effect which clearly would not be seen if antiretroviral drugs caused AIDS."

Something that struck me in the article though was that AZT was shown to have anti-HIV properties, but the author continually mentioned the drug was given to AIDS patients. Maybe I am missing something?!

Originally posted by CynicalDrivel
reply to post by Xtrozero

---

That's how they used cow pox against small pox.

And that is a valid question and observation. Objectively I suppose we should all ask can one contract AIDS without ever being subjected to HIV?

We know that those who are diagnosed as HIV+ have the potential of never progressing to AIDS. Could someone healthy contract AIDS?

Leading biochemical scientists, including University of California at Berkeley retrovirus expert Peter Duesberg and Nobel Prize winner Walter Gilbert, have been warning for years that there is no proof that HIV causes AIDS. The warnings were met first with silence, then with ridicule and contempt. In 1990, for example, Nature published a rare response from the HIV establishment, as represented by Robin A. Weiss of the Institute of Cancer Research in London and Harold W. Jaffe of the U.S. Centers for Disease Control. Weiss and Jaffe compared the doubters to people who think that bad air causes malaria. "We have . . . been told," they wrote, "that the human immunodeficiency virus (HIV) originates from outer space, or as a genetically engineered virus for germ warfare which was tested in prisoners and spread from them. Peter H. Duesberg's proposition that HIV is not the cause of AIDS at all is, to our minds, equally absurd." Viewers of ABC's 1993 Day One special on the cause of AIDS-almost the only occasion on which network television has covered the controversy-saw Robert Gallo, the leading exponent of the HIV theory, stomp away from the microphone in a rage when asked to respond to the views of Gilbert and Duesberg.

Gallo: There is no organized body of science that thinks it is anything but comedy with Peter right now. That's the fact. Why does the Institute of Medicine, WHO (World health Organization), CDC (Centers for Disease Control), National Academy of Sciences, NIH, Pasteur Institute and the whole body of science 100 percent agree that HIV is the cause of AIDS? If there was anything to what Peter is saying, wouldn't it occur to you that there would be some other scientists that would agree with Peter? Can you tell me anyone?

SPIN: Walter Gilbert of Harvard.

Gallo: Wally Gilbert believes HIV doesn't cause AIDS?!!

SPIN: He says it remains an open question. He says Duesberg has shown that at least.

Gallo: Wally Gilbert said that?! You want to get that in writing? Get Wally Gilbert to say that in writing! I don't believe Wally Gilbert ever said anything of the sort. He probably doesn't know all the facts. We have had detailed study by the best qualified people and the answer is overwhelming.

[Duesberg] is absolutely correct in saying that no one has proven that AIDS is caused by the AIDS virus. And he is absolutely correct that the virus cultured in the laboratory may not be the cause of AIDS. ~Hippocrates (Sept./Oct. 1988)~

Such displays of rage and ridicule are familiar to those who question the HIV theory of AIDS. Ever since 1984, when Gallo announced the discovery of what the newspapers call "HIV, the virus that causes AIDS," at a government press conference, the HIV theory has been the basis of all scientific work on AIDS. If the theory is mistaken, billions of dollars have been wasted-and immense harm has been done to persons who have tested positive for antibodies to HIV and therefore have been told to expect an early and painful death. The furious reactions to the suggestion that a colossal mistake may have been made are not surprising, given that the credibility of the biomedical establishment is at stake. It is time to think about the unthinkable, however, because there are at least three reasons for doubting the official theory that
HIV causes AIDS.

STAGE 1 : Primary HIV infection This stage of infection lasts for a few weeks and is often accompanied by a short flu-like illness. In up to about 20% of people the HIV symptoms are serious enough to consult a doctor, but the diagnosis of HIV infection is frequently missed.

During this stage there is a large amount of HIV in the peripheral blood and the immune system begins to respond to the virus by producing HIV antibodies and cytotoxic lymphocytes. This process is known as seroconversion. If an HIV antibody test is done before seroconversion is complete then it may not be positive.

Primary HIV infection is the first stage of HIV disease, when the virus first establishes itself in the body. Some researchers use the term acute HIV infection to describe the period of time between when a person is first infected with HIV and when antibodies against the virus are produced by the body (usually 6- 12 weeks).

Some people newly infected with HIV will experience some "flu-like" symptoms. These symptoms, which usually last no more than a few days, might include fevers, chills, night sweats and rashes (not cold-like symptoms). Many other people either do not experience acute symptoms, or have symptoms so mild that they may not notice them.

Given the general character of the symptoms of acute infection, they can easily have causes other than HIV, such as a flu infection. For example, if you had some risk for HIV a few days ago and are now experiencing flu-like symptoms, it might be possible that HIV is responsible for the symptoms, but it is also possible that you have some other viral infection.

1. Pointed at the end; sharp.
2. Of or relating to a disease or a condition with a rapid onset and a short, severe course.
3. Of or relating to a patient afflicted with such a disease.

Before these facts were well understood, Robert Gallo and his followers insisted that the virus does its damage by directly infecting and killing cells. In his 1991 autobiography, Gallo ridiculed HIV discoverer Luc Montagnier's view that the virus causes AIDS only in the company of as yet undiscovered "cofactors." Gallo argued that "multifactorial is multi-ignorance" and that, because being infected by HIV was "like being hit by a truck," there was no need to look for additional causes or indirect mechanisms of causation.

All that has changed. As Warner C. Greene, a professor of medicine at the University of California, San Francisco, explained in the September 1993 Scientific American, researchers are increasingly abandoning the direct cell-killing theory because HIV does not infect enough cells: "Even in patients in the late stages of HIV infection with very low blood T4 cell counts, the proportion of those cells that are producing HIV is tiny-about one in 40. In the early stages of chronic infection, fewer than one in 10,000 T4 cells in blood are doing so. If the virus were killing the cells just by directly infecting them, it would almost certainly have to infect a much larger fraction at any one time."

Gallo himself is now among those who are desperately looking for possible co-factors and exploring indirect mechanisms of causation. Perhaps the virus somehow causes other cells of the immune system to destroy T-cells or induces the T-cells to destroy themselves. Perhaps HIV can cause immune-system collapse even when it is no long present in the body. As Gallo put it at an AIDS conference last summer: "The molecular mimicry in which HIV imitates components of the immune system sets events into motion that may be able to proceed in the absence of further whole virus."

Leading AIDS researchers at the Centers for Disease Control and Prevention now offer similar views, and even Gallo has lightened up a bit. He now says, “Some of Joe Sonnabend’s postulations catalyzed us to move faster” in studying the immune system’s response to HIV. As for his 1987 repudiation of AIDS cofactors, Gallo now says, “I was brasher and younger then.” He still argues that no cofactor is necessary for AIDS, but says he believes several may contribute to disease progression.

Harden: Dr. Gallo, it has been some time since we conducted the earlier interviews. We will try to pick up where we left off last time. We were talking about your laboratory's research on the basic molecular biology of HIV. I am interested in some of the spin-offs of the research. I know that you found one or two new human herpesviruses which might be cofactors in AIDS. I would like you to describe the whole idea of cofactors and whether these new herpesviruses are now viewed as cofactors in HIV infection.

Gallo: Just talking generally, the spin-off in terms of the herpesvirus actually did not come out of molecular biology; it came more out of virology/biology experiments with a design, in fact, a plan, to discover new herpesviruses. As usual, the general idea bears fruit, but it is never for the reasons that you predicted. I will come to that in just a second and then we will talk about cofactors.

But, in terms of molecular biology spin-offs, I think the biggest ones are the discovery of new genes within HIV, within the genome of HIV, that have rather novel molecular mechanisms of action, that have, in fact, contributed to molecular biology. Some of those new genes have also become targets for people trying to interfere with HIV replication. Some of them are genes, the tat gene being an example, essential to HIV replication.

Let us turn to the issue that you wanted to talk about, the cofactors. Many people have the idea that if you do not always get a disease from a microbe that causes the disease, then either the microbe does not cause the disease, or something else is required as a cofactor. But this is not true. A microbe may cause disease in a very small percentage of people. That is usually the case. In fact, the usual case is that it causes no disease at all. The determination of whether somebody gets disease or not from a microbe depends on a very large number of factors.

The number one factor is, of course, the nature of the microbe. Some are efficient in causing disease, some are not.

Second, it sometimes depends on the host. Most of the time it depends on genetic factors in the host. Sometimes it depends on chance events–the dose–and if that seems trite, there are experimental examples that actually prove that in a number of systems.

Staying with retroviruses, it is clear that in nature–I probably used this example in earlier discussions, but I will use it again–when a cat gets infected by the feline leukemia retrovirus, it usually does not get leukemia; it is usually carrying the virus without leukemia occurring. My belief is that if cats lived long enough, let us say, for 100 years, the majority would get leukemia. There is a chance of genetic events occurring due to the integration of the provirus that eventually leads to leukemia. But it is known that if you inoculate the right dose in a young enough kitten, you get leukemia all the time. This is typical. The same is true with chicken leukemia retrovirus. If you inoculate newborn chicks with a proper dose, most will get leukemia. But, in nature, when chickens get infected as adults, it is unusual for them to get leukemia. So, it sometimes depends on the age of the individual, or on the age of the organism, or on the dose of the microbe. These are chance events. People often do not appreciate that.

The third is that sometimes it depends on the genetics of the host and how it handles a given microbe.

The determinants, for example, of HIV, are still unknown, but it could be that there is so much virus variation that different variants may have different virulence. But all the other factors I have just listed may be important.

Now, in my mind, when we talk about cofactors, we have to give a definition. Most people, when they think of cofactors, start to believe that you mean something that is absolutely required to get the disease. I would divide them into categories. I would say that there are essential and non-essential cofactors or, maybe it would be better, to call something a cofactor if it is truly required. Other things are just catalysts or promoters of the probability of getting disease and of the probability of the disease being more rather than less vicious, or more acute rather than it taking a long time to develop the disease. Let us go directly to HIV.

But researchers have not been able to confirm experimentally any of the increasingly exotic causal mechanisms that are being proposed, and they do not agree about which of the competing explanations is more plausible. When The New York Times interviewed the government' s head AIDS researcher, Anthony Fauci, in February, reporter Natalie Angier summarized his view as a sort of stew of all the leading possibilities: "It [HIV] overexcites some immune signaling pathways, while eluding the detection of others. And though the main target of the virus appears to be the famed helper T-cells, or CD-4 cells, which it can infiltrate and kill, the virus also ends up stimulating the response of other immune cells so inappropriately that they eventually collapse from overwork or confusion." No other virus is credited with such a dazzling repertoire of destructive skills

Perhaps it is the HIV scientists who are collapsing from overwork or confusion. The theory is getting ever more complicated, without getting any nearer to a solution. This is a classic sign of a deteriorating scientific paradigm. But as HIV scientists grow ever more confused about how the virus is supposed to be causing AIDS, their refusal to consider the possibility that it may not be the cause is as rigid as ever. On the rare occasions when they answer questions on the subject, they explain that "unassailable
epidemiological evidence" has established HIV as the cause of AIDS. In short, they
rely on correlation.

The seemingly close correlation between AIDS and HIV is largely an artifact of the misleading definition of AIDS used by the U.S. government' s Centers for Disease Control. AIDS is a syndrome defined by the presence of one or more of 30 independent diseases-when accompanied by a positive result on a test that detects antibodies to HIV. The same disease conditions are not defined as AIDS when the
antibody test is negative. Tuberculosis with a positive antibody test is AIDS;
tuberculosis with a negative test is just TB.

The Centers for Disease Control and Prevention (CDC) uses a definition for AIDS that includes a positive HIV blood test along with either a major opportunistic condition or a blood CD4 count of less than 200/mm3. (A normal CD4 count is about 500 to 1,500 cells per cubic millimeter of blood – written mm3.) The opportunistic conditions incl

The Mayo Clinic offers this definition for AIDS:

AIDS is a chronic, potentially life-threatening condition caused by the human immunodeficiency virus (HIV). By damaging your immune system, HIV interferes with your body's ability to fight the organisms that cause disease.

The WHO maddeningly offers this:

Since 1982, many different definitions have been used for national and international reporting. The following list of documents, mostly in PDF format, gives an overview of the most commonly used definitions. We have also included an Excel file with a list of WHO Member States with definitions they are currently using.

Continued...

The 1985 WHO AIDS surveillance case definition was heavily criticised, for both medical and political reasons. The 1994 expanded World Health Organization AIDS case definition was introduced in 1994 to incorporate the statement that HIV testing should be done. However, if testing was unavailable, then the Bangui definition should be used.

The skewed definition of AIDS makes a close correlation with HIV inevitable, regardless of the facts. This situation was briefly exposed at the International AIDS Conference in Amsterdam in 1992, when the existence of dozens of suppressed "AIDS without HIV" cases first became publicly known. Instead of considering the obvious implications of these cases for the HIV theory, the authorities at the CDC, who had known about some of the cases for years but had kept the subject under wraps, quickly buried the anomaly by inventing a new disease called ICL (Idiopathic CD4+Lympho-cytopenia)--a conveniently forgettable name that means "AIDS without HIV."[/ex]

I have all ready linked a page briefly describing ICL and Maslo and I briefly debated the ramifications of this, but it rapidly turned into a debate over the toxicity of AZT, because as Reason has all ready pointed out, this issue just keeps getting more complex and more complex.

There are probably thousands of cases of AIDS without HIV in the United States alone. Peter Duesberg found 4,621 cases recorded in the literature, 1,691 of them in this country. (Such cases tend to disappear from the official statistics because, once it's clear that HIV is absent, the CDC no longer counts them as AIDS.) In a 1993 article published in Bio/Technology, Duesberg documented the consistent failure of the CDC to report on the true incidence of positive HIV tests in AIDS cases. The CDC concedes that at least 40,000 "AIDS cases" were diagnosed on the basis of presumptive criteria-that is, without antibody testing, on the basis of diseases such as Kaposi's sarcoma. Yet these diseases can occur without HIV or immune deficiency. Perhaps some of the patients diagnosed as having AIDS would have tested negative, or actually did test negative, for HIV. Physicians and health departments have an incentive to diagnose patients with AIDS symptoms as AIDS cases whenever they can, because the federal government pays the medical expenses of AIDS patients under the Ryan White Act but not of persons equally sick with the same diseases who test negative for HIV antibodies.

Duesberg had argued that the HIV virus did not meet Koch's postulates, but members in this site claim this has been "debunked", and of course "AIDSTruth" "debunks" this by simply arguing the opposite and declaring that HIV does meet Koch's postulates, and how is this so? Why by ignoring the "non-HIV AIDS" patience and declaring them victims of ICL!

Avert offers this explanation:

The definition of AIDS usually requires a positive HIV test. This means that any connection between HIV and AIDS is artificially strengthened because any cases of "HIV-free AIDS" are discounted. In other words, the definition already assumes that HIV causes AIDS, so it can't be used to prove that theory. However, it is possible to redefine AIDS without reference to HIV or even to any other diseases.

The alternative definition of AIDS requires a CD4+ cell count consistently below 200 cells per cubic millimetre of blood, which cannot be explained by any factor other than HIV (such as cancer, malnutrition, radiation or chemotherapy). No HIV test is required.

It turns out that the vast majority of people diagnosed with AIDS fit these criteria. They form a population that barely existed before 1980, but which now numbers hundreds of thousands in the USA and Europe alone. People with such severe immune deficiency are at very high risk of developing serious illnesses and usually die within months (unless they take antiretroviral drugs).10 11 12 We can use this simple, unambiguous definition to test the association between HIV and AIDS.13 14

Continued...

The claimed correlation between HIV and AIDS is flawed at an even more fundamental level, however. Even if the "AIDS test" were administered in every case, the tests are unreliable. Authoritative papers in both Bio/Technology (June 1993) and the Journal of the American Medical Association (November 27, 1991) have shown that the tests are not standardized and give many "false positives" because they react
to substances other than HIV antibodies. Even if that were not the case, the tests at best confirm the presence of antibodies and not the virus itself, much less the virus in an active, replicating state. Antibodies typically mean that the body has fought off a viral infection, and they may persist long after the virus itself has disappeared from the body. Since it is often difficult to find live virus even in the bodies of patients who are dying of AIDS, Gallo and others have to speculate that HIV can cause AIDS even
when it is no longer present and only antibodies are left.

Just as there are cases of AIDS without HIV, there are cases of HIV-positive persons who remain healthy for more than a decade and who may never suffer from AIDS. According to Greene's article in Scientific American, "It is even possible that some rare strains [of HIV] are benign. Some homosexual men in the U.S. who have been infected with HIV for at least 11 years show as yet no signs of damage to their immune systems. My colleagues . . .and I are studying these long-term survivors to ascertain whether something unusual about their immune systems explains their response or whether they carry an avirulent strain of the virus."

The faulty correlation between HIV and AIDS would not disprove the HIV theory if there were strong independent evidence that HIV causes AIDS. As we have seen, however, researchers have been unable to establish a mechanism of causation. Nor have they succeeded in confirming the HIV model by inducing AIDS in animals. Chimps have repeatedly been infected with HIV, but none of them have developed AIDS. In the absence of a mechanism or an animal model, the HIV theory is based only upon a correlation that turns out to be primarily an artifact of the theory itself