By Matt Irwin


Disagreement about HIV's role in causing AIDS has been curiously absent from public and scientific debate, even though many of the 700 M.D.'s and/or Ph.D.'s of The Group for the Scientific Reappraisal of the HIV/AIDS Hypothesis have published their reasons for their concern (Philpott 1999). Members of this group include current and former professors of molecular and cell biology at Harvard, Berkeley, and other prestigious universities, as well as two Nobel Prize winners in chemistry, Walter Gilbert and Kary Mullis. HIV is a "retrovirus", and Peter Duesberg, one of the earliest people to call for reappraisal, has been called the "father of retrovirology". David Rasnick, the president of the Society for the Scientific Reappraisal of AIDS, holds nine patents on protease inhibitors, the drugs claimed to have saved many people from the brink of death. And yet, Dr. Rasnick adamantly maintains that these drugs are contributing to, or directly causing their deaths rather than helping them. For a topic which has become so entrenched in the national and world-wide mindset, such a large number of dissenting voices among people with the highest credentials in their fields is unusual, to say the least, and yet researchers, health professionals, and the public have not been informed about the magnitude of the debate, or about the reasons why these dissenting scientists are questioning conventional dogma.

HIV is claimed to cause a wide variety of symptoms in people who test positive on the HIV antibody test, but even for the most common symptoms, like immunosuppression and low CD4 T-cells, there is continued difficulty and disagreement in understanding the mechanism involved (Balter 1997), a fact that has led the original discoverer of HIV, Luc Montagnier, to state that he does not think HIV can cause AIDS without other unidentified cofactors (Balter, 1991).

Problem#1: Mechanism of Action

An article in the journal, Science by Balter (1997) gives a description of the ongoing state of confusion and disagreement among the leading scientists regarding HIV's proposed mechanisms of action. This article by Balter describes a conference in the fall of 1997 that focused specifically on the disagreement and conflicting reports regarding how HIV supposedly kills CD4 T-cells. Here is an introductory comment from the article that summarizes the problem:

It might be said that AIDS researchers know the virus that causes the disease, HIV, inside and out. They have isolated its proteins, sequenced its genome, and identified the receptors it uses to dock onto the CD4 T lymphocytes that are the viruses primary target. Yet the central mystery of AIDS remains unresolved: How does the virus cause the severe loss of CD4 T-cells, which wrecks the immune system, that is the hallmark of the disease? (p.1399)

The article also quotes Harvard Medical School professor of immunology Paul Johnson, who is one of the leading figures in this area of research:

We are still very confused about the mechanisms that lead to CD4 depletion, but at least now we are confused at a higher level of understanding. (Balter 1997, page 1400).

The reason for this confusion, as outlined in the article, is primarily because there are competing hypotheses, none of which has held up under scrutiny. This situation is not at all new to HIV, and has actually plagued it since Robert Gallo first claimed in 1984 that it killed CD4 T-cells directly, as other viruses do, by direct rupturing of the cell. It quickly became clear that this was not possible, however, as researchers discovered that this did not occur in test tube experiments. Also, there were extremely low levels of HIV in people's blood which were insufficient to explain any lowering of CD4 counts, let alone the dramatic lowering observed in people diagnosed with AIDS. The mechanisms proposed originally by Robert Gallo have had to be abandoned, only to be replaced by new theories which are now in the process of being abandoned, as well (Balter 1997, Gorochov 1998, Grossman 1997, Pakker 1998, Roederer 1998).

A detailed summary of problems with the idea that HIV can damage T-cells, as well as problems with several other hypotheses about HIV, was published in the journal, Genetica (Papadopulos-Eleopulos et al. 1995). The article, which is entitled, "A critical analysis of the HIV-T4-cell-AIDS hypothesis" argues that HIV cannot harm T-cells, and that HIV cannot harm the immune system. The authors, who are professors of biophysics and pathology at the University of Western Australia and the Royal Perth Hospital, are members of the group of scientists who are openly calling for a reappraisal of the causes of AIDS.

The "viral load" hypothesis

Two papers published in 1995 in the journal, Nature, appeared to resolve the dilemma of either not being able to find any actual HIV particles, or only finding extremely small quantities of HIV, in people diagnosed "HIV positive" (Ho 1995, Wei 1995). They used a new genetic detection system, called "quantitative PCR", which relies on a complex mathematical formula to quantify the amount of virus in people's blood. This abstract quantification system is what is still used today to find what is called a person's "viral load", and has become a major method used by clinicians to determine the health status of people diagnosed HIV-positive. Contrary to what most people believe, however, PCR does not actually directly detect any intact viral particles, but instead is entirely based on the detection of tiny fragments of HIV's genetic material. Thus, "viral load" is not found by counting even one single intact particle of HIV, but rather by using a complex mathematical system of estimation. This quantification system has serious problems that have been largely ignored, in spite of being clearly reported in the medical literature, and yet it has become the primary marker of health both in research as well as in treatment decisions with people diagnosed HIV positive.

How many HIV particles does "viral load" really represent?

Viruses can only cause damage if they are infectious. That is how they are supposed to cause damage, by infecting cells and then causing cell death. Researchers attempting to see what proportion of the huge numbers of HIV reported by quantitative PCR represent active, infectious viruses, have found that as few as 1 in 10 million are actually infectious. This is done by "culturing" the virus, which usually means trying to infect other cells with it. The way that researchers try to find out if other cells are infected is by looking for surrogate markers of HIV, which has problems that will be discussed in the section entitled "Problem #7: How Reliable Are HIV Antibody Tests?"

A virus that cannot infect another cell is essentially sterile, since it cannot harm any cells if it cannot infect them. Here are some comments on the results from one major study published in Science in 1993, where researchers found that the vast majority of "viral particles" found by viral load/quantitative PCR were non-infectious (Piatak 1993):

Circulating levels of plasma virus determined by (quantitative) PCR correlated with, but exceeded by an average of 60,000-fold, numbers of infectious HIV-1 that were determined by quantitative culture of identical portions of plasma... Total virions have been reported (in other studies) to exceed culturable infectious units by factors of 1000 to 10,000,000, ratios similar to those we observed in plasma. (page 1752)

This means that these researchers estimated that only about 1 in 60,000 "virions" found using "quantitative" PCR were actually infectious, and that other studies have found similar results when examining the meaning of a person's "viral load" in more detail. They also admit in a footnote that the actual amount in their study is likely to be even lower than 1 in 60,000.

Even more surprising, they were not able to culture any virus at all in more than half (35 of 66) patients, even though all the patients studied had large "viral loads". People with no infectious virus at all had "viral loads" as high as 815,000 "copies per milliliter"! The study subjects had all tested positive on the ELISA and western blot antibody tests, the two tests currently used to diagnose people as being "HIV-positive", they all had high "viral loads", and yet the majority of them had no "culturable infectious units" of HIV. Results like these bring up some obvious questions about who proved that testing positive on antibody tests meant that a person had an active infection, and how they proved it. Unfortunately, in the world of HIV science, the answers to these questions remains elusive.

This difficulty in finding active HIV particles is not surprising to those familiar with the literature on this topic, since similar results have been found by many researchers who have tried to confirm the presence of HIV in people's blood (Chiodi 1988, Gallo 1984, Learmont 1992, Popovic 1984, Sarngadharan 1984, Schupbach 1984). Based on results like these, the abstract system used by "quantitative PCR technology", in which tiny bits of genetic material are amplified by a complex set of mathematical equations into frighteningly large numbers, is highly questionable. Most people diagnosed HIV positive, even with high viral loads, may have no infectious virus in them, at all. As will be discussed in the next section, many people who test negative on both the ELISA and western blot have substantial viral loads when tested using "quantitative PCR", which brings up the question of whether PCR is capable of mistaking tiny bits of a person's own genetic material for genetic material of HIV. This is more likely when one considers that the human genome has about 3 billion base pairs, while that of HIV has only about 10,000, and that PCR only looks for about 3% of HIV's genetic material, or about 300 base pairs. It appears likely that some of the 3 billion base pairs in the human genome could happen to have the same coding sequence as that attributed to HIV, and could produce RNA that would be detected by PCR technology.

As mentioned before, "viral load" has become the only measure of health in clinical trials of new drugs. News reports about people "doing well" on the new anti-retroviral cocktails often speak about people whose "disease is controlled" on the drugs, or whose "disease came roaring back" after stopping the drugs. What they are referring, however, to is not clinical health, at all. Careful reading of such news articles reveals that the person in question often feels much better off of the drugs, due to their often extremely high toxicity. The description of the disease "roaring back" is based entirely on the fact that their "viral loads" have risen, even though they may be feeling much better.

As often occurs in studies like this one that fundamentally challenge HIV science, however, the authors (Piatak et al.) appear unphased by their results, and focus completely in the discussion section of their paper on other aspects of their study that fit better with conventional views about what it means to be "HIV-positive" and to have a high "viral load". They do not even mention in their discussion that the majority of their subjects had no infectious viral particles. While it is of questionable significance to have such high "viral loads" if only a tiny minority, or none of the particles is actually infectious, it can still be terrifying to be told that one has several million copies of HIV in every milliliter of blood. This type of news has a powerful symbolic meaning to clinicians and patients, which can result in profound immunosuppression whether HIV is causing damage, or not.

High viral loads in people who are "HIV-negative"

Adding further confusion to the issue, PCR technology has found extremely high "viral loads" in people who are HIV negative by the antibody tests. For instance, Schwartz et al. (1997) found a person with a viral load of 100,000 who was negative on the ELISA and Western Blot antibody tests. The authors concluded that lab error had led to this reading, which would be a reasonable explanation but for the presence of other studies finding similar results. Another study, for example, examined the blood of health care workers who accidentally received needle sticks of HIV-infected blood. This was published in the Journal of Infectious Disease in 1994 (Gerberding et al.). As will be described in detail in the section entitled "Can HIV be transmitted through needle sticks?", only a very tiny risk existed that any of them would seroconvert to HIV-positive status, a risk that is within the error of the antibody tests. They attempted to track the status of these health care workers by doing regular PCR's on them, as well as other tests, and found that false positive PCR's occurred in about one of every thirty people. Since only about 1 in 240 people in the general population of the United States are estimated to be "HIV positive", this means that a random screening would turn up nearly ten times as many "false positives" as "true positives".

More questions about David Ho's hypothesis

David Ho's hypothesis did not stop with PCR and "viral load", however. He also hypothesized that the immune system was waged in a life-and-death struggle, with the person's own CD8/ cytotoxic T-cells killing CD4 T-cells. The CD8 cells were killing the CD4 cells, according to Ho, because the CD4 cells were infected with HIV. This is how Ho et al believed that CD4 T-cell depletion was occuring, and it also explains the elevated CD8 cells often observed in AIDS, since lots of CD8-cells would be produced by the body. He also claimed that billions of CD4 cells were being produced daily in a desperate attempt to replace the infected ones which were being killed. This would explain why CD4 cells in test tubes do not die when infected with HIV, since the entire process must take place inside a human body where CD8 cells can be programmed to attack. Although they could only provide circumstantial evidence for this hypothesis, it quickly caught the attention of the media as well as the scientific community, and led to David Ho's selection as Time's "Man of the Year" award for 1995.

This theory for the mechanism of action of HIV has also failed to withstand the test of time. An article by Roederer (1998) gives a good overview of the reasons why David Ho's theory is no longer considered viable by most scientists who focus in this area of research.

These reports (Ho 1995, Wei 1995) received enormous publicity in the popular press, with vivid portrayals of a "massive immunological war" in which billions of CD4 T cells were produced and destroyed daily. However, there has been considerable debate about this simple hypothesis. The Nature papers ignited a heated controversy that resulted in publication of several well-designed studies which raised serious doubts about this "war". In this issue of Nature Medicine, reports by Pakker et al (1998) and Gorochov et al (1997) provide the final nails in the coffin for models of T-cell dynamics in which a major reason for changes in T cell numbers is the death of HIV-infected cells. (page 145)

Roederer does not question the hypothesis that HIV is causing AIDS, however, which he appears to accept without question. He goes on in his article to discuss new mechanisms proposed by a different set of researchers, which he thinks are more plausible.

It seems impossible that fifteen years of research with so many billions of dollars devoted to it would not reveal a more clearly delineated mechanism of action. As will be outlined in AIDS and Voodoo Hexing*, however, the mechanisms by which chronic stress affects the immune system, are much better understood, as are the mechanisms of toxicities from AZT and other drugs used to treat people diagnosed HIV positive.

Problem #2: Low CD4 Counts are Common in People Who Are HIV-Negative

Low CD4 T-cell counts have been called the "signature" of HIV, and yet research has found that low CD4 counts are a non-specific reaction to any state of psychological or physical stress. The same is true of the CD4/CD8 ratio, which is found to be inverted in people diagnosed with AIDS. An "inverted" ratio simply means that there are a lot more CD8 cells than CD4 cells, resulting in a ratio of less than 1, while normally the opposite is true, and the ratio is greater than 1.

Conditions found to cause profoundly lowered CD4 counts include a variety of viral illnesses, bacterial infections, sepsis, septic shock, multiple organ system failure, tuberculosis, coccidioidomycosis, burns, trauma, and transfusions (Feeney 1995). Only a few of these studies will be reviewed here. CD4 counts in people with these conditions often dip below the level that would be considered "AIDS-defining" in a person who is HIV-positive.

Low CD4 counts in mononucleosis

Mononucleosis, commonly called "mono", is a common viral illness, especially in young people of college age, and can last for several months. It usually causes cold and flu symptoms, and fatigue. In 1981 a group of researchers looked at CD4 and CD8 counts in ten consecutive patients with acute mononucleosis, and compared their counts with those of ten healthy volunteers (Carney 1981). The CD4 counts in people with mononucleosis were greatly reduced, with the healthy volunteers having 73% more cells per ml than was found in people with mono. The CD8 cells in people with mono were increased, resulting in an inverted CD4/CD8 ratio in every single patient. The average ratio was only 0.2, compared to the normal average of 1.7 found in controls. Of the nine patients whose CD4 counts were measured, the three with the lowest CD4 counts had 194, 202 , and 255 cells/mm3. People who are HIV positive with less than 200 CD4 cells are immediately diagnosed with AIDS, and the assumption is made that HIV is attacking their T-cells. This assumption seems ill-advised in light of findings like this one, especially since people diagnosed HIV positive often suffer from more infections than the general population.

Low CD4 counts in chronic illness

More recently, another group of researchers looked at CD4 counts in HIV negative people, this time in 102 consecutive Intensive Care Unit (ICU) patients who were admitted for a variety of reasons (Feeney 1995). Fully 30% of these patients had CD4 counts less than 300. The authors do not discuss how many were below 200, the level diagnosed as "AIDS" in people with a positive HIV antibody test. They also did not find that low CD4 counts were linked with poor health, nor were they linked with a poor prognosis. Here are the author's comments on their findings.

Our results demonstrate that acute illness alone, in the absence of HIV infection, can be associated with profoundly depressed lymphocyte concentrations. Although we hypothesized that this depression would be directly related to the severity of illness, this was not seen in our results. The T-cell depression we observed was unpredictable and did not correlate with severity of illness, predicted mortality rate, or survival rate. This study was consistent with prior studies that have shown similar decreases in T-cell counts in specific subsets of acutely ill patients. These subsets included patients with bacterial infections, sepsis, septic shock, multiple organ system failure, tuberculosis, coccidioidomycosis, viral infections, burns, and trauma patients. Most of these studies reported decreases in lymphocyte populations, some of which were severe and included CD4/CD8 ratio inversions...

In the largest study to date of hospitalized patients, Williams et al (1983) evaluated T-cell subsets in 146 febrile patients with serious acute infections... with 19 of 45 patients having a CD4 count of less than 300 per microliter.

We also found that CD4 counts were linearly related to total lymphocyte concentrations, as Blatt et al. (1991) reported in HIV-positive patients. (page 1682-1683)

Curiously, although these researchers did find the low CD4 cell counts as seen in AIDS, they did not find that such counts were very good measures of immune function. One major double-blind study of AZT use in over 2000 HIV positive people found the same result. AZT increased the number of CD4 T-cells, but in spite of this people who received AZT died at a faster rate (Seligman 1994). This study was the major reason AZT fell out of favor as the sole drug used on HIV positive people, but it also seriously questioned the value of CD4 T-cells as a marker for immune health. This study, commonly referred to as the Concorde Study, will be reviewed in "Can AZT and other anti-HIV drugs cause AIDS?", where the toxicities of anti-HIV medications are discussed.

Low CD4 counts caused by drug injections

In an article published in 1987 in the journal, AIDS, lymphocytes were found to be reduced in HIV positive injection drug users as a direct function of how many injections they received (Des Jarlais et al. 1987). The authors comment in their abstract:

Continued drug injection was associated with the rate of CD4 cell loss... While it is not possible to distinguish the mechanism underlying the relationship between continued drug injection and CD4 cell loss, seropositive IV drug users should be warned that continued injections may lead to increased HIV-related immunosuppression. (page 105)
The authors also found that HIV positive individuals had lower CD4 counts, on average, than HIV negative individuals, which they assume was caused by HIV. Such correlations have been used repeatedly as evidence that HIV kills CD4 T-cells, but this type of evidence (correlation) is the weakest evidence that science can provide, especially since there were a large number of HIV-positive individuals with higher CD4 counts than many HIV-negative individuals. There are also many other explanations for the general trend of lowered CD4 T-cells in HIV-positive IV drug users. For example, the study above by Bruneau et al (1997) suggests that increased injections are associated with increased risk for seroconversion, even when clean needles from needle exchange programs are used. Since we see here that increased drug injections are also associated with lower CD4 T-cell counts, it is very possible that both seroconversion to HIV-positive status and lower CD4 T-cells are caused by increased drug injections, not by a virus. This also fits the hypothesis that testing positive on the antibody tests is a non-specific marker for an activated immune system, possibly due to injecting foreign proteins or to other infections, which puts cells under stress. We have already seen that all sorts of infections cause lowered CD4 T-cell counts and inverted CD4/CD8 ratios. Another explanation is that the diagnosis, HIV-positive, can cause emotional and psychological stress, which in turn can cause inverted ratios and lowered CD4 T-cell counts.

Problem #3: HIV Rates Do Not Reflect an Infectious Epidemic

Another major problem with AIDS science is that the official estimates for the number of people in the United States who are HIV positive have never actually resembled an epidemic. One of the first estimates of HIV prevalence in the US was published in the New England Journal of Medicine in 1985. Sivak and Wormser (1985) estimated that about 1,765,470 people in the United States were infected at that time. A few years later the Centers for Disease Control in Atlanta, Georgia estimated only about 1,500,000, a drop of nearly 300,000 cases. Today the estimates hover around 750,000 to 1,000,000, representing a further drop of at least 30%. An article in the Washington Post on September 2, 1997 commented on these confusing figures:

The most recent estimate of the number of Americans infected (with HIV), 750,000, is only half the total that government officials used to cite over a decade ago, at a time when experts believed that as many as 1.5 million people carried the virus. They later revised that figure, saying that in the mid-1980's only about 450,000 people were infected. (Okie 1997).

Similar results were reported by Katz et al (1997) for HIV infection rates in San Francisco, supposedly the "epicenter of the epidemic". They found that the rates of new HIV infections peaked in 1982 at 7500, long before the introduction of any safe sex campaign and even longer before the introduction of anti-HIV drugs. The rates dropped quickly, finally plateauing at only 500 new infections every year from 1988 through 1997.

Another study found that HIV rates among applicants to a government youth social service program, Job Core, were dropping steadily during the 1990's (Valleroy 1998). All 357,443 applicants over the seven year period from 1990, to 1996 were tested for HIV antibodies. The rates for both female and male applicants in 1996 were half the rates found in 1990. Curiously, the authors still refer in their opening line to HIV as an "epidemic among youth in the United States", even though the rates of HIV positives had been cut in half in only six years.

If HIV rates have dropped in the United States, what about AIDS rates?

The number of AIDS deaths and new AIDS cases, according to the CDC, did rise steadily during the 1980's in a manner resembling an epidemic. This does not prove that the epidemic was infectious in nature, however, and the rise could also be explained by more and more doctors becoming aware of how to diagnose AIDS, as well as increased use of the HIV antibody test which occured during those years. The number of new AIDS cases continued to increase each year until 1993, at which point the number of new AIDS cases began to decline, according to the CDC's 1998 Year-End HIV/AIDS Surveillance Report. Shortly after that, as would be expected, death rates from AIDS also began to fall. This decrease in death rates began in the end of 1994 and the beginning of 1995. The common explanation for this fall in death rates, however, completely overlooks this obvious correlation, and gives all the credit to the introduction of protease inhibitor combination therapies, which were introduced in 1995. Since the fall in new AIDS cases occured in 1993, protease inhibitors could not possibly have made a difference. As will be discussed in "Can AZT and other anti-HIV drugs cause AIDS?", there are no randomized trials showing statistically significant reductions in death rates by using these drugs. In addition, only two such trials have been published, and they both showed considerable toxicity, with 50% of people having chronic diarrhea, and another 50% experiencing chronic nausea from taking the drugs.

The number of new AIDS cases, and deaths from AIDS, would have begun falling years earlier if the definition of AIDS had not been continually updated to include more and more conditions that were formerly not considered "AIDS-defining". These included conditions like low CD4 T-cell counts and cervical cancer. The final definition change, which occured in 1993, doubled the number of cases of AIDS overnight by including people who had low T-cell counts, but who had no opportunistic infections. In other words, these people were still in good health, but were now defined as having AIDS. Low CD4 cells are not by any means unique to AIDS, and occur in a variety of conditions including other viral illnesses and chronic psychological stress. Thus, much of the appearance of an epidemic depended on the changing of the definition of AIDS to include more and more people, rather than by having more and more people develop a current "AIDS-defining" condition.

The "Epidemic" in Africa is based entirely on inflated predictions that have not come true, and were likely based in racist stereotypes.

Africa is commonly pointed to as an example of rampant spread of HIV, and has been repeatedly presented as what will happen in the future to other countries where the "epidemic" is considered to be relatively new. African AIDS is covered in more detail in "A Critical Reappraisal of African AIDS Research and Western Sexual Stereotypes", an article written by Charles Geshekter, a professor of African History at California State University whose research has focused on AIDS in Africa for many years. He argues that the widely believed stories about Africa are primarily products of overactive imaginations and misplaced financial incentives. While it is certainly true that many people in Africa are suffering and dying, he argues that they are dying of the same illnesses they always have, including malnutrition, lack of public sanitation, and resulting infectious diseases. Death rates have not changed in Africa, and the populations continue to rise, something that would be unlikely if the media proclamations about Africa were true. The only places where increases in death rates has occurred are countries that have been torn by drought and economic hardship. (Geshekter 1998)

The statistics for African AIDS are even more tenuous than those in the United States, because the HIV antibody tests are rarely used there. They are simply too expensive. Since Africa was thought to have infection rates as high as 25% over ten years ago, one would expect that about a quarter of the population would have died by now, something that is very far from the truth. In fact, as Dr. Geshekter's paper documents, the World Health Organization's Weekly Epidemiological Record reported in November 1998 that the cumulative number of AIDS cases in Uganda, a country that has been called the "epicenter" of the African AIDS "epidemic", to be only 53,000 over the 15 year period from 1982 to 1997. The cumulative death rates reported for other countries were much smaller, with the exception of Tanzania. While it is possible that these estimates are mistaken, it would be expected that someone would document this fact, rather than just claim that it is mistaken because of widely believed media reports. Even these 53,000 deaths may not reflect the influence of HIV, however, since the diagnosis of AIDS in Africa is highly suspect.

The Definition of AIDS in Africa

So how does one diagnose AIDS without an HIV antibody test? The official definition of AIDS in Africa was decided at a WHO conference in 1985 in the Central African Republic, and has been called the "Bangui definition" of AIDS. It consists of four clinical signs and symptoms, none of which are in any way unique to HIV. They are:

  1. Persistent cough
  2. Fever
  3. Weight loss of 10%
  4. Diarrhea

The two physicians who pushed for this definition, Joseph McCormick and Susan Fisher-Hoch, were from the CDC, an organization whose major goal is to count cases of various diseases. AIDS and HIV also represented a great opportunity for the CDC, both politically and economically. The problem was that counting cases of AIDS in Africa was, and continues to be, very difficult if the Western definition is used. This is because in the West a positive HIV antibody test is considered fundamental, but in Africa the HIV tests are unavailable, except for the small minority of people who can afford private health care.

The two CDC physicians undoubtedly believed in their cause, but their zeal allowed them to gloss over the fact that these symptoms had been present in Africa for centuries, and were caused primarily by malnutrition. McCormick and Fisher-Hoch admit in a book that they wrote about their experiences that their definition was not based in an effort to achieve an accurate counting, but rather to achieve any kind of counting. They write,

If we could get everyone at the WHO meeting in Bangui to agree on a simple definition of what an AIDS case was in Africa, then, imperfect as the definition might be, we could actually start to count the cases. (McCormick & Fisher-Hoch 1995, page 189).

Problem #4: Can HIV Really Be Transmitted Sexually?

Another aspect that does not fit the predictions made over a decade ago is the fact that HIV remains confined primarily to the original risk groups, unlike what would be expected from an infectious epidemic. Africa, where men and women are affected equally, has been pointed to since the early 1980's as what Europe and the United States will soon look like. Fifteen years into the epidemic, however, CDC reports clearly indicate that nearly 90% of all AIDS in the U.S. is still occuring in male homosexuals and IV drug users. Press reports to the contrary are based in "projections" and assumptions, not on the only official source of such data, the CDC. Also, as we have seen, HIV rates have actually fallen in the past 15 years, according to the best available epidemiological data. This lack of epidemic behavior may be explained by studies that call into question whether the virus can really be spread from one person to another via sexual or blood to blood contacts. These studies have been completely ignored by the media and the scientific community, and yet there are no studies to refute the picture that they present.

Perhaps the most well-controlled study to date that tried to see how often HIV is transmitted in heterosexual relationships was published in the American Journal of Epidemiology in 1997 (Padian et al. 1997). A group of researchers followed 175 HIV positive people who were involved in monogamous heterosexual relationships with partners who were HIV negative. Fully 75% of the couples were not using condoms at entry to the study. While some couples changed their behavior over time, and started using condoms, 47 of the couples continued to have sexual intercourse without using condoms for the duration of the study. Amazingly, not even one single case of seroconversion was documented. This is one of the very few studies that followed people over time, giving it a better chance of accurately documenting seroconversion, although it still would not be able to prove that the seroconversion occured due to sexual intercourse since other factors could well be at play, including false positives on the antibody tests. The one thing that it could show quite accurately, however, would be that people who have unprotected sex do not seroconvert, and this is exactly what happened.

Their abstract is confusing, or perhaps even misleading, because they claim that they did a "prospective study" and determined that it would take slightly over 1000 sexual contacts, on average, before a female partner of an HIV positive male seroconverted. The "1 in 1000" sexual contact risk was not based in any of the 175 couples, however, since none of them seroconverted, but was rather based entirely on finding a small minority of couples in which both partners were already HIV positive at the outset of the study, and assuming that they must have transmitted it from one to another through sexual intercourse. In any case, even 1000 sexual contacts is quite a large number. They estimate that it would take eight times that number of sexual contacts for a woman to transmit HIV to a man, for a grand total of 8000, but even these findings are likely to be false, since there is no solid evidence of any kind that the couples where both members were already HIV positive had transmitted an infectious virus through sexual intercourse. Here are the author's own comments on their surprising findings:

We followed 175 HIV-discordant couples (couples where one member was positive and one negative) over time for a total of approximately 282 couple-years of follow up (table 3)... The longest range of follow-up was 12 visits (6 years). We observed no seroconversions after entry into the study... To our knowledge, our study is the largest and longest study of the heterosexual transmission of HIV in the United States. (p. 354)

No transmission occured among the 25% of couples who did not use their condoms consistently, nor among the 47 couples who intermittently practiced unsafe sex during the entire duration of follow-up. This evidence argues for low infectivity in the absence of either needle sharing and/or other cofactors. (page 356)

"Low infectivity" may be a monumental understatement given the public and scientific stance on how HIV is spread. In spite of their remarkable findings, and in spite of this being the "largest and longest" study of its kind, according to the authors, they do not even raise the question of whether HIV can be sexually transmitted, but instead conclude that it has "low infectivity". If HIV had been shown to be infectious in other studies, the authors of this article would have included the references. Since none are included, it is likely that none exist.

Why not do a simple animal study to prove that HIV can be transmitted sexually?

It would seem easy to do a study on animals to see if HIV can be transmitted sexually. Since HIV does not make animals sick, it would even be a study which causes minimal harm to the animals. But perhaps the reason that researchers have trouble infecting animals with HIV is that HIV is not actually infectious, a factor that no one seems to be considering. It is also possible that the reason animals do not get sick is because HIV cannot harm the immune system. The logical questions are, who demonstrated that HIV was transmitted sexually, and how did they demonstrate that, and who demonstrated that a positive HIV antibody test would result in a destroyed immune system in 100% of the people infected, or even in 50%? These should both be demonstrated in the absence of other co-factors, including drug use, malnutrition, "antiretroviral" medications, and chronic stress, all of which can cause immune deficiency whether a person is "HIV positive", or not.

Problem #5: Can HIV Really Be Transmitted By IV Drug Use?

Another way of spreading HIV, according to conventional HIV science, is through the shared needles of intravenous (IV) drug users. This idea, like sexual transmission, is widely believed, but it is uncertain how this belief was established scientifically. It is the reason behind clean needle exchange programs where free needles are given to IV drug users in an attempt to slow the spread of the "epidemic". The largest and best controlled study to date of this issue, however, actually found that people who used only clean needles from needle exchange programs were at a greatly increased risk for seroconversion (Bruneau et al. 1997). This study, like the one by Padian which was just reviewed, appeared in the American Journal of Epidemiology in 1997. In the abstract the authors state that people who use needle exchange program are three times as likely to seroconvert, even after controlling for all known potential confounding variables like "unsafe" sex. It is astounding to find this result of triple risk in users of clean needles, but if one reads the text of the article (not just the abstract) one finds, as occurred with Padian et al's study of sexual transmission, that the authors have again grossly underestimated their findings. It appears that exclusive users of clean needle exchange programs have between 12 and 30 times increased risk of seroconversion, when compared to IV drug users who never use clean needle exchange programs. This information was undoubtedly a blow to many people, including those who fought diligently for such programs to be established, as well as to those who think that HIV is spread through sharing of contaminated needles. In this light, it was courageous of the authors to report even their tripling of risk, which was found through a comparison of "ever users" of needle exchange programs to "never users". The 12 to 30 times increased risk occurred when "exclusive users" were compared to "never users", which is the opposite of what one would expect if HIV was infectious.

The authors compared four groups of people based on how consistent they were in using only clean needles from needle exchange programs; the first group used clean needles from the needle exchange program 100% of the time, a second group used them greater than 50% of the time, a third group used them less than 50% of the time, and the final group (the "controls") did not participate at all in clean needle exchange programs. The authors found that people who exclusively used clean needles were nearly 30 times more likely to seroconvert than people who did not participate at all in clean needle exchange programs. This number was reduced, after controlling for confounding variables, to 10 times increased risk, which is still quite remarkable, and after controlling for even more "confounding variables", the risk increased to 13 times. These astounding figures, which showed as much as a 30-fold increased risk in exclusive users of clean needles, is not presented in the text or in the abstract. The reader has to read Table 5 to see these results (p. 1000). The only discussion of this subject states:

As shown in table 5, there was a clear tendency for risks of seroconversion to increase with frequency of needle exchange program use over time. Upon adjustment for confounders, significant elevations remained among self-reported consistent users for all subjects and for males only. (page 998)
Thus we see that the authors of two major studies (Padian et al 1997, Bruneau et al. 1997) which have effectively undermined one of the basic premises regarding HIV and AIDS, vastly underestimated their findings when writing the abstracts of their data. Following are some direct quotes from the text of Bruneau et al:

Needle exchange programs are designed to prevent HIV transmission among injection drug users. Although most studies report beneficial effects in terms of behavior modification, a direct assessment of the effectiveness of needle exchange programs in preventing HIV infection has been lacking. A cohort study was conducted to assess the association between risk behaviors and seroprevalence and seroincidence among injection drug users in Montreal, Canada. ... In the cohort study, there were 89 incident cases of HIV infection with a cumulative probability of HIV seroconversion of 33% for needle exchange program users and 13% for non-users. (p<0.0001) ... Risk elevations for HIV infection associated with needle exchange program attendance were substantial and consistent in all three risk assessment scenarios in our cohort of injection drug users, despite extensive adjustment for confounders. In summary, in Montreal, needle exchange program users appear to have higher seroconversion rates than non-users. (p. 994)
The authors also provide a research review showing that needle exchange programs are successful in lowering the number of "risk behaviors".

In London, England, and Glasgow, Scotland, a significant reduction in injecting behaviors was observed among recent needle exchange program attenders.. In the UK a prospective survey between 1987 and 1988 reported higher levels of risk behaviors among non-attenders. ... In Tacoma, Washington, in a case control study among injection drug users entering a methadone program, the nonuse of the needle exchange program was associated with a significant risk for hepatitis B (p. 995)

It is curious that hepatitis B, which is supposedly transmitted the same way as HIV, through sexual contact and blood to blood contact, shows reduced rates in clean needle exchange program users, while HIV actually shows increased rates. As will be seen in the next section, this dilemma presents itself even more clearly in studies of health care workers whose skin is accidentally pierced by needles contaminated with HIV-infected blood.

Finally, their discussion section has a number of revealing comments. Even though the authors do not openly question the basic dogma that HIV is transmitted via contaminated needles, it appears that they are calling for a reappraisal in much the same way as the "Group for the Scientific Reappraisal of AIDS".

Most of the excess risk appeared to be experienced by those reporting consistent and exclusive attendance at needle exchange programs, which was their primary source of new intravenous equipment.

We hypothesized initially that the direction of this association represented simply the net confounding effect of behavioral characteristics biasing ... toward an effect that would be opposite from the expected protective one. Interviews conducted at entry and on multiple opportunities during follow-up elicited detailed information on numerous potential confounders... All plausible sociodemographic, behavioral, and drug consumption variables available were examined as potential confounders...

The fact that the association between needle exchange program attendance and HIV infection risk persisted after being scrutinized with such a conservative analytical approach bolsters our conclusion that it is internally valid and merits further attention. (pp. 999-1000)

This study by Bruneau et al. (1997) suggests a totally different way that people can seroconvert to "HIV positive" status, which, although unproven, explains these results very well. The group of researchers from the University of Western Australia and the Royal Perth Hospital who were mentioned earlier, headed by Eleni Papadopulos-Eleopulos, have hypothesized that when people test positive on "HIV antibody" tests, it is not because they have been infected by a virus at all, but rather because their cells are undergoing oxidative damage which starts a process in which the immune system is hyperstimulated to release antibodies of many different types, which results in false positives on a number of antibody tests, including those for HIV (Papadopulos-Eleopulos et al. 1993a, 1993b, 1995). Oxidative stress can occur in a number of ways, one of which is the injection of foreign proteins into one's body. This is exactly what occurs when IV drug users inject drugs into their arms, whether or not there is any HIV on the needles. It is also what happens when a hemophiliac gets a factor VIII transfusion, whether or not there is any HIV in the factor VIII. Thus, if the exclusive users of clean needle exchange programs were using drugs much more often than the IV drug users who never used clean needle exchange programs, which is certainly plausible, it would follow that they would also be much more likely to seroconvert. Their theory also explains why hemophiliacs tested positive for HIV, even though the factor VIII that they receive is stored in a manner that would kill any HIV particles present in the original samples. It was stored in this way in the 1970's and 1980's, when it is claimed that many hemophiliacs became HIV positive through factor VIII that was contaminated with HIV.

If the data found by Bruneau et al. could be used to answer this question, perhaps with controlled studies in collaboration with the Perth group, their results would serve the purpose they were designed to serve, which is the advancement of knowledge concerning how one seroconverts from "negative to "positive" on the HIV antibody tests. Foreign proteins, such as factor VIII, could be injected into volunteers, as long as this did not pose a risk to the volunteers. Since no HIV would be injected, this would not be a concern.

The evidence that HIV cannot be transmitted sexually, as reported by Padian et al. (1997), also adds strength to the hypothesis of the Perth group. As the next section will indicate, there is also reason to doubt whether HIV-infected needle sticks can transmit HIV, which adds even more evidence in favor of a non-infectious model of AIDS.

It is reasonable that while we wait for further studies, as recommended by both Padian et al. and Bruneau et al., people diagnosed HIV positive should be informed of the results of these studies, especially if they are engaged in any of the behaviors in question. The risks of being treated for HIV infection with long-term courses of "antiretroviral" medications when one is actually showing a false positive are considerable, not to mention the risks of believing that one's immune system is under a siege that it cannot survive, and the risks of social isolation created by the belief that one is infected with a deadly, and contagious virus.

Problem #6: Can HIV Be Transmitted Through Needle Sticks?

Being stuck with a needle that has HIV infected blood, as has happened to thousands of health care workers, is a terrifying experience, but it very rarely results in HIV infection. Studies of such exposures find that only about 1 in 333 people who experience HIV-infected needle sticks seroconvert (Cardo 1997, Gerberding 1994, Henderson 1990), and that a total of only about 50 seroconversions from infected needles have been reported worldwide since HIV was targeted as the cause in 1984. This is an incredibly small number when compared to other blood borne diseases that are of similar prevalence.

This risk of seroconversion after a needle stick, 1 in 333, is less than the prevalence of HIV in the general population of the United States, which is about 1 in 250 people (Okie 1997). This raises the question whether these people really got HIV from the needle stick, since picking randomly from the population will result in more HIV positive people (1 in 240) than picking randomly from people who have been stuck by a needle (1 in 333). One could even argue, somewhat facetiously, that being stuck by a needle reduces your risk, just as using "dirty" needles for IV drug injections might reduce your risk. The 50 cases of seroconversion that are claimed to have occured in the world were reported in a multitude of small studies, with only one or two seroconversions per study. An in depth analysis of these studies would be quite revealing, but is unfortunately beyond the scope of this book. Instead, two of the largest and best controlled studies will be discussed, to serve as examples.

Gerberding (1994) found one case of seroconversion out of 327 cases of HIV-infected needle sticks. These all occurred over the space of 10 years in a clinic that specialized in HIV and AIDS. This single case of seroconversion was a woman who developed a flu-like illness about two weeks after the needle stick occurred, and then tested HIV positive two weeks after that. Another study by Henderson et al. (1990) reports a similar circumstance, where the HIV positive test occurred two weeks after a "severe mononucleosis-like illness, characterized by persistent fever, malaise, and weight loss". These types of anecdotal cases are what led to the conclusion that, at least in some cases, the initial stages of HIV seroconversion result in flu-like symptoms.

There is a completely different way to view this result, however.

Both the flu and mononucleosis have been found to cause false positives on HIV antibody tests (Cordes 1995, Challakeree 1993, MacKenzie 1992). False positives occur for all antibody tests, and are much more likely to occur after people have had an infectious illness, at which time there is a high quantity of many different types of antibodies present in a person's blood. No reports are made by Gerberding et al or Henderson et al of any repeat tests in the two health care workers who seroconverted to confirm the diagnosis, and thus it is not known whether these people may have converted back to HIV negative status after their levels of antibodies returned to normal, which can take a number of months. People who experience a needle stick from HIV infected blood experience several months of stress and social isolation, which people who are HIV positive experience on a permanent basis. This may have also weakened their immune system and made them more susceptible to the flu and other common infections, thus increasing their likelihood of a false positive result. False positives, and other problems with the antibody tests, will be covered in more detail in "Problem#7: How Reliable Are HIV Antibody Tests?"

A final aspect of Gerberding's findings presents another serious question about whether HIV can be transmitted via blood-contaminated needle sticks. They compared the extremely low rate of HIV antibody seroconversion to rates of hepatitis B seroconversion among the health care workers at their HIV-AIDS clinic. Hepatitis B is transmitted the same way that HIV is supposedly transmitted, via direct blood to blood contact or by intimate sexual contacts, and yet, in their own words, "the incidence of hepatitis B was 55 times greater than that of HIV, and 38 times greater than hepatitis C" (p. 1415). Since the setting of this study was a clinic specializing in HIV and AIDS, the prevalence of hepatitis B in the patients seen at the clinic was not expected to be much higher than the 25% to 40% prevalence of HIV positivity. Although not the subject of this paper, problems are also revealed with regards to Hepatitis C infectivity, and there are many other inconsistencies with this virus, as well (Duesberg 1996).

Problem #7: How Reliable Are HIV Antibody Tests?

There are two tests that are primarily used in the West to diagnose HIV infection. These are the ELISA and Western Blot tests. The ELISA is used as a screening test, and if the ELISA result is positive, the Western Blot is used as a confirmatory test. If the ELISA result is negative, no furthur testing is performed. In order to be considered "HIV positive" one must test positive on both tests. If someone tests positive on the ELISA but negative on the Western Blot, they are considered "HIV negative", although a recommendation will usually be made for them to be retested at a later date. The manufacturers of these tests know that their tests are of questionable accuracy, although it is doubtful that they realize just how questionable the accuracy really is. They reveal this knowledge through the following disclaimers that they include with their test kits:

1) Abbott Laboratories puts the following statement in their ELISA test kit: "ELISA testing alone cannot be used to diagnose AIDS." (Abbott 1997) This warning is not surprising, since current practice, at least in the United States, suggests that the Western blot test is the true way to assess infection.

2) Epitope, the maker for one of the Western Blot kits warns in their package insert: "Do not use this kit as the sole basis for HIV infection." (Epitope 1997). This is somewhat more concerning, since the Western blot is supposed to be a highly accurate test, used to confirm that the ELISA is not a false positive. As will be seen below, there are serious questions about the Western Blots true specificity.

3) Roche, the maker of a popular "viral load" test kit which they call "Amplicor", state: "The amplicor HIV-1 monitor test is not intended to be used as a screening test for HIV, nor as a diagnostic test to confirm the presence of HIV infection." (Roche 1996). This is also not surprising, since viral load is not normally used to diagnose HIV infection, and since people who are negative on ELISA and Western blot tests often have positive "viral loads".

Because of the difficulty that Robert Gallo and other researchers have had in isolating viruses from patients, the logical question arises: how was the accuracy of these tests established? It has been found, in studies that are published in major medical journals, that the antigens used in these tests are apparently not specific to HIV, since they occur in many people who are HIV negative, as well as a number of animals. This makes it very difficult to be sure what they are measuring. Since no one has obtained a pure isolate of HIV, as described below by Etienne de Harven, Ph.D., who is one of the world's leaders in retroviral isolation, the accuracy of each test has been primarily decided by testing them against one another, a method that is questionable.

Serious challenges of the specificity of the HIV antibody tests have been raised by several researchers (de Harven 1998a,b, Giraldo 1998/1999, Papadopulos-Eleopulos 1993b). If the rate of HIV seroconversion after a needle stick is truly 1 in 333, and the rate in the general population is 1 in 240, then extremely specific tests would be needed, in which false positives would occur in much less than 1 in 333 tests. This means that the HIV antibody tests would have to be extremely accurate, and yet researchers like Etienne de Harven and Eleni Papadopulos-Eleopulos are claiming that the accuracy of the HIV tests is completely unknown.

Everyone Tests Positive on the ELISA test

The most remarkable study of the ELISA test has unfortunately not yet been published in a peer-reviewed medical journal. The study was described by the physician who performed it, Roberto Giraldo, M.D., in an article that he published in the magazine, Continuum (Giraldo 1998/1999). Dr. Giraldo has worked in a laboratory of clinical immunology at Cornell University Hospital in New York City since 1993. This lab regularly performs the ELISA, Western blot, and Viral load tests on the serum of people who are patients in the hospital. He became suspicious of the ELISA test because when the test is run, the person's serum must be diluted 400 times with a special diluent that is provided by the manufacturer of the lab, Abbott Laboratories. What is particularly unusual about this is that no other antibody tests require such a high dilution. Most are run on straight serum, with no dilution at all. Dr. Giraldo's remarks:

This extraordinarily high dilution of the person's serum (400 times) took me by surprise. Most serologic tests that look for the presence of antibodies use undiluted ("neat") serum. For example, the tests that look for hepatitis A and B viruses, rubella virus, syphilis, hystoplasma, and cryptococcus, to mention a few of them, use straight, undiluted, serum. (page 8)
The closest comparison is the rheumatoid factor (RF) antibody test, which is run at a dilution of 40:1. It is well known, however, that RF is an antibody that all humans produce, and it is used as a non-specific marker for autoimmune processes where the body is attacking itself. Thus RF is referred to as an "autoantibody", and is only elevated when the immune system is hyperstimulated, as occurs in illnesses like rheumatois arthritis and lupus. It is therefore reasonable to dilute the serum before testing for it, since the idea is to find out who is making too much of it, not to find out whether a person has it, or not.

Given these facts, Dr. Giraldo wondered what would happen if he took serum that had tested negative for HIV when diluted 400 times, and ran the ELISA test on it when undiluted, as is done with tests for other viral antibodies. Here is Dr. Giraldo's description of the results:

I first took samples of blood that, at 1:400 dilution, tested negative for antibodies to HIV. I then ran the exact same serum samples through the test again, but this time without diluting them. Tested straight like this, they all came up positive.

Since that time I have run about 100 specimens and have always gotten the same result. I even ran my own blood, which, at 1:400, reacts negative. At 1:1 (undiluted) it reacted positive. (page 8)

This remarkable result is difficult to explain. As suggested by the comparison with RF antibodies mentioned above, one explanation is that HIV antibodies are actually something that all people produce, but for some unknown reason are more elevated in some. This suggests that HIV antibodies might actually be "autoantibodies", rather than antibodies to a viral invader. The other obvious explanation, that all people have been exposed to HIV, is equally disconcerting if one considers what is currently believed about HIV infection and what it means to have "HIV antibodies" in one's blood.

Many conditions cause "false positives"

All tests are known to have "false positives". In the case of an antibody test, this is much more likely to occur if antibodies are present in large quantities, as often occurs when the immune system has been stimulated by multiple infections or by having foreign agents injected into the bloodstreams. All of these things are common experiences of people in all the major risk groups for testing HIV positive in the United States and Europe, including IV drug users, male homosexuals, and hemophiliacs.

Several reports discussing false positives, published by researchers who support the use of these tests and who support the conventional explanations for AIDS, shed light on why such concerns have been raised. MacKenzie et al (1992), for example, found seven people who had repeated false positives on the ELISA test, apparently due to flu vaccination, and estimate that "0.6% to 1.7% of blood donors who received influenza vaccine this season had multiple false positives." This rate is much higher than the prevalence of HIV in the US population, which is about 0.4%, so that people who receive a flu vaccine are much more likely to get a false positive than a true positive.

How, did they decide that the ELISA results were "false positives"? They based their decision that these were false positives on the fact that their Western Blots, used as confirmatory tests, were negative or, in one case, indeterminate, and that about 3 months later the six people available for follow-up tested negative. The significant question to be asked is, what about people whose Western Blot is positive? How does one know they are not false positives, also? People with positive Western Blots are not normally retested months later, but even if they were, how is one to know that the repeat test is not also a false positive? Interestingly, this study also looked at false positives to hepatitis C virus, and found that after 11 weeks, four of seven false positives remained positive, which indicates that the ELISA test for hepatitis C antibodies is possibly even less reliable than the ELISA test for HIV.

A letter to the Western Journal of Medicine (Challakere 1993) reported finding 5 false positives in a sample of 127 people, for a false positive rate of 4%. Through careful history taking they determined that the flu vaccine as well as previous viral infections like herpes simplex 2 were the probable causes of these false positives. This means that 1 in 25 people had a false positive, which would lead to ten times as many false positives as true positives, since only about one in 250 people in the United States are "HIV positive" according to the most recent CDC estimates. These researchers also relied on negative Western Blots to decide which tests were true positives and which were false, showing again how critical the accuracy of the Western Blot is to current practices regarding the diagnosis of HIV infection. A summary article on the use of HIV antibody tests that appeared in Infectious Disease Clinics of North America (Proffitt et al. 1993) discussed some of the known causes of false positives on the ELISA HIV-1 antibody test.

The predictive value of an ELISA screening test depends on the prevalence of HIV infection in the population being tested. In a population at low risk of HIV infection where the prevalence of HIV is low (0.1% or less), a reactive test is much more likely to be false positive than true positive. Thus, the predictive value of a reactive test is low, whereas that of a nonreactive test is high.

False positive ELISAs have been observed with serum from patients with a variety of medical conditions unrelated to HIV infection. These include hematologic malignancies, infections with DNA viruses, autoimmune conditions, multiple myeloma, primary biliary cirrhosis, and alcoholic hepatitis, among others.

Notable causes of false positive reactions have been antibodies that sometimes occur in multiparous women and in multiply transfused patients. Likewise, antibodies to proteins of other viruses have been reported to cross react with HIV determinants. False positive HIV ELISA's also have been observed recently in persons who received vaccines for influenza and hepatitis B virus. (page 205)

Since such heavy reliance is placed on the Western Blot test, one rightfully needs to know how specific it is, and how this specificity was determined. As it turns out, false positives and "indeterminates" for the Western Blot test are also quite common, and the claimed specificity of the test is highly questionable.

How accurate is the Western Blot HIV antibody test?

The Western Blot has ten "bands", each of which have a different protein ("antigen") that is supposedly only produced by HIV. The ELISA test also uses these "HIV proteins", but they are present as a mixture. In the Western Blot the proteins are placed separately on a strip so it is possible to see which of the ten bands the patient's serum will react. If it reacts with a protein in a given band, that is considered to mean that the patient's serum contains antibodies to that protein. Not all ten bands have to be positive in order for a person to be considered, "HIV positive", however, and the combinations needed vary greatly from country to country. This fact alone sounds suspicious, but this is only the beginning.

Proffitt et al. describe the inconsistent guidelines for the reading of the Western Blot test:

Indeed, not even the interpretation guidelines in the brochures of each FDA-licensed manufacturer of HIV Western Blots are the same. However, the majority of the laboratories have accepted the recommendations of the ASTPHLD. Following those recommendations, a negative Western Blot would have no bands, a positive would have at least two of the key bands, and an indeterminate would have a single band or a combination that does not fit the interpretation of positive. ( Proffitt 1993, page 208)
This first comment hardly inspires confidence that these interpretations are based on sound scientific principles, and explains why different countries have widely varying criteria for how to decide when a test is "positive" and when it is "indeterminate". The most disturbing evidence they cite, however, is the rate of indeterminates that appear for Western Blots, even when the ELISA is negative. An "indeterminate", as described above, occurs when an insufficient number of bands come up positive, or when the combination "does not fit the interpretation of positive". One would expect, since all of the bands are loaded with proteins that are supposedly specific to HIV, that "indeterminate" results would be quite rare, but this is hardly the case.

Problems may be encountered when an HIV Western Blot is done on someone at no identifiable risk of infection. For example, recent studies of blood donors in whom no risk of HIV infection could be ascertained, who were nonreactive on the ELISA, and for whom all other tests for HIV were negative, revealed that 20% to 40% might have an indeterminate Western Blot... (Proffitt 1993, page 209)
This means that any one of us, if given a Western Blot HIV antibody test, will have a 20% to 40% chance of having our serum react with proteins that are supposedly specific to HIV! Such a high rate of indeterminates on a test that supposedly determines life or death issues is outragiously high, and yet Proffitt et al. do not mention anywhere in their article that they have any doubts about whether this is an appropriate test to use as the final decision when diagnosing HIV infection.

Upon hearing results like these, it is reasonable to wonder how the extremely high specificity which is claimed for this test can possibly be true. The specificity that is claimed is that only 1 in 20,000 tests will give a "false positive". A later article from 1995, that also supports the use of these tests, places these two seemingly irreconcilable claims in the very same sentence.

Thus, incidences of inaccurate results (on the Western Blot) vary from a false positive rate of 1 in 20,000 to indeterminate results in 20% to 40% of cases in which the ELISA test was serum negative. (Cordes 1995, page 185)
The only conclusions that Proffitt et al. draw from this extremely high "false indeterminate" rate is that the Western Blot should not be used as an initial screening test, and the only harm mentioned is that "the anxiety an indeterminate result creates in a test subject is understandably intense" (Proffitt 1993, page 209).

If an indeterminate result creates intense anxiety, a result considered to be a "true" positive can create levels of stress and anxiety that are many times more intense, and yet the decision about what is "true", "false" or "indeterminate" appears highly arbitrary. It is also notable that the false positive nature of the Western Blot is established by negative ELISAs, but false positives on the ELISA are established by negative Western Blots. Thus one does not know which test, if any, can truly be relied upon, a fact that is even more significant when one considers that as many as 40% of people with negative ELISAs will have indeterminate Western Blots.

A recent study looked at a number of cases of people who had experienced what they considered to be repeated false positives on the Western Blot, even though their ELISA reults were also positive (Sayre et al. 1996). They decided these were false positives based on the fact that only the minimum number of Western Blot bands were positive and that there were no risk factors. While this criteria would be considered suspect by many who hold frimly to the conventional model of HIV and AIDS, it is reasonable to ask them how they know that their interpretation of these tests is any better than the researchers cited below, a question that no one seems to be asking.

Recently, a group in Australia reported identifying low risk, uninfected blood donors whose sera reacted nonspecifically with gp 41 and gp120/160 (two of the proteins used in the Western Blot), which resulted in apparently false positive interpretations... We report here on studies on initial donations and follow up samples from four U.S. blood donors with similar reactivity, as well as data documenting the increasing frequency with which these patterns have been observed in the blood donor setting... (page 46)

The four donors were identified by the individual blood centers as having possibly false positive Western Blots, on the basis of the donor's denial of HIV risk factors and the restricted reactivity of the Western Blots performed. (page 48)

Our results document a fourth source of false positive HIV-1 Western Blot results, which is the reproducible but nonspecific reactivity to (proteins from HIV)... Preliminary studies suggest that the basis for this cross reactivity with HIV-1 gp 41 proteins may be infection by paramyxoviruses, carbohydrate antibodies, or autoantibodies against cellular proteins. (page 48-49).

The authors also looked at rates of these types of false positives among all tests performed on blood donors in the U.S., and conclude that 1992 had the highest rates to date of 52 out of 683, or 8% of positives actually being false positives, if these criteria are used. The question is, how do they know that only these people are false positives? If two bands can represent a false positive, why not three or more bands? In fact, all of the bands of the Western Blot test commonly react as "indeterminate" readings, suggesting that none of them are actually specific to HIV.

The quote above from Sayre et al. (1996) mentions false positives due to reactions with the proteins called "gp 41" and "gp 120/160" (these proteins are sometimes referred to with only a "p", instead of with "gp"). However, there have been problems with the proteins in all the other bands used in the Western Blot, as well, and it has been shown in a number of studies that none of the ten proteins is actually specific to HIV. "Gp" stands for "glycoprotein", which is just a protein with some sugar molecules attached to it. Glycoproteins of all shapes and sizes are extremely common components of cells in both plants and animals. The number after the letters gp represents the molecular weight of the protein, in kilodaltons. So even the name "gp 41" or "gp 120" is a non-specific marker.

The research calling into question whether any of the "HIV proteins" is really specific to HIV is presented in detail in an article published in Bio/Technology, by the group of researchers from Perth, Australia, entitled "Is a Positive Western Blot Proof of HIV Infection" (Papadopulos-Eleopulos et al.1993). They point out that even Luc Montagnier's original papers found gp 41 to occur in normal cells which were not infected by HIV, and that Montagnier's group concluded that gp 41 "may be due to contamination of the virus by cellular actin which was present ... in all the cell extracts" (Barre-Sinoussi et al. 1983). Actin is an extremely common protein that is present in all cells, including bacteria and viruses. The gp 120/160 protein was shown in 1989 to actually be several gp 41 proteins hooked together ("oligomers" of gp 41), so it is equally non-specific. (Pinter 1989)

Another protein, gp24, is of special significance because it is often used by itself to test for the presence of HIV. This is commonly done in newborn children, where the ELISA and Western Blots are thought to give false positives due to antibodies that have been supplied by the Mother, who has already been found to be positive for "HIV antibodies". In addition, when "cultures" of HIV are done, the way they test to see if HIV is there is by looking for gp 24. Thus, this glycoprotein has special importance, and one would expect that it would be extremely rare to find it in people considered not to be infected with HIV. As Papadopulos-Eleopulos et al. put it:

Detection of p24 is currently believed to be synonymous with HIV isolation and viremia. However, ... Gallo and his colleagues have repeatedly stated that the p24's of HTLV-1 (a different retrovirus) and HIV cross-react. (Papadopulos-Eleopulos et al.1993 page 697, Wong-Staal & Gallo 1985)
Papadopulos-Eleopulos et al. continue with further examples showing how incredibly common it is to find gp 24 and antibodies to gp 24 in people who are "HIV negative":

Genesca et al (1989) conducted Western Blot assays in 100 ELISA-negative samples of healthy blood donors. 20 were found to have positive bands which ... were considered indeterminate Western Blots, with p24 being the predominant band (70% of cases). Among the recipients of Western Blot indeterminate blood, 36% were Western Blot indeterminate 6 months after transfusion, but so were 42% of individuals who received Western Blot-negative blood samples. (!!!) Both donors and recipients of blood remained healthy. They concluded that Western Blot indeterminate patterns "are exceedingly common in randomly selected donors and recipients and such patterns do not correlate with the presence of HIV-1 or the transmission of HIV-1... Most such reactions represent false positives.

Antibodies to gp 24 have been detected in 1 out of 150 healthy, ELISA-negative individuals, 13% of randomly selected otherwise healthy patients with generalized warts, 24% of patients with cutaneous T-cell lymphoma, and 41% of patients with multiple sclerosis (Ranki et al. 1988). ...

Conversely, the p24 antigen is not found in all HIV positive or even AIDS patients. In one study... in patients at various stages from asymptomatic (HIV positive) to AIDS, p24 was detected in only 24% (Delord et al. 1991). (Papadopulos-Eleopulos et al. 1993b, pages 697-699).

The incredible reliance of patients, doctors, and scientists on tests with such obvious inconsistencies is a cause for alarm, and yet it appears that the only people sounding the alarm are not being heard, or at least not being listened to. The rest of the article by Papadopulos-Eleopulos et al. goes on to discuss similar findings with the rest of the Western Blot "HIV proteins", and concludes with a relatively conservative call for reappraisal:

We conclude that the use of the HIV antibody tests as a diagnostic and epidemiological tool for HIV infection needs to be reappraised. (page 696)
No "gold standard"

Papadopulos-Eleopulos et al. (1993a,b, 1995) have argued repeatedly that since no one has completely isolated the HIV virus, the specificity of these tests is completely unknown. Only by checking the accuracy of the tests against a "gold standard" of purified HIV can specificity be established. All available electron micrographic pictures of HIV show impure solutions in which what is said to be HIV only represents a small minority of the visible elements (Verney-Elliott 1999, de Harven 1998a,b), and therefore there is no way to know whether the proteins found in such samples are from HIV or from the other cellular components present within the sample.

The opinions of Papadopulos-Eleopulos et al. are shared by Etienne de Harven, Ph.D., who has been one of the world's leaders in electron microscopy for over forty years. Dr. de Harven spent most of his 37 year research career studying retroviruses associated with leukemias in animals. He spent 25 years at the Sloan Kettering Institute, where, in 1958, he published the first electron micrographs of the Friend leukemia virus, a retrovirus his colleague Charlotte Friend had discovered in mouse leukemic cells. His electron micrographs stand in stark contrast to micrographs claimed to show pictures of HIV. This is because his micrographs of the Friend leukemia virus show purified viral particles, with only three small impurities viewed in a field of hundreds of viruses. The only micrographs claimed to be of HIV are 99% impurities, which makes it impossible to know for sure what you are looking at (Verney-Elliott 1999, de Harven 1998a,b). De Harven, like Duesberg, became disillusioned with retrovirology as he saw more and more researchers trying to side-step the frustration of having their work disproved. They "side-stepped" by lowering their scientific standards, and using less precise measures that would give them the results that they wanted. He began to see that the idea that retroviruses could cause disease was highly unlikely, and he was upset to see that retrovirologists studying the issue, instead of admitting that this was so, used unproven and untested hypotheses to keep their research alive.

When, in 1984, Gallo claimed that a retrovirus was causing AIDS, de Harven, who was an emeritus professor of Pathology at the University of Toronto at the time, was highly skeptical. He was not only skeptical that HIV could be the cause of AIDS, as Duesberg was, but also skeptical as to whether they had even found a real retrovirus. He describes how he had seen many researchers claim to have a new retrovirus, only to find upon attempted isolation and microscopy that there was no virus present. This is why isolation was dropped by most researchers, according to de Harven, and why the term "isolation" is now used when the presence of questionable surrogate markers are identified. This means that one of the pioneers of retroviral isolation does not think that HIV has ever been identified as a real retrovirus, and that what are thought to be "markers" of HIV may simply be a collection of proteins produced by the body's own cells when under stress. Here are some direct quotes from Dr. de Harven.

When, around 1980, Gallo and his followers attempted to demonstrate that certain retroviruses can (cause disease in humans), to the best of my bibliographical recollection, electron microscopy was never used to demonstrate directly viremia (the presence of viruses in the blood) in the studied patients. Why? Most probably electron micrographic results were negative, and swiftly ignored! But over-enthusiastic retrovirologists continued to rely on the identification of so-called "viral markers" attempting to salvage their hypothesis. ...

ELISA, then Western Blot tests were hastily developed, at sizable profits eagerly split between the Pasteur Institute and the U.S.. "Seropositivity" (based on these two tests) became synonymous with the disease, itself, plunging an entire generation into behavioural panic, and exposing hundreds of thousands of people to "preventative" antiviral AZT therapy which actually hastened the appearance of severe or lethal immunodeficiency syndrome. ... (de Harven 1998b, page 21)

De Harven concludes his article with the following plea:

Obviously, the hiv/aids hypothesis has to be scientifically reappraised. And, most urgently, the funding for aids research should no longer be restricted to laboratories working on a hypothesis which has never been proven. (page 21)
Problem #8: False "Viral loads"

Gerberding's study of HIV contaminated needle sticks, described above (Gerberding 1994) also uncovered data that call into question the value of PCR testing. PCR, or "Polymerase Chain Reaction" is the test used to determine a person's "viral load". Gerberding gave PCR tests to 133 of the 327 healthy workers who had experienced needle sticks in their clinic. All of these 133 subjects remained HIV negative on the ELISA antibody test, but seven of them had "indeterminate" PCR results, and four others had one or more actual positive results, for a false positive rate of 3%. If the "indeterminate" results are counted as well, the false positive rate is 8%. For a very rare infection like HIV, with an estimated prevalence of only 0.4%, these rates of false positive results in perfectly healthy people are extremely high. The ratio of 3% to 0.4% reveals that for every 30 people with "positive PCR's" only 4 will be considered true positives. The decision that these are actual positives is based on the ELISA and Western Blot antibody tests, which also have lots of false positives, as previously shown. Gerberding et al. comment on their findings with PCR as follows:

The failure to demonstrate seroconversion... among those with positive PCR tests suggests that false positives occur even under stringent test conditions. The low predicitive value of a positive or indeterminate PCR test... contraindicates the routine use of gene amplification in this clinical setting. (page 1415)
Other cases of people with positive PCR tests but who were negative on the ELISA test were reported quite recently (Rich 1999). They report on three such cases which occurred over a two month period. The third case has a particularly interesting series of conflicting results:

(Case 3) had a positive result on ELISA and an indeterminate result on a Western Blot (WB) test... During a four month period after her initial indeterminate result, she had a positive result on ELISA and another indeterminate result on WB test, on separate occasions. Five months later, both ELISA and WB tests yielded negative results, but the patient had a plasma viral load of 1300 copies/mL. (page 38).
Another study looking at this question, published in 1992 in the Journal of AIDS (Busch et al. 1992). They did PCR tests on 151 ELISA-negative people and found that 18.5% (28 people) had positive PCRs. Furthurmore, they found that only 25.5% of people diagnosed HIV-positive had "positive" PCR's!

Finding viral loads and false positive PCR's in HIV-negative people should be a major wake-up call to people diagnosed "HIV-positive", their doctors, scientists working in the field, and the public at large, because these tests are repeatedly used to make clinical decisions about treatment. What results like these even more surprising is that they were never reported in the media, nor were they discussed in the research community, nor were they presented to physicians at AIDS conferences, and finally, they were definitely never told to people diagnosed "HIV-positive".

Perhaps this is why Kary Mullis, the scientist who won the Nobel Prize in Chemistry in 1993 for inventing the PCR test, says that the "viral load" is meaningless (Duesberg 1996). Kary Mullis is one of the signatories of the statement calling for a reappraisal of the causes of AIDS.

Problem #9: Weak Correlation Between HIV and AIDS

The evidence that HIV causes AIDS has been based from the very beginning on correlations between testing positive on the HIV antibody test and later developing AIDS. Even this correlation, however, breaks down under scrutiny.

There is a significant minority of HIV positive patients who have not gotten AIDS, most of whom have never taken any anti-HIV medications. Some of them were diagnosed as far back as 1984, when the virus was first discovered by Robert Gallo and Luc Montagnier. They are often called "long-term non-progressors", and represent from 7% to 10% of all people infected with HIV (Learmont 1992). Conventional science has focused narrowly on a search for genetic protective factors to explain their "resistance to the virus", while ignoring many survivors' own explanations for why they have remained healthy for so many years. A group of such non-progressors have organized the "Long-term Survivor's Network". They have concluded that two of the major factors they have in common are that they do not believe that HIV is a deadly infection, and that they have also refused to take anti-HIV medications (Walton 1999).

Uncountable numbers of people would have been diagnosed with AIDS, except that a negative HIV test result was used to exclude AIDS as a diagnosis. To clarify, outside of Africa the very definition of AIDS requires a positive HIV antibody test result. This means that people with symptoms of AIDS or with one of the 31 "AIDS-defining conditions", but who test negative on the HIV antibody tests, are not diagnosed with AIDS. People with the exact same illnesses and symptoms are given different diagnoses based solely on the result of an HIV antibody test, which creates a completely artificial correlation between HIV and AIDS. Tuberculosis with a positive HIV antibody test is AIDS, but tuberculosis with a negative test is just tuberculosis, even if it is occurring in an IV drug user with multiple opportunistic infections.

"AIDS-defining Conditions" without HIV

Even the syndrome of chronic infections and extremely low CD4 T lymphocyte counts has been found in many people who are HIV negative. A wave of reports of this syndrome, dubbed "non-HIV AIDS" (Bird 1996) and occurring in IV drug users, male homosexuals, and hemophiliacs, surfaced in the early 1990's. While this represented a major challenge to the correlation between HIV and AIDS a solution was quickly found. This syndrome, which looked just like AIDS, was given a new name. When the syndrome was found in people who were HIV negative, it would be called "Idiopathic CD4 Lymphocytopenia". If they were HIV positive, it would be called "AIDS". This was decided at a conference in 1993, and dramatically reduced the number of HIV-free AIDS cases that were reported. While it is true that people diagnosed with "Idiopathic CD4 Lymphcytopenia" are less likely to die than people diagnosed "HIV positive", the possibility of a self-fulfilling prophecy would easily explain this finding. It is interesting that reports of this phenomenon have focused on how this syndrome differs from AIDS (Bird 1996), while these differences may be due to the fact that these people are not engulfed in the death-education that surrounds an HIV positive diagnosis, nor are they treated with powerful and highly toxic medications.

Many researchers now believe that Kaposi's Sarcoma (KS), considered the signature disease of AIDS in the early 1980's, is probably not caused by HIV, at all. This began to be obvious because KS occurs exclusively in male homosexuals, and not in other risk groups. While it does occur much more often in male homosexuals who are HIV-positive, if it is really caused by HIV, it would be expected to occur in other HIV-positive individuals, as well, which it does not. Some researchers, still narrowly focused on infectious explanations, have targeted another virus, human herpes virus 8 (HHV-8). Other researchers, however, including Robert Gallo, have pointed out that human herpes virus 8 would also unlikely to affect male homosexuals, exclusively, since any virus causing KS would have spread outside of that risk group. Here is a quote from an article that appeared in Science in 1995, entitled "Controversy: Is KS Really Caused by New Herpes Viruses?" (Cohen 1995):

If HHV-8 is the cause of KS, said Gallo, "this would be the most unorthodox virus in nature." Gallo noted that AIDS-KS is found almost exclusively in gay men and very rarely in women or injection drug users who are infected with HIV. yet herpes viruses are famous for spreading freely throughout populations. (page 1847)
The article goes on to say that Gallo still believes that HIV plays a central role in causing KS, which, if true, is extremely odd given that HIV is as unable as HHV-8 to tell whether its host is gay or heterosexual.

Drugs as a cause of "AIDS-defining conditions" without HIV

Duesberg has long maintained that the initial epidemic of AIDS that occurred in a small subset of male homosexuals and IV drug users was caused by recreational drug abuse (Duesberg 1992, 1996). He argues that overuse of prescription drugs is also a major factor, especially after the introduction of AZT in 1987, at which point most of the deaths from AIDS have either been directly caused or contributed to by AZT and other "antiretroviral" medications. This argument is discussed in more detail in "Can AZT and other anti-HIV drugs cause AIDS?".

Duesberg and others argue, for instance, that Kaposi's Sarcoma is well-correlated with the use of amyl nitrite inhalants, commonly called "poppers", which are widely used in the gay community. Nitrite inhalants have also been found to cause immunosuppression, as well as lowered CD4 counts. The same is true of other drugs, including cocaine, heroin, alcohol, and many others. Duesberg (1992) is not the only researcher to document this correlation, or to point out that the subgroup of male homosexuals who are at risk for AIDS also have a high rate of drug use. This was especially true in the early 1980's, when the AIDS epidemic was restricted to male homosexuals involved in the "gay party scene". A book published in 1988, entitled "Psychological, Neuropsychiatric, and Substance Abuse Aspects of AIDS", includes many well-referenced scientific articles on these issues (Bridge et al 1988). All of the authors of the various articles in the book agree that HIV is the cause of AIDS, and are focusing on psychological stress and drug abuse only as cofactors. As we have seen, this is commonly the case even when the author's data clearly challenge the HIV hypothesis. Here are some quotes that make this point clear, from an article in the book that focuses mainly on opiates as causes of a state of immunodeficiency that leads to some of the 31 "AIDS-defining" opportunistic infections:

Although needle-sharing is unquestionably a major factor in the spread of AIDS by addicts [in spite of their use of the word "unquestionably", this article was written before Bruneau et al., or anyone else, had actually tried to test the hypothesis that needle-sharing spreads HIV as is indicated by their lack of a reference to support their statement], the fact that various abused drugs are themselves immunomodulatory and immunocompromising has led to the suggestion that such drugs may directly alter susceptibility to HIV-1 and exacerbate the complications of AIDS...

From as early as 1907, evidence has accumulated that opiate addiciton leads to depressed immune function. In the 1960's and 1970's, the observations that opiate addicts often suffered from opportunistic infection and cancer were believed to indicate that they were experiencing immunosuppression ... In 1980, McDonough et al., from our laboratory, showed that opiate addicts had depressed levels of total T-cells... This information corroborated the earlier (in vitro) findings of Wybran et al. (Bridge et al. pages 145-146)

Finally, the groups of people at risk for AIDS, even when HIV-negative, have increased rates of "AIDS-defining conditions". The study above by Des Jarlais (1987), that found lowered CD4 T-cells as a function of increased drug injections, also found that HIV-negative IV drug users had high rates of lymphadenopathy, weight loss, fevers, night sweats, diarrhea, and mouth infections. Hemopheliacs have long suffered from high rates of opportunistic infections, especially pneumonia and tuberculosis (Johnson et al. 1985).

Problem #10: Where Is the Virus?

Finally, it is very difficult to find even non-specific markers of actual HIV viruses in most people who have antibodies to HIV, and even in people diagnosed with "full blown AIDS". This is done by doing things like looking for gp24 protein in a person's serum or lymph nodes. As discussed earlier, gp 24 occurs in many people who are ELISA negative, including 41% of people diagnosed with multiple sclerosis (Ranki et al. 1988). Robert Gallo only claimed to have found markers of actual viruses in about 40 to 50% of his patients with AIDS, as reported in his original articles in the journal, Science (Gallo 1984). He claimed in those articles that this low rate was probably due to contamination, but does not explain how contamination could remove all traces of the viruses. Even if one realizes that the tests used are only finding non-specific markers for HIV, one would expect very close to a 100% correlation in order to make claims that people are "infected", since the presence of antibodies without any other signs of a virus normally means that the virus had been eliminated by the person's immune system.

Attempts since Gallo have also failed to find markers of actual viruses in most patients diagnosed "HIV-positive", with percentages ranging from 20% to 80% (Chiodi 1988, Learmont 1992). These dismal results are similar to those of Piatak et al who found that most people with "viral loads", even as high as 800,000, had no infectious virus at all. Even people who are found to have markers of HIV in them only have tiny amounts, which has resulted in the difficulties in coming up with a mechanism for how HIV could be causing the damage, as outlined at the beginning of this chapter.

Here is a brief summary of the problems with HIV science covered here:

  • Proposed mechanisms by which HIV supposedly kills CD4 T-cells have been revised several times, and remain in debate.
  • HIV rates in the general population do not reflect an infectious epidemic, and have been declining since 1984 according to all available sources.
  • Evidence of infection by unprotected sex or blood to blood contact is weak or non-existent.
  • ELISA, Western Blot, and PCR are all prone to false positives, and are used amongst themselves incestuously to prove each other's validity.
  • There are a large number of HIV-free cases of AIDS, so many that a new diagnosis was invented to describe them, "Idiopathic CD4 Lymphocytopenia". The very definiton of AIDS includes a positive HIV antibody test, creating an artificially correlation between HIV and AIDS.
  • The major risk groups for AIDS suffered from atypically high rates of "AIDS-defining Conditions" for decades before the HIV hypothesis was introduced.
  • Researchers only find markers of actual HIV in 20% to 80% of people who test positive on the HIV antibody tests, and PCR reports "viral loads" in about one in thirty "HIV-negative" people.
  • Even a perfect correlation would not prove causation, and HIV=AIDS is not at all perfect.

Of even greater concern than the existence of these problems is the fact that no one in the conventional medical and scientific establishment seems to be asking questions about them. When researchers like Etienne de Harven and the Perth group do begin asking questions, they often find themselves labelled as "dissidents", as if they were political refugees, which succeeds only in stifling the opportunity for open scientific discourse. The fact that the media also fails to report on such studies suggests that it is not only a problem within the scientific community, however, but more likely something that is occurring on a societal level. In many ways, "science" has replaced religion as the mediator between God/Nature and humanity, and people prefer to believe in the infallibility of science, much as Christians believed in the infallibility of the Pope. Belief in such infallibility is what led to people like Galileo being excommunicated and imprisoned for reporting that he had seen moons around Jupiter in his telescope, and it appears that a modern version of excommunication is happening today.

Matt Irwin MD is a family practice resident who wrote several literature reviews on HIV and AIDS while attending medical school at George Washington University. He also holds a Master's degree in social work from the Catholic University of America. In addition to his interest in alternative views of HIV and AIDS, he specializes in health promotion with nutritional, psychological, social, and spiritual interventions, as well as classical homeopathy. He has a practice near Washington, D.C.


Balter M (1991). Montagnier pursues the mycoplasm-AIDS link. Science 251; 271.

Balter M (1997, November 21). How does HIV overcome the body's T-cell bodyguards? Science 278: 1399-1400.

Bird AG (1996). Non-HIV AIDS: nature and strategies for its management. Journal of Antimicrobial Chemotherapy 37 Suppl B, 171-183.

Bruneau J, Lamothe F, Franco E, et al. (1997). High rates of HIV infection among injection drug users participating in needle exchange programs in Montreal: Results of a cohort study. American Journal of Epidemiology; 146; 994-1002.

Cameron DW et al. (1998). Randomised placebo controlled trial of ritonavir in advanced HIV-1 disease. Lancet; 351; 543-549.

Cardo DM et al. (1997). A case-control study of HIV seroconversion in health care workers after percutaneous exposure. New Engl J Med 337(21); 1485-1490.

Challakeree K, Rapaport MH (1993, August). False positive HIV-1 ELISA results in low risk subjects. Western Journal of Medicine; 159(2); 214-215.

Chiodi F, Albert J, Olausson E, et al.(1988) Isolation Frequency of Human Immunodeficiency Virus from Cerebrospinal Fluid and Blood of Patients with Varying Severity of HIV Infection. AIDS Res Hum Retrovirol ;4:351-358.

Cordes RJ & Ryan ME (1995). Pitfalls in HIV testing. Postgraduate Medicine 98(5); 177-189.

de Harven E (1998). Retroviruses: the recollections of an electron microscopist. Reappraising AIDS 6(11); 4-7.

Des Jarlais DC, Friedman SR, Marmor M, Cohen H, Mildvan D, Yancovitz S, Mathur U, el-Sadr W, Spira TJ, Garber J, et al (1987). Development of AIDS, HIV seroconversion, and potential co-factors for T4 cell loss in a cohort of intravenous drug users. AIDS. 1987 Jul;1(2):105-11.

Duesberg PH (1992). AIDS acquired by drug consumption and other non-contagious risk factors. Pharmacology and Therapeutics ;55:201-277.

Duesberg PH (1993). The HIV gap in national AIDS statistics. Bio/Technology 11; 955.

Duesberg P (1996). Inventing the AIDS Virus. Regnery: Washington, DC.

Feeney C, Bryzman S, Kong L, Brazil H, Deutsch R, Fritz LC (1995, Oct). T-lymphocyte subsets in acute illness. Crit Care Med; 23(10):1680-5.

Gallo RC, Salahuddin SZ, Popovic M, et al (1984). Frequent Detection and Isolation of Cytopathic Retro-viruses (HTLV-III) from Patients with AIDS and at Risk for AIDS. Science; 224:500-502.

Gerberding JL (1994). Incidence and prevalence of HIV, hepatitis B virus, and cytomegalovirus among health care personnell at risk for blood exposure: Final report from a longitudinal study. J Infect Dis 170; 1410-1417.

Geshekter CL (1998). A Critical Reappraisal of African AIDS Research and Western Sexual Stereotypes. Presentation to General Assembly Meeting, Council for the Development of Social Science Research in Africa [CODESRIA], Dakar, SENEGAL, December 1998

Giraldo RA (1998/1999). Everybody reacts positive on the ELISA test for HIV. Continuum; 5 (5): 8-10.

Gorochov G, Neumann AU, Kereveur A, Parizot C, Li T, Katlama C, Karmochkine M, Raguin G, Autran B and Debré P (1998). Perturbation of CD4+ and CD8+ T-cell repertoires during progression to AIDS and regulation of the CD4+ repertoire during antiviral therapy. Nature Medicine 4: 215-221.

Grossman Z and Herberman RB (1997). T-cell homeostasis in HIV infection is neither failing nor blind: modified cell counts reflect an adaptive response of the host. Nature Medicine 3: 486-490

Hammer SM et al. A controlled trial of two nucleoside analogues plus indinavir in persons with human immunodeficiency virus infection and CD4 cell counts of 200 per cubic millimeter or less. N Engl J Med 1997 Sep 11;337(11):725-33

Henderson DK et al. (1990). Risk for occupational transmission of HIV type 1 associated with clinical exposures: a prosepctive evaluation. Ann Intern Med 113; 740-746.

Ho DD et al. (1995). Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection. Nature 373; 123-126.

Katz et al (1997). Projected incidences of AIDS in San Francisco: The peak and decline of the epidemic. Journal of Acquired Immune Deficiency and Human Retrovirology 16:182-189.

Learmont J, Tindall B, Evans L, et al (1992). Long-term symptomless HIV-1 infection in recipients of blood products from a single donor. Lancet ;340:863-867

MacKenzie WR, Favis JP, Peterson DE et al. (1992). Multiple false positive serologic tests for HIV, HTLV-1, and Hepatitis C following influenza vaccination. JAMA; 268(8); 1015-1017.

Okie S (September 2, 1997). AIDS: Health officials launch a new campaign to determine how widespread the virus is. The Washington Post, Health Section page 12.

Padian NS, Shiboski SC, Glass SO et al. (1997). Heterosexual transmission of HIV in Northern California: Results from a ten-year study. American Journal of Epidemiology 146(4); 350-357.

Pakker NG, Notermans DW, de Boer RJ, Roos MTL, de Wolf F, Hill A, Leonard JM, Danner SA, Miedema F and Schellekens PTA (1998) Biphasic kinetics of peripheral blood T cells after triple combination therapy in HIV-1 infection: a composite of redistribution and proliferation. Nature Medicine 4: 208-214.

Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM (1993a). Has Robert Gallo proven the role of HIV in AIDS? Emergency Medicine; 5: 135-147.

Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM (1993b). Is a Positive Western Blot Proof of HIV Infection? Biotechnology (N Y). 1993 Jun;11(6):696-707.

Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM (1995). A critical analysis of the HIV-T4-cell-AIDS hypothesis. Genetica 95; 4-24.

Philpott P (1999). Personal communication. The statement and list of the original 500 signatories can be viewed at:

Piatak M, Saag MS, Yang LC, et al. (1993). High levels of HIV-1 in plasma during all stages of infection determined by quantitative competitive PCR. Science 259; 1749-1754.

Pinter A, Honnen WJ, Tilley SA, Bona C, Zaghouani H, Gorny MK, Zolla-Pazner S. (1989) Oligomeric structure of gp41, the transmembrane protein of human immunodeficiency virus type 1. J Virol.;63(6):2674-9

Popovic M, Sarngadharan MG, Read E, et al. (1984) Detection, Isolation,and Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science; 224: 497-500.

Proffitt MR & Yen Lieberman B (1993, June). Laboratory diagnosis of HIV infection. Infectious Disease Clinics of North America 7(2).; 203-215.

Rich JD, Merriman NA, Mylonakis E et al (1999). Misdiagnosis of HIV infection by HIV-1 plasma viral load testing: A case series. Ann Internal Med 130(1); 37-39.

Roederer, M. (1998) Getting to the HAART of T cell dynamics. Nature Medicine 4: 145-146.

Sarngadharan MG, Popovic M, Bruch L, et al (1984). Antibodies Reactive to Human T-Lympho-trophic Retroviruses (HTLV-III) in the Serum of Patients with AIDS. Science:224:506-508.

Sayre KR, Dodd RY, Tegtemeier G et al. (1996). False positive HIV-1 Western Bloy tests in noninfected blood donors. Transfusion 36; 45-52.

Schwartz DH et al. (1997). Extensive evaluation of a seronegative participant in an HIV-1 vaccine trial as a result of a false positive PCR. The Lancet 350; 256-259.

Sivak SL & Wormser GP (1985). How common is HTLV-III infection in the United States? New England Journal of Medicine 313; 1352.

Schupbach J, Popovic M, Gilden RV, et al (1984). Serological analysis of a Subgroup of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS. Science;224:503-505.

Valleroy LA, Mackellar DA, Karon JM, Janssen RS, Hayman CR (1998). HIV infection in disadvantaged out-of-school youth: Prevalence for US Job Corps entrants, 1990 through 1996. Journal of Acquired Immune Deficiency and Human Retrovirology 19: 67-73.

Verney-Elliott M (1999). `Virtual viral load' tests. Continuum 5(5); 56-58.

Walton C (1999). What makes a survivor? Continuum 5(5); 16-18.

Wei et al. (1995). Viral dynamics in HIV-1 infection. Nature 373; 117-122.