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.
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.
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)
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.
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.
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)
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 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 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 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.
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:
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).
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. ...
De Harven concludes his article with the following plea:
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)
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)