Document:Questions on HIV Tests
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Questions on HIV-Antibody Tests
By Matthew Irwin
- 1 Introduction
- 2 Problems with the ELISA test
- 3 Problems with the Western Blot antibody test
- 4 Problems with the "viral load" test
- 5 References
As an introduction to the problems with these tests, here is a quote from the conventional literature about indeterminates on the Western Blot, which is currently the heavily relied upon "confirmatory" test for HIV infection:
"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 et al 1993, page 209)
This shows that indeterminate results are hardly rare. It also shows the remarkable finding that any person, if given a Western Blot HIV antibody test, will have a 20% to 40% chance of having their serum react with proteins that are supposedly specific to HIV. An indeterminate result by definition means that the person's serum reacted to at least one of the "HIV-proteins" used in the Western Blot. A 20% to 40% 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. This is a common reaction from people who are entrenched in the HIV-causes-AIDS belief system. The finding of how incredibly common indeterminate results are on the Western Blot is only the tip of the iceberg regarding the problems with these 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 Western Blot test is performed, and the person is declared "HIV-negative". 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. Following is a detailed discussion of problems with the ELISA, Western Blot, and viral load tests.
Problems with the ELISA test
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, MD, 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, as is the case for hepatitis A and B virus, rubella virus, and many others. In Dr. Giraldo's own words:
"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." (Giraldo 1998/1999, page 8)
The closest comparison to this level of dilution 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 rheumatoid arthritis and lupus. Another test that uses diluted serum is the Western Blot test, which uses a ratio of 50:1. This may explain why the Western Blot test is almost always positive when the ELISA is positive, because serum that reacts at a dilution of 400:1 on the ELISA test is even more likely to react if only diluted 50:1 on the Western Blot. One wonders what would happen if Western Blot tests were run on healthy blood donors and others undiluted serum, since even when diluted 50 times the indeterminate rate is between 20% and 40%. Unfortunately, no one has yet tried to repeat Dr. Giraldo's experiment or do similar tests with the Western Blot.
Given the unusual dilution required by the ELISA test, Dr. Giraldo wondered what would happen if he took serum that had tested negative for HIV when it was diluted 400 times, and rerun the ELISA test on the same serum without diluting it at all 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." (Giraldo 1998/1999, page 8)
This remarkable result seems significant enough to immediately halt all ELISA testing until it and more detailed experiments are done, which may be why Dr. Giraldo states that "No one will be willing to publish my results because they are too threatening to the HIV establishment." (Giraldo, personal communication). As suggested by the comparison with RF antibodies mentioned above, one explanation is that HIV antibodies are actually something that all people produce and that are not specific to any virus. This suggests that HIV antibodies might actually be "autoantibodies", rather than antibodies to a viral invader. The other obvious explanation is that all people have been exposed to HIV, but some people produce more antibodies than others. This is equally disconcerting if one considers the psychological terrorism that accompanies the diagnosis, "HIV-positive".
Papadopulos-Eleopulos et al. (1993) have argued repeatedly that since no one has completely isolated the HIV virus, the specificity of the tests used to diagnose HIV-infection 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 that are used in the ELISA and Western Blot tests 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 from 1958 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 (Verney-Elliott 1999, de Harven 1998a,b).
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. According to Dr. de Harven they did this by lowering their scientific standards, and by using less precise measures in order to get the results that they wanted. De Harven 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 more and more dubious scientific methods in an attempt 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 had worked with many researchers in the past who claimed to have isolated a new retrovirus, only to find upon electron microscopy that there was no virus present. This is why true isolation was discontinued by most researchers, according to de Harven, and why the term "isolation" is now used when the presence of questionable surrogate markers are identified. He and Papadopulos-Eleopulos et al. argue 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 regarding these problems and how they relate to the ELISA and Western Blot tests:
"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." (de Harven 1998b, page 21)
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 comon experiences of people in all the major risk goups for testing HIV positive in the United States and Europe, including IV drug users, male homosexuals, and hemophiliacs. The argument that ELISA and Western Blot tests are simply picking up false positives due to very high antibody levels is supported by an article by Shallenberger on low CD4 counts. (Shallenberger 1998). He argues that AIDS is not infectious at all, but rather that it is caused by an imbalance of the immune system with a hyperstimulated antibody-mediated immunity. He documents that this is exactly what happens to people in the risk groups for AIDS, and that a hyperactive antibody-mediated arm causes a suppression of cellular immunity. He does not discuss the HIV antibody tests, but it appears that the finding that the HIV test must be run on heavily diluted blood shows that it is a measure for excess antibodies in the blood, also called "hypergammaglobulinemia".
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 on the ELISA test (the Western Blot was not repeated). Thus we see that the accuracy of the ELISA test is gauged by the results of Western Blot tests.
A letter to the Western Journal of Medicine (Challakeree 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. A rate of 4% 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 diagnosed HIV positive according to the most recent CDC estimates. Challakere 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 1993) discussed some of the known causes of false positives on the ELISA HIV-1 antibody test:
"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.
Problems with the Western Blot antibody test
The specificity of the Western Blot is called into question by reports such as the one below which is also from Proffitt et al.'s 1993 article. The Western Blot has ten "bands", all of which have a protein ("antigen") that is supposedly only produced by HIV. The ELISA test also uses these "HIV proteins", but they are present as a mixture and so only one band needs to be used. The patient's serum is run separately through all ten bands of the Western Blot to see how it will react with each one, individually. 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 diagnosed HIV-positive, however, and the combinations needed vary greatly from country to country. This fact alone shows how arbitrary the test limits are, since a person diagnosed HIV-positive in one country may be considered "indeterminate" in another.
The following quote from Proffitt et al. describes the inconsistent guidelines for the reading of this test (Proffitt 1993):
"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." (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 in healthy blood donors as discussed previously. An indeterminate 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 contain 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..." (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! As mentioned before, such a high rate of indeterminates on a test that supposedly determines life or death issues is outrageous, in my opinion, and yet Proffitt et al. do not question its accuracy in any way.
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 will create levels of stress and anxiety that are many times more intense. I have called the fear and social isolation caused by a positive HIV antibody test result "psychological terrorism" because of how devastating it can be, and yet the decision about what is "true", "false" or "indeterminate" does not appear to be based in any well controlled experiments, and appears to ignore many conflicting results.
The arbitrary nature of the Western Blot has been analyzed in detail by Papadopulos-Eleopulos et al. (1993), who document that all of the proteins used in the Western Blot which are supposedly specific to HIV have been commonly found in people who are HIV-negative on the other HIV tests. They also point out that HIV was never isolated so there is no way to know if these proteins are from HIV or from other cells and viruses. Before analyzing their work, however, here is a quote from a team of researchers who reported a number of false positive results on the Western Blot tests.
"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." (Sayre et al. 1996, 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 concluded that 1992 had the highest rates to date with 52 out of 683, or 8% of Western Blot positives on donated blood actually being false positives.
The quote above from Sayre et al. (1996) mentions false positives due to reactions with the "gp 41 proteins", which include 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 a protein with some sugar molecules attached to it, and the number after the letters represents the molecular weight of the protein, in kilodaltons. Glycoproteins of all shapes and sizes are extremely common components of cells in both plants and animals.
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 Papadopulos-Eleopulos et al., entitled "Is a Positive Western Blot Proof of HIV Infection?" (Papadopulos-Eleopulos et al. 1993). This article is available online. The authors 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. This was reported by Pinter et al in 1989 in the Journal of Virology in an article entitled, "Oligomeric Structure of gp41, the transmembrane Protein of HIV-1" (Pinter et al. 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 furthur examples showing how incredibly common it is to find gp 24 and antibodies to gp 24 in people who are considered 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. 1993, pages 697-699).
Here we have researchers discussing the "exceedingly common" occurence of Western Blot indeterminate results, and deciding that they represent false positives because the ELISA is negative. When we looked at ELISA false positives, they were said to be false positives because the Western Blot was negative! 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)
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.
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.
Viruses can only cause damage if they are infectious. That is how they are supposed to cause ill health, 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 and looking for surrogate markers of HIV like gp 24. As outlined above, these proteins are actually quite non-specific and are often found in people who are HIV-negative.
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 et al. 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 even more dismal results. Because they use the presence of gp24, which is a non-specific protein found in 41% of patients with multiple sclerosis (Ranki et al. 1988), to determine if a cell has become infected, even their estimate of 1 in 60,000 is probably exaggerated.
Even using a non-specific marker like gp 24 they were not able to culture any virus at all in more than half (35 of 66) of patients. 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 extremely 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, no one seems to be asking questions about these tests. Instead, articles commonly quote amazing levels of specificity and sensitivity.
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". This 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. Since the human genome has about 3 billion base pairs, while that of HIV has only about 10,000, and 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 accidentally be attributed to HIV.
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 to, however, is not clinical health, at all. Careful reading of such articles reveals that the person in question often feels much better off of the drugs because of the numerous toxic effects that they have. 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. 1993) 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 may result in profound immunosuppression whether HIV is causing damage, or not.
High Viral Loads in People Who Are "HIV-Negative"
Adding furthur confusion to the issue, PCR technology has found extremely high viral loads in people who are HIV negative by the ELISA and Western Blot 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.
Gerberding et al. (1994) conducted a study of HIV contaminated needle sticks, and in the process also uncovered data that call into question the value of viral load/PCR testing. They did PCR tests on 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 regarding which are actual positives is based on the ELISA and Western Blot antibody tests, which are also highly questionable as discussed above. 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." (Gerberding et al. 1994, page 1415)
Other cases of people with positive PCR tests but who were negative on the ELISA test were reported by Rich et al. (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 1,300 copies/mL." (page 38).
Another study looking at this question was 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 makes 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 a statement calling for a reappraisal of the causes of AIDS.
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:
- 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.
- 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.
- 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.
So, here we have it. All the test makers deny that their test is accurate to diagnose HIV infection when used "alone". Combining three inaccurate tests will create yet another inaccurate test, especially given the evidence cited above showing how severe the accuracy problems are. I continue to be amazed that these tests are relied upon daily to make life or death decisions, and I would propose that simple but thorough experiments be carried out by an independent and unbiased body of researchers composed of some conventional and some dissenters. In the meantime, I could not in good conscience recommend that anyone take one of these tests.
- Abbott Laboratories ELISA test kit disclaimer.
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