Document:Durban Declaration Rebuttal

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Durban Declaration Rebuttal
A rebuttal to the "Durban Declaration"
published in Nature on July 6 2000
Revised September 28, 2001
Compiled by Robert Johnston1, Matthew Irwin, MD2 and David Crowe3

Rethinking AIDS

The views of dissident scientists challenging the mainstream HIV/AIDS hypothesis have been receiving increased attention recently. President Thabo Mbeki of South Africa caused a controversy by convening a panel of AIDS experts among them many prominent dissidents. This event, along with Mbeki's skepticism of orthodox AIDS theory and treatments, generated a great deal of media coverage. Apparently some AIDS researchers invested in HIV orthodoxy now feel compelled to circulate a petition to academics of any discipline asking them to pledge allegiance to a declaration that HIV is unquestionably the cause of AIDS. This document implies that all dissent costs lives and that dissenting voices should be suppressed. What follows is a rebuttal in the form of a review of scientific evidence that challenges every substantial point in the "Durban Declaration".

Full text of the declaration with interlinear comments:



     Seventeen years after the discovery of the human immunodeficiency virus (HIV), thousands of individuals from around the world are gathering in Durban, South Africa, to attend the XIII International AIDS Conference, which starts next week (9 July). At the turn of the millennium, figures released last week reveal that an estimated 34.3 million people worldwide are living with HIV or AIDS, 24.5 million of them in sub-Saharan Africa.(1) Last year alone, 2.8 million people died of AIDS, the highest rate since the start of the epidemic. If current trends continue, southern and Southeast Asia, South America and regions of the former Soviet Union will also bear a heavy burden in the next two decades.

COMMENT: These frightening figures from UNAIDS are grossly exaggerated and represent typical efforts to ignore 17 years of evidence to the contrary. These estimates are based on computer projections from very small samples. Hysterical projections have been issued through the media since the beginning of the AIDS 'epidemic'. Common predictions were:

  • "By 1990 one in five heterosexuals will be dead of AIDS" — Oprah Winfrey, 1987
  • "By 1991, HIV will have spread to between 5 and 10 million Americans" — Newsweek, 1986
  • "By 1996, three to five million Americans will be HIV positive and one million will be dead of AIDS" &mdas; NIAID Director Anthony Fauci, New York Times, January 14, 1986
  • "Without massive federal AIDS intervention, there may be no one left." — HHS Secretary Donna Shalala, 1993, Washington Times, June 8, 1999

None of these predictions have proven to be true. HIV rates in the United States have never reflected an infectious epidemic, and the figures UNAIDS cites for Africa are even more wildly inflated.

In the U.S., HIV rates have actually been falling steadily since HIV rates were first estimated in 1985. At that time Sivak and Wormser (Sivak 1985) published an article in the New England Journal of Medicine estimating that about 1,765,470 people in the United States were infected with HIV. A few years later the Centers for Disease Control (CDC) in Atlanta estimated only about 1,500,000, a drop of nearly 300,000 cases, but claimed that the earlier estimate had been exaggerated. By the mid 1990s the CDC's estimates had dropped even further, to about 750,000. An article in the Washington Post on September 2, 1997, commented on these confusing figures, as follows:

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)

Okie does not question the validity of these new estimates, which is what usually occurs even when the information being presented directly contradicts the most basic beliefs about HIV and AIDS. An unbiased observer, however, might conclude that the CDC is creating estimates to fit their belief that HIV infection "must be increasing", rather than facing the reality that their own published data show exactly the opposite. These data are supported by other results. For instance, HIV rates fell by 50% from 1990 to 1996 among applicants to President Clinton's youth Job Corps program, a finding in direct contradiction to the claim that HIV was spreading among youth during those years. (Valleroy 1998) Katz et al (Katz 1997) also found that new HIV infections in San Francisco, supposedly the "epicenter of the epidemic", peaked in 1982. This was long before the introduction of any safe sex campaign, and was two years before HIV was even selected as the probable cause of AIDS. Both of these findings were published in the Journal of Acquired Immune Deficiency and Human Retrovirology, but in spite of this they were completely ignored by the media, the scientific community, and the medical establishment.

AIDS rates began dropping in 1993, contrary to all predictions except those of dissident scientists. They actually started dropping in the 1980's but serial definition changes allowed more and more people to be diagnosed with AIDS, creating the illusion of an epidemic. (Maggiore 1999) As the CDC's HIV/AIDS surveillance reports clearly demonstrate, the official decline in new AIDS cases began several years before protease inhibitors had even received FDA approval. Two years after this decline in new AIDS cases, AIDS mortality also began to decline, as would be expected. Mortality also began declining before protease inhibitors were approved. (CDC 1998) Thus, it is impossible for these drugs to be responsible, in spite of widely repeated claims to the contrary. The effectiveness of protease inhibitors and other "antiretroviral" medications will be discussed in more detail later in this article.

If figures in the United States can be so wildly misrepresented, African estimates would be expected to be even more susceptible to bias, and even more inaccurate. In Africa there is not even enough funding to perform HIV antibody tests on the vast majority of people diagnosed with AIDS, let alone on the general population, a fact that is completely left out of the media's portrayal of a continent being decimated by the virus.

UNAIDS trumpets 24.5 million "living with HIV or AIDS" in sub-Saharan Africa. Meanwhile, the WHO's Weekly Epidemiological Record from November 1998 quietly reports the total cumulative number of AIDS cases in Africa since 1982, when AIDS record-keeping began, is 794,444 or an average of about 44,000 per year -- numbers starkly at odds with the latest UNAIDS scare figures, which claim 2.8 million AIDS deaths throughout Africa for 1999 alone. If it is true that "African countries south of the Sahara have some of the best HIV surveillance systems in the world", as UNAIDS (UNAIDS 1999) claims, then this huge disparity cannot be due to under-reporting.

Given the history of failed predictions, how seriously can we take the claim that "half of all 15-year olds in the African countries worst affected by AIDS will eventually die of the disease even if the rates of infection drop substantially in the next few years"? (Altman 2000)

African historian Dr. Charles Geshekter points out that part of the problem is the way these estimates are created. South Africa is more advanced than most African countries in that it conducts HIV tests in surveys of about 18,000 pregnant women annually. (Geshekter 2000) The HIV-positive numbers are then extrapolated - even though it is known that pregnancy makes a false positive test result more likely. Estimates are made from these very small surveys because the vast majority of people in Africa can barely afford basic necessities of living, and cannot even afford antibiotics, let alone expensive blood tests. The women are given a blood test known as ELISA, which frequently gives a false positive result. (Burke 1988) (Challakeree 1993) (Johnson 1998) (Kashala 1994) (MacKenzie 1992) (Meyer 1987) In wealthier nations, ELISA tests are used only as a screening test, and a person is only diagnosed positive if they also test positive on a Western Blot test. Western Blot tests are not used in these surveys, even though two Russian studies have found that less than 1% of people who tested positive on the ELISA also tested positive on the Western blot. (Voevodin 1992) (Papadopulos 1993) Here is a quote directly from the packet insert in the ELISA test kit:

… the EIA [or ELISA] was designed to be extremely sensitive. As a result, non-specific reactions may be seen in samples from some people, who, for example, due to prior pregnancy, blood transfusion, or other exposure, have antibodies to the human cells or media in which the HIV-1 is grown for manufacture of the EIA. Because of these and other nonspecific reactions, it is appropriate to investigate specimens found to be reactive on EIA in a manner that gives improved predictability that HIV-1 antibody, in fact is present. (Abbott 1997)

Abbott Labs test kit instructions also contain the disclaimer: "There is no recognized standard for establishing the presence or absence of HIV-1 antibody in human blood." (Abbott 1997)

Other conditions common in underprivileged and impoverished communities that are known to cause false positive results are tuberculosis, malaria, hepatitis and leprosy. (Burke 1988) (Challakeree 1993) (Johnson 1998) (Kashala 1994) (MacKenzie 1992) (Meyer 1987) In fact, these are the primary health threats in Africa; several million cases of tuberculosis and malaria are reported in Africa each year - more than all the AIDS cases reported in Africa since 1982. (WHO 1998)

AIDS spreads by infection

     AIDS spreads by infection, like many other diseases, such as tuberculosis and malaria, that cause illness and death particularly in underprivileged and impoverished communities. HIV-1, which is responsible for the AIDS pandemic, is a retrovirus closely related to a simian immunodeficiency virus (SIV) that infects chimpanzees. HIV-2, which is prevalent in West Africa and has spread to Europe and India, is almost indistinguishable from an SIV that infects sooty mangabey monkeys Although HIV-1 and HIV-2 first arose as zoonoses (2) — infections transmitted from animals to humans — both now spread among humans through sexual contact; from mother to infant; and via contaminated blood.

     An animal source for an infection is not unique to HIV. The plague came from rodents and influenza from birds. The new Nipah virus in Southeast Asia reached humans via pigs. Variant Creutzfeldt-Jakob disease in the United Kingdom is identical to 'mad cow' disease. Once HIV became established in humans, it soon followed human habits and movements. Like many other viruses, HIV recognizes no social, political or geographic boundaries.

COMMENT: It is widely claimed that HIV and AIDS spread by infection, but much of the scientific evidence shows that AIDS does not always act like an infectious disease. In the US and other affluent countries, contrary to wild predictions of the 1980's, AIDS has not spread outside the original risk groups — homosexual men, IV drug users, hemophiliacs and blood transfusion recipients. CDC HIV/AIDS surveillance reports clearly show that AIDS has dropped in the heterosexual population, and yet media reports continue to claim (quoting deceptive percentages) that it is increasing.(CDC 1999) While it has been argued that other infectious diseases are similarly limited by behavior, many facts cast serious doubt on the idea that a single, sexually-transmissible agent can account for all cases of AIDS. In Africa the loose AIDS definition (described below) and lack of HIV testing sweep most illness into the AIDS basket. In fact, the AIDS definitions differ so drastically from one part of the world to another that it is not credible for UNAIDS or WHO to claim to be tracking a distinct disease. Following is a series of examples from the medical literature that directly contradict the claims made above in the Durban Declaration. The claims of an infectious spread through sexual and blood to blood contact can only survive by ignoring or disregarding the results below.

  • The infectious disease theory cannot explain why an extensive study of IV drug users showed that those who exclusively used clean needle exchange programs were 10 times MORE likely to be HIV-positive than those who never used clean needle exchange programs. (Bruneau 1997)
  • A 10 year study of sexual partners (one HIV+, one HIV-) recorded NO cases of sexual transmission. This same study concluded that it would take about 1,000 instances of heterosexual intercourse to transmit HIV once. (Padian 1997)
  • A study of 21 haemophiliacs revealed only two HIV+ wives, neither of whom had AIDS, and only one of whom had an abnormal immune cell count. (Kreiss 1986)
  • The CDC admits that transmission of HIV through discarded needles is extremely rare as HIV is quickly inactivated when dried - yet the preparation of Factor VIII and IX involves extensive heating, freezing and drying and supposedly HIV comes through unscathed. Other explanations for why hemophiliacs test positive are more compelling (more on this to follow).
  • If HIV is transmitted in blood and other bodily fluids, one would expect health care workers who are most likely to be exposed to these substances to be infected quite regularly. Of 733,374 AIDS cases reported in the U.S. through the end of 1999, only 25 are believed to have been occupationally transmitted. And, this conclusion is from negative evidence (i.e. health care workers who are HIV-positive, but not homosexual, drug abusers, haemophiliacs or blood transfusion recipients are assumed to have been infected occupationally). The CDC has reported not a single case of confirmed occupational transmission in surgeons and paramedics. (CDC 1999)

The evidence that AIDS is caused by HIV is clear-cut

     The evidence that AIDS is caused by HIV- I or HIV-2 is clear-cut, exhaustive and unambiguous, meeting the highest standards of science.(3) (4) (5) (6) (7) The data fulfill exactly the same criteria as for other viral diseases, such as polio, measles and smallpox:

COMMENT: Regarding "highest standards of science", HIV does not meet Koch's postulates, which are the established methods of showing that a microbe is causing a disease. They were adopted due to constant false claims by microbe hunters that they had found microbes causing diseases. Many of the diseases in question turned out to be non-infectious, such as scurvy, beri-beri, and pellagra, which are all vitamin deficiency diseases, and more recently with the Japanese "SMON virus", which was found to be caused by a specific medication, clioquinol. (Duesberg 1996) Koch's postulates are straightforward logic, describing the necessary steps to prove that a virus or microbe is the cause of a disease:

  • First, the germ must be found growing abundantly in every patient and every diseased tissue.
  • Second, the germ must be isolated and grown in the laboratory.
  • Third, the purified germ must cause the disease again in another host.(Duesberg 1996)

Following is a short summary showing how poorly HIV meets any of the three postulates:

First, the germ must be found growing abundantly in every patient and every diseased tissue.

There are thousands of people who have been diagnosed with AIDS and then later found to be HIV negative on the antibody tests. (Duesberg 1993) In addition, HIV antibody tests are rarely used in Africa and other poor nations where the majority of people with AIDS supposedly reside, so there is no way of knowing how many test positive on the HIV antibody tests. Secondly, it is very possible that even people who test positive on the antibody tests do not have any virus in them. There are no tests that actually detect HIV itself. They all rely on surrogate markers like antibodies and tiny RNA and DNA fragments. While these surrogate markers are thought to prove that a person is infected by HIV, this has never actually been established with proper isolation techniques. Even using these markers as a proxy for "isolation", HIV researchers have observed that "not all seropositive individuals have virus recoverable from their PMCs and that isolation from serum is not a common event". (Michaelis & Levy 1987) Signs of "virus" were found in only "about 30% of specimens from seropositive persons, generally at a concentration of less than 10 IP/mL [10 infectious particles per milliliter]" (Levy 1988) & a minuscule amount. Although most people think that the viral load test looks for actual viruses, it does not. It looks for tiny strands of RNA that are claimed to be specific to HIV, and then uses a complex mathematical formula that generates the number commonly referred to as "viral load". Piatak et al. (Piatak 1993) were able to successfully "isolate"* virus from only 53% of people with viral loads in the hundreds of thousands. One patient had a viral load of 815,000 "copies per milliliter", and yet they could not "isolate" any active virus. Thus the diagnosis "HIV-positive" is of questionable scientific value and needs to be reappraised. Finally, since positive HIV tests are required in most first world/western/rich countries to diagnose AIDS, even people suffering from one of the 29 "AIDS indicator diseases" with symptoms exactly like those of AIDS, are not diagnosed with AIDS. This creates a ridiculous artificial correlation in which the definition of AIDS requires an HIV positive test, and then people use the artificial correlation to try to show that HIV must be causing AIDS.

Second, the germ must be isolated and grown in the laboratory.

HIV has never been isolated. Eleni Papadopulos-Eleopulos and colleagues remind us that isolation of a virus requires an electromicrograph of pure viral particles, which has never been done with HIV. (Papadopulos 1998) Attempts have been made without success, as described by Etienne de Harven, one of the pioneers of the use of electron microscopy for identifying retroviruses. (de Harven 1998) The discoverer of HIV, Luc Montaignier, has also admitted that they have not isolated the virus.(Tahi 1997) When the word "isolation" is used in scientific articles about HIV, it refers to finding surrogate markers like proteins that are said to be specific to HIV. Thus "isolation" does not mean finding even one single intact virus. All of the proteins used as surrogates for isolation, which are supposedly specific to HIV, have been found in humans and animals who test negative on the antibody tests. For example, antibodies to p24, one of the proteins commonly used as a surrogate marker when "isolation" is claimed, have been found in 14% of healthy, HIV-negative blood donors, (Genesca et al. 1989) 41% of HIV-negative people with multiple sclerosis, and 13% of people with generalized warts. (Ranki et al. 1988) (Papadopulos et al. 1993)

Third, the purified germ must cause the disease again in another host.

Not one paramedic, emergency medical technician or surgeon in the U.S. has contracted AIDS from on-the-job exposure. (CDC 1999) Out of 733,374 total U.S. AIDS cases through 1999, only 25 are thought to be occupationally acquired, based on presumptive evidence as described previously. (CDC 1999) In Canada, out of 16,235 AIDS cases through 1998, only 3 are reported as occupationally acquired,(LCDC 1998) based on circumstantial evidence.(CCDR 1992) Consider that the 1 million needle-stick injuries among health care workers in the U.S. each year result in about 1,000 cases of hepatitis among health care workers annually. That means that in the 18 years of AIDS, health care workers contracted 18,000 cases of hepatitis and 25 cases of AIDS. Pretty strange if HIV is a blood-borne virus!

Patients with acquired immune deficiency syndrome are infected with HIV

  • Patients with acquired immune deficiency syndrome, regardless of where they live, are infected with HIV. (3) (4) (5) (6) (7)

COMMENT: Not true. As mentioned above, there have been thousands of people diagnosed with AIDS who were later found to be HIV-negative. (Duesberg 1993) In the United States and affluent countries the current definition of AIDS requires that the patient be HIV-positive, although thousands of assumed-positive, but actually HIV-negative, AIDS cases have slipped through. HIV-negative patients with AIDS-like symptoms are excluded by definition and are required to be reported as ordinary cases of the old 29 "AIDS indicator" diseases or as Idiopathic CD4 Lymphocytopenia, a fancy name for HIV-negative people who have CD4 T-cell counts low enough to be diagnosed with AIDS. This category was created to draw off these troublesome HIV-negative people who defy Koch's postulates.

In Africa, the continent supposedly being decimated by HIV, HIV tests are rarely ever done, as mentioned previously, so the idea that all patients with AIDS in Africa are infected with HIV is based entirely on supposition. At a WHO conference in the Central African Republic in 1985, U.S. Centers for Disease Control (CDC) introduced the "Bangui Definition" of AIDS in Africa. The CDC officials later explained, "The definition was reached by consensus, based mostly on the delegates' experience in treating AIDS patients. It has proven a useful tool in determining the extent of the AIDS epidemic in Africa, especially in areas where no testing is available. Its major components were prolonged fevers (for a month or more), weight loss of 10% or greater, and prolonged diarrhea..." (McCormick & Fisher-Hock 1995) In describing why they felt it was reasonable to adopt this extremely non-specific definition of AIDS, they wrote:

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-Hock 1995, page 189)

In their haste to start counting, they seem to have overlooked that their "AIDS symptoms" are common results of malnutrition, advanced tuberculosis, and many other illnesses that are widespread in Africa. Where AIDS is diagnosed clinically, large numbers of AIDS patients test negative for HIV. As no HIV testing is required in Africa we have no idea how many AIDS cases there are HIV positive. (De Cock 1991) (Gilks 1991) (Widy-Wirski 1988)

Robert Gallo's team designed and patented their HIV tests in order to identify people who have, or who are likely to have, AIDS diseases. Gallo presumed - but did not prove - that these tests would also indicate infections with a common virus that caused these diseases. Gallo's team settled on testing standards that produced positive results in 88% (43 of 49) of his risk group test subjects who had AIDS diseases, 79% (11 of 14) of his risk group test subjects who had "pre-AIDS," 40% (9 of 22) of his risk group subjects with no AIDS conditions, and less than 1% (1 of 164) of AIDS-free test subjects who did not belong to the official risk groups. This is a far from perfect correlation, and these were just looking for antibodies, not for actual viruses. By the higher standard of so-called isolation, HIV was detected in only 36% of Gallo's AIDS patients - barely a third.(Gallo 1984) The frequency of isolation has not improved in the ensuing years,(World Health Organization 1994) and PCR viral load is no better at identifying active "HIV infections" when cross referenced to either p24 antigen tests or plasma culture. (Piatak 1993)

We are often reminded by HIV researchers that HIV has a relationship to AIDS. Certainly there is a loose correlation between HIV-positive antibody results and AIDS, but it is not enough to fulfill Koch's first postulate. Perhaps the reason the HIV antibody tests tend to identify AIDS patients is that it functions like the erythrocyte sedimentation rate (ESR) test and other non-specific antibody tests like rheumatoid factor (RF), and anti-nuclear antibody (ANA) tests. (Turner 1997) After all, no one has ever established a gold standard, such as purification of HIV from fresh patient plasma or even cell culture, as Luc Montaignier admits. (Tahi 1997) Therefore, any of 70 conditions already identified could be the cause of "HIV positivity" in any or all cases. (Johnson 1998) The erythrocyte sedimentation rate (ESR) is a blood test that is frequently ordered in internal-medicine and infectious-disease offices. The test measures the rate that red blood cells (erythrocytes) fall to the bottom of a test tube under controlled conditions. An increased rate, usually defined as greater than 10 in a young adult, generally reflects an inflammatory process somewhere in the body. The ESR can be elevated in a multitude of disorders, from a mild infection, to a severe infection, malignancy or even kidney failure. A normal ESR can virtually exclude some disorders, but it is never diagnostic of any one particular disease.

Other very non-specific antibody tests like the Rheumatoid Factor (RF) and the Anti-nuclear Antibody (ANA) tests, are positive mostly in people with certain autoimmune diseases, but are also often positive in healthy adults. These tests use diluted serum, because otherwise most people would test positive. They are not as nearly diluted as the 400-fold dilution of the HIV ELISA test, however. When the ELISA is run on straight serum, as is done for the majority of antibody tests like hepatitis B antibodies, 100 out of 100 HIV-negative blood samples became positive! (Giraldo 1998/1999) The Western Blot also uses diluted serum, but no studies could be found by these authors in which it was tested on straight serum. This would be an essential test of the Western blot's specificity, especially given that even when diluted, indeterminate readings are quite common. An article in a leading journal presents this issue:

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)

Amazingly, the authors of the above study do not even mention that this extremely high "indeterminate" reading might raise questions about the specificity of the Western blot, which is currently relied on heavily to diagnose AIDS.

Most people with HIV show signs of AIDS within 5-10 years

  • If not treated, most people with HIV infection show signs of AIDS within 5-10 years.(6) (7) HIV infection is identified in blood by detecting antibodies, gene sequences or viral isolation. These tests are as reliable as any used for detecting other virus infections.

COMMENT: Studies of long-term survivors or non-progressors show that the majority do not take AIDS drugs and that many of them refuse viral load tests as well as other surrogate marker tests and lead normal lives - some of them since 1984 when HIV was first targeted as "the probable cause of AIDS". (Buchbinder 1994) (Cao 1995) (Garbuglia 1996) (Harrer 1996) (Hogervorst 1995) (Hoover 1995) (Montefiori 1996) (Pantaleo 1995) (Root-Bernstein 1995)

Is the "HIV Test" Valid? The test kit manufacturer's own literature admits:

"ELISA testing alone cannot be used to diagnose AIDS, even if the recommended investigation of reactive specimens suggests a high probability that the antibody to HIV 1 is present" — Abbott Laboratories, 1994, 66-2333/R4.
The insert for one of the kits for administering the Western Blot warns: "Do not use this kit as the sole basis of diagnosis of HIV-1 infection" — Epitope/Organon Teknika Corporation, PN201-3039 Revision # 6.
"Sensitivity and Specificity: At present there is no recognized standard for establishing the presence and absence of HIV-1 antibody in human blood. Therefore, sensitivity was computed based on the clinical diagnosis of AIDS and specificity based on random donors. The ABBOT studies show that: Sensitivity based on an assumed 100% prevalence of HIV-1 antibody in AIDS patients is estimated to be 100% (144 patients tested). Specificity based on an assumed zero prevalence of HIV-1 antibody in random donors is estimated to be 99.9% (4777 random donors tested)." — Abbott Laboratories HIVABtm HIV-1 EIA

Assumed because it is not possible to isolate HIV from fresh patient plasma. Thus it has never been proven that any "HIV" antibody positive patient has an active "HIV" infection.

The insert that comes with a popular kit to run viral load warns:

"The Amplicor HIV-1 Monitor test is not intended to be used as a screening test for HIV or as a diagnostic test to confirm the presence of HIV infection" — Roche Diagnostic Systems, 06/96, 13-08-83088-001.

HIV test results vary depending on where you live. In the U.S., Canada, most of Europe but not in England or Wales, the Western Blot test confirms ELISA tests. Dr. Valendar Turner explains how HIV antibody test results can be interpreted very differently by nine different international standards. For instance it is possible for any person to be any of the following on a single test result: positive in Australia, but not in France; positive in France, but not in Australia (for different reasons); positive in Africa and not positive everywhere else in the world. A Martian might be forgiven for wondering whether wine tasting was less subjective. (Turner 1995)

Durban rebuttal image001.gif
Criteria varying worldwide for a positive HIV test result on Western Blot.
AFR = Africa; AUS = Australia; FDA = US Food and Drug Administration; RCX = US Red Cross; CDC = US Center for Disease Control; CON = US Consortium for Retrovirus Serology Standardization; GER = Germany; UK = United Kingdom; FRA = France; MACS = US Multicenter AIDS Cohort Study 1983-1992. Courtesy Dr. V. Turner

As for the recent thrust to test pregnant women regardless of risk, the American Foundation for AIDS Research (AmFAR), among others, makes it clear that this idea will lead to disaster:

Take, for example, self selected and previously tested blood donors from the general population. Here the prevalence of infection might be 1 case per 100,000 people … If the test has a specificity of 99.9%, it means 0.1% — about 100 of the test results will be false positives … This means that a positive test result in this population has only a 1% chance of being a true positive! (AmFAR 1999)

People who receive HIV-contaminated blood develop AIDS

  • People who receive HIV-contaminated blood or blood products develop AIDS, whereas those who receive untainted or screened blood do not. (6)

COMMENT: The Darby study of hemophiliacs is the only evidence referenced by the authors to support their statement. The Darby study, at first glance, seems to convict HIV, but a closer look at this study and other evidence reveals that the weak correlation between "HIV-positive" and illness actually supports the view that other factors, not HIV, are responsible.

HIV testing was introduced in 1985, and administered to most of Darby's subjects by the end of that year. When annual mortality was next calculated, at the end of 1986, hemophiliacs who had tested HIV-positive had increased mortality. No increased mortality was observed for those who tested HIV-negative. (Both trends continued through the course of the study.) But if HIV was responsible for the increased death rate, there should have been some indication before the HIV-positive subjects knew their status. AIDS appeared in the other major risk groups before HIV testing. Could the psychological impact of the HIV test and subsequent prophylactic and "anti-viral" treatment be the root of the problem for "HIV-positive" hemophiliacs? (Philpott 1995) Is "HIV-positivity" just a marker for hemophiliacs who suffer from foreign-protein-mediated immunodeficiency? (Biasi 1991) (Duesberg 1995) (Johnson 1985) (Kreiss 1986) (Papadopulos 1995)

Robert S. Root­Bernstein provides a review of the evidence that many HIV negative hemophiliacs may have developed compromised immune systems due to problems with factor VIII and other treatments for hemophilia:

Severity of hemophilia is independently predictive of development of AIDS, possibly due to increased frequency of use of clotting concentrates, transfusions, viral contaminants, and steroidal, colloidal gold, and opiate drugs associated with joint injury treatment (Rosendaal, Smit & Briet, 1991; Root-Bernstein,1993).
Additional evidence for controllable cofactors in AIDS comes from studies of HIV­seronegative hemophiliacs who display pronounced decreases in CD4 counts, decreased capacity to produce interleukin II, and immune suppression (Watson & Ludlum, 1992; Hassett et al., 1993; Madhok et al., 1990; Hay, McEvoy & Duggan­Keen, 1990). This immune suppression has been related to factor VIII therapy (ibid., and Farrugia, 1992), active cytomegalovirus and hepatitis C infections, and lymphocytotoxic autoantibodies. It is believed that affected hemophiliacs are consequently predisposed to HIV infection and an increased rate of development of AIDS (Sabin et al., 1993; Goldsmitk et al., 1991; Higgins & Goodall, 1991; Madhok et al., 1991; Schulman, 1991; Webster et al., 1989; Daniel et al., 1989). Replacing medium purity blood clotting factor concentrates with high purity, antibody purified, or recombinant factor that lacks viral and alloantigenic contaminates for the treatment of both HIV­seronegative and HIV­infected hemophiliacs has resulted in stabilization of T­cell counts, and in some patients, increasing T­cell counts over several years (Hilgartner et al., 1993; Mannucci et al., 1992; Gompert et al., 1992; De Biasi et al., 1991; Schulman, 1991).
… most hemophilia studies differentiate between hemophiliacs age 25­44 and those over the age of 44, because the rate of AIDS development in the over 44 group is two or four times faster than that of the 25­44 age group. [...] The so­called age factor in hemophiliacs is unique to this group, and must therefore be related to the very significant changes in the treatment of hemophilia over the past few decades (e.g., the switch from heavily virus contaminated plasma, to less contaminated factor concentrate, to ultrapurified and recombinant DNA derived clotting factor), which has saved young hemophiliacs from many cumulative immunosuppressive cofactors that affect older hemophiliacs (Rosendall, Smit & Briet, 1991; Root­Bernstein, 1990a, 1993). Cofactors known to cause immune suppression and to significantly increase the rates of AIDS development, which are also known to be much more common in older than younger hemophiliacs, include infections (sometimes chronic) with herpes viruses, hepatitis virus types B and C, and cytomegalovirus (Sullivan et al., 1986; Goedert et al., 1989; Webster et al., 1989; Higgins & Goodall, 1991; Sabin et al., 1993) and exposure to alloantigens in impure factor concentrates themselves (Hilgartner et al., 1993; Schulman, 1991; Goedert et al., 1989; Sullivan et al., 1986). All of these cofactors are also present in other AIDS risk groups at unusually high rates compared to the general population (Root­Bernstein, 1993). Attenuation or elimination of these cofactor exposures through changes in hemophilia treatment since the 1960s resulted in a rise in the average life expectancy of hemophiliacs from 33 years in 1960 to nearly 57 years in 1980 (Aronson, 1988; Rosendaal, Smit & Briet, 1991). (Life expectancy has unfortunately plunged again to 40 years during the period 1987­1989 due primarily to AIDS, but also to increases in non­AIDS­associated pathologies as well [Lorenzo, et al., 1993; Mares, Sartori & Girolami, 1992; Ritter, 1994]*). (Root­Bernstein, 1995)
*OR: Life expectancy plunged again to 40 years during the period 1987­1989 due primarily to the introduction of "HIV tests" (nocebo effect) and toxic high dose AZT treatment.

Papadopulos-Eleopulos and colleagues remind us that some HIV/AIDS researchers are of the opinion that HIV cannot be transmitted through "...products prepared from blood, such as albumin, plasma, protein fractions, or hepatitis B vaccine." (Blattner 1989) Of course, that includes blood clotting Factor VIII. As quoted earlier in this paper, Jay Levy (1988) comments that infectious HIV particles are found in only about 30% of people diagnosed HIV-positive, with a concentration of only about 10 infectious particles per milliliter (IP/mL). 10 IP/mL is virtually none. Commenting on his and his colleagues' findings Levy wrote: "These studies demonstrate further that not all seropositive individuals have virus recoverable from their PMCs and that isolation from serum is not a common event" [PMCs=peripheral blood mononuclear cells].(Michaelis & Levy 1987) "Thus, cell-free virus in body fluids is unlikely to be a meaningful source of HIV transmission." (Levy 1988) (Papadopulos 1995a)

Here are a few of the points made by Eleopulos and colleagues:

  • Even the CDC accepts that a positive test in hemophiliacs is not proof of HIV infection. "It is possible that antibody to LAV[=HIV] is acquired passively from immunoglobulins found in factor VIII concentrates..... Likewise, it is possible that seropositivity is caused not by infectious virus but by immunization with noninfectious LAV or LAV proteins derived from virus disrupted during the processing of plasma into factor VIII concentrate." (Evatt 1985)
  • Levy and his colleagues have shown that the titre of HIV in plasma of HIV infected individuals three, six or twelve hours after phlebotomy [blood donation] "dropped from up to 500 TCID/ml to 0" [TCID=tissue culture infectious dose].
  • In January 1994, the CDC (CDC 1994) communicated the following experimental data and conclusion:
"In order to obtain data on the survival of HIV, laboratory studies have required the use of artificially high concentrations of laboratory grown virus...the amount of virus studied is not found in human specimens or anyplace else in nature, does not spread or maintain infectiousness outside its host. Although these unnatural concentrations of HIV can be kept alive under precisely controlled and limited laboratory conditions, CDC studies have shown that drying of even these high concentrations of HIV reduces the number of infectious viruses by 90 to 99 percent within several hours.
Since the HIV concentrations used in laboratory studies are much higher than those actually found in blood or other body specimens, drying of HIV-infected human blood or other body fluids reduces the theoretical risk of environmental transmission to that which has been observed-essentially zero."

Since: (a) in most instances, if not all, the time between phlebotomy and conversion of pooled plasma to factor VIII concentrate is considerably greater than 3 hours; (b) factor VIII is made from plasma which is cell free; (c ) [since] the late 1970s factor VIII has been supplied as a dry powder which may spend weeks or months waiting use; how can one reconcile the above facts with the view that hemophiliacs are infected with HIV via contaminated factor VIII concentrates? (Papadopulos 1995b)

A more likely explanation for HIV positive hemophiliacs is that after years of receiving foreign proteins intravenously they develop high titres of a wide variety of antibodies, which results in false positive test results with no actual HIV infection. Since hemophiliacs with worse disease require more infusions, they are more likely to test HIV positive, which explains why those that are HIV positive will have a higher death rate. There is also the possibility of a self-fulfilling prophecy being created when they learn that they are "HIV positive".

Children who develop AIDS are born to HIV-infected mothers

  • Most children who develop AIDS are born to HIV-infected mothers. The higher the viral load in the mother, the greater the risk of the child becoming infected. (8)

COMMENT: Diseases in children who are not HIV positive will not be classified as AIDS - at least by the First World definitions. The presence of so-called HIV antibodies may often (certainly not always) correlate with ill health. Children inherit antibodies from their mothers, so children of less healthy mothers are more likely to inherit "HIV" antibodies and are more likely to be unhealthy themselves because their nourishment within the uterus and through breast feeding is less adequate. It should also be noted that the use of AZT therapy to reduce transmission of HIV has serious health consequences, and is likely responsible for the injury and death of many children when they and/or their mothers are exposed to this drug:

"Comparison of HIV-1-infected children whose mothers were treated with ZDV [AZT] with children whose mothers were not treated showed that the former group had a higher probability of developing severe disease [57.3% (95% CI 40.9-74.3) versus 37.2% (95% CI 30.0-45.4); log-rank test 7.83, P = 0.005; adjusted hazard ratio 1.8 (95% CI 1.1-3.1)] or severe immune suppression [53.9% (95% CI 36.3-73.5) versus 37.5% (95% CI 30.0-46.2); log-rank test 5.58, P = 0.018; adjusted hazard ratio 2.4, (95% CI: 1.3-4.3)]" — The Italian Register for HIV Infection in Children. Rapid disease progression in HIV-1 perinatally infected children born to mothers receiving zidovudine monotherapy during pregnancy. AIDS. 1999 May 28; 13: 927-33.

For a list of citations see APPENDIX: Concerns about AZT

"Viral load" is a very misleading term. It refers not to a count of infectious virus, but to a mathematical equation based on a very inaccurate estimate of the number of occurrences of a small portion (3%) of what is believed to be the HIV genome. Because viral load is based on calculating the beginning of an exponential process from the end point it is much like estimating the original number of American settlers from the present population of the U.S.. Duesberg and Bialy thoroughly debunked "viral load" in a letter to Nature:

Here we would point out only that the central claim of the Ho et al.2 and Wei et al.3 papers - that 105 HIV virions per ml plasma can be detected in AIDS patients with various nucleic-acid amplification assays - is misleading. The senior author of the Wei et al. paper has previously claimed that the PCR method they used overestimates by at least 60,000 times the real titre of infectious HIV5: 100,000/60,000 is 1.7 infectious HIVs per ml. hardly the "virological mayhem" allud-ed to by Wain-Hobson6. Further, Ho and a different group of collaborators have just shown7 that more than 10,000 "plasma virions", detected by the branched-DNA amplification assay used in their Nature paper, correspond to less than one (!) infectious virus per ml. And infectious units after all, are the only clinically relevant criteria for a viral pathogen.
Finally, in view of Wain-Hobson's statement6 that "the concordance of their [Wei and Ho's] data is remarkable", note that Loveday et al.8 report the use of a PCR-based assay and find only 200 HIV "virion RNAS" per ml of serum of AIDS patients - 1,000 times less than Ho and Wei. So much for the "remarkable concordance". (Duesberg 1995)

In the laboratory, HIV infects CD4 lymphocytes

  • In the laboratory, HIV infects the exact type of white blood cell (CD4 lymphocytes) that becomes depleted in people with AIDS. (3) (4) (5)

COMMENT: But HIV doesn't kill CD4 cells - that's how Gallo got his HIV test patented. (Gallo 1985) Theories for the indirect mechanism of action of HIV have also failed to withstand scientific scrutiny. An article by Roederer (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 (Pakker 1998) and Gorochov et al (Gorochov 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)

Depletion of CD4 lymphocytes has been found to be a common event that appears to be a non-specific response by the body to any type of physical or psychological stress, a finding that AIDS researchers continue to ignore. The reduction of CD4 cells is often found to be below that required to diagnose AIDS in someone who is HIV-positive. (Carney 1981) (des Jarlais 1987) (Feeney 1995) (Kennedy 1988) (Kiecolt-Glaser 1984) (1991) (1992) (Pariante 1997) (Williams 1983)

Drugs that block HIV replication reduce virus load

  • Drugs that block HIV replication in the test tube also reduce virus load in people and delay progression to AIDS. Where available, treatment has reduced AIDS mortality by more than 80%. (9)

COMMENT: First of all, the reference (9) (9) is to a CDC HIV AIDS Surveillance Report, which presents no evidence for the effectiveness of any drugs. They do not cite controlled clinical trials because there are no trials showing reduced death rates. In fact, it is impossible for the new drug regimens to be responsible for the drop in AIDS deaths, because they were introduced after the drop began, according to the CDC's own data. It is remarkable that this fact is repeatedly overlooked. Clinical trials have also shown these drugs to be highly toxic, and their long term toxicities are likely to be the true cause many of the health problems that are blamed on HIV.

In 1995, the number of people dying from AIDS in the United States began to drop. When deaths due to AIDS continued to drop in 1996, around the time protease inhibitors started to be prescribed widely, this was quickly offered as proof that the new drugs were working. However, CDC statistics clearly show that new AIDS cases started dropping in 1993, several years before protease inhibitor cocktails were introduced. This would seem to be the most obvious explanation for any decrease in AIDS death rates. Intriguingly, the drop in HIV-related deaths was more than 25% between 1995 to 1996, which was before the widespread use of HAART in the United States. (HAART = Highly Active Anti-Retroviral Therapy) Between 1996 and 1997, the drop was 42%, which was before the majority of patients were using HAART. One might argue that AIDS cases and deaths have dropped because the number of new HIV infections in the United States peaked in 1982.(Stine 1998) Both NIAID Director Anthony Fauci and Helene Gayle of the CDC have confirmed that the earlier decrease in U.S. new infections played a significant role in the decrease in deaths (Goldberg, 2000). In addition, in 1993 the number of AIDS cases doubled overnight when the definition of AIDS was changed for the third time. This is almost entirely because the 1993 definition change allowed people who had low T-cell counts, but no illnesses, to be listed as AIDS cases. Since then two-thirds of AIDS cases have been people who are clinically completely healthy. This created an artificial inflation of AIDS cases. These new cases were at low-risk, and thus the average life-expectancy of people diagnosed with AIDS would be expected to increase, no matter what medications were used. The CDC itself states that the new figures for AIDS prevalence have been artificially inflated by the definition changes:

Durban rebuttal image002.gif

Figure 1. Adult/adolescent AIDS cases reported 1987 through 1997, United States. "AIDS case reports received after January 1, 1993 were influenced by the expanded AIDS surveillance case definition and chiefly represent reporting of persons who had CD4+ cell counts below 200/ul with or without illness. This change greatly altered the pattern of case reports and was most pronounced in the first quarter of 1993." (CDC 1997)

AZT, 3TC, d4T , protease inhibitors and other drugs termed "antiretrovirals" have been hailed as breakthroughs in AIDS treatment. So what studies exist that support the widespread claims that new AIDS medications have revolutionized the treatment of AIDS? One would expect a lot of very clear and striking study results showing reduced illness and reduced death with statistically significant reductions. To most people's surprise, a careful search of the medical literature finds that these claims are not based on controlled studies, but rather on clinical observations and media reports. This is not to say that there are no studies of protease inhibitor cocktails. The problem is that they all ignore clinical health, and instead focus on viral load reduction. Only two controlled studies have actually looked at clinical health. All of the others focused exclusively on viral load, which this paper has shown to be a questionable marker for the presence of HIV, let alone for clinical health.

The two studies that do claim health benefits, and not just viral load were published in 1997 and 1998. (Hammer 1997) (Cameron 1998) They did not find statistically significant reduced death rates. Both were stopped early, which biases the results in favor of the drugs. The Hammer study suffered from very incomplete reporting, making it difficult to assess toxicity or results. In addition, the Hammer study researchers broke their own study design in order to increase their study's statistical significance. By combining two separate treatment groups, the statistical "P value" was artificially increased. In addition, the gross underreporting of "AIDS-defining" events make this study of little or no value, since it only reports on one or two of the thirty one "AIDS-defining illnesses".

The second study by Cameron et al (Cameron 1998) was of better quality, but many more of the study participants experienced toxicity rather than benefit. People given the full drug regimen had extremely high toxicities compared to placebo recipients, including 50% with diarrhea, another 52% with nausea, 29% vomiting, 28% circumoral parasthesia (numbness and tingling around the mouth), and 25% weakness. With these extremely high toxicities, it is easy to see how the double-blind could be penetrated by both patients and clinicians. Fully 21% of the people taking the triple drug combination dropped out of the study before the 4.5 months were up, which biases the results. In spite of all these favourable biases, although there was a reduction in opportunistic infections, the authors found little or no reduction in mortality, as a graph on page 546 clearly indicates. They mask this failure by lumping death statistics in with opportunistic infection statistics, citing reductions in the probability of "AIDS progression or death", a practice which seems designed to confuse or mislead people who read the study rather than to educate them. The toxicities described here occurred over the short space of 4.5 months, and the risk of giving these drugs for years on end has never been assessed.

Both these studies claim to have used a placebo (i.e. inert substance to take the place of an active medicine), but actually used a completely unproven combination of AZT with another DNA chain terminator like ddI or ddC. This alone eliminates these studies from any meaningful scientific discourse, unless the placebo combination has been shown to be at least safe, something that can only be done by testing it against a true placebo. This was not done.

One must rightfully ask how this entire multi-billion dollar industry of anti-AIDS medications was established with studies that have statistically insignificant results. When billions of dollars and thousands of careers are at stake, the potential for bias is enormous, and one must be very careful about making conclusions from such incomplete reporting.

The argument thus far is simply that the new protease inhibitor cocktails are completely unproven, open to bias, and any reported benefits may be due to placebo effects, or possibly due to a short term benefit from a broad antimicrobial effect. Many prominent scientists, however, take the argument quite a bit further. They argue that the very drugs used so wantonly with people diagnosed HIV-positive, could very well be causing much of the illness and death that is blamed on HIV. For example, Glaxo Wellcome puts the following warning in large, bold-faced, capital letters at the start of the section in the 1999 Physician's Desk Reference that describes AZT:


"Granulocytopenia", is a deficiency of the most numerous cells of our immune system, which in turn leads to opportunistic infections. Thus, AZT, by its maker's own admission, can attack a person's immune system, which is the very thing that HIV is supposedly attacking. An earlier version of the Physician's Desk Reference, published in 1992 made the connection even clearer:

It is often difficult to distinguish adverse events possibly associated with Zidovudine administration from underlying signs of HIV disease or intercurrent illness.

AZT's brand names are Retrovir and Zidovudine, and it continues to be one of the most commonly used drugs in people diagnosed HIV-positive. Up until 1993, it was used by itself in about triple the dose used today, but today it is used in combination with other drugs. Many of the newer "antiretrovirals" like ddI, 3TC, and d4T, have analogous mechanisms of action and similar toxicities to AZT. Warnings like this should bring about a great deal of concern, especially given the litany of contradictions and confusion surrounding the science of "HIV" as the cause.

For a list of citations see APPENDIX: Concerns about HAART

Monkeys inoculated with SIV DNA develop AIDS

  • Monkeys inoculated with cloned SIV DNA become infected and develop AIDS. (10)

COMMENT: The declaration cites a study by Liska et al. (10) If that study set out to prove that SIV causes AIDS in monkeys then it was very poorly designed. Three monkeys with no control group that happen to become ill hardly constitutes rigorous scientific evidence. A proper experiment would require as a control group monkeys injected with a similarly processed substance differing only in the absence of SIV. The authors were probably aware of this as they chose to emphasize their technical success "stably maintaining the entire genome of SIVmac239 as a plasmid clone" or "construct". Apparently live SIV does not cause "SAIDS" in wild monkeys. (Duesberg 1996)

In any case, the real issue is HIV, which has never caused any immune deficiency in animals including chimpanzees, the closest known animal to humans. In an interview in the November-December 1999 issue of Modern Maturity, Jane Goodall, the world-renowned scientist and activist for saving the chimpanzee, commented on failed attempts to give them AIDS by injecting them with HIV positive blood. She also commented on the horrid conditions that these chimps are forced to live under:

Since the early '80s they've been doing everything in their power to give chimps AIDS. They've injected them in the spinal cord, in the brain, in the blood, in the muscles -- but they have not succeeded in giving a single chimp AIDS. Even Gallo now says chimps are useless in AIDS research...
I'd heard some chimps were being kept at the NIH campus in Bethesda, Maryland, where we were meeting, so I asked him (Robert Gallo) to see if that was true. He went down this long, dark underground corridor with animal rooms on both sides. He opened one of the doors, and there was a chimp in a very small cage rocking from side to side, hitting the side of the cage. Rocking and hitting its head, rocking and hitting its head, rocking and hitting its head. There was a young woman in the room in a white coat blowing soap bubbles. He asked the woman what she was doing that for. She said, "To enrich the lives of the chimps."

Under such inhumane living conditions, even if the chimpanzees became sick, one would rightfully question whether any virus was necessary. Sadly, this question would probably never be raised by those eager to defend the HIV hypothesis. The preponderance of weak animal analogies highlights the fact that there are many hypotheses for how HIV could cause AIDS in humans, but none of them have held up under scientific scrutiny. (Roederer 1998)

Further compelling data are available

     Further compelling data are available. (4) HIV causes AIDS. (5) It is unfortunate that a few vocal people continue to deny the evidence. This position will cost countless lives.

COMMENT: Open Scientific dialogue about all aspects of this complex issue can only serve to further our understanding of it. Closing the doors on open dialogue only serves to protect the status quo. What if the HIV theory is mistaken like infectious theories of scurvy, pellagra, beriberi and SMON? What if the very diagnosis becomes a self-fulfilling prophecy by a combination of social isolation, over-medication, and an undermining of people's beliefs in their own health, like a medical voodoo hex? How many lives will it have cost?

In different regions of the world, HIV/AIDS can show altered patterns of spread and symptoms

    In different regions of the world, HIV/AIDS can show altered patterns of spread and symptoms. In Africa, for example, people infected with HIV are 11 times more likely to die within five years, (7) and more than 100 times more likely than uninfected people to develop Kaposi's sarcoma, a cancer linked to yet another virus. (11)

COMMENT: That "HIV/AIDS shows altered patterns of spread and symptoms" in different regions of the world is not surprising because there is not, surprisingly enough, anywhere near a single definition of AIDS. In most Western countries a diagnosis of AIDS is made based on the presence of one or more of about 30 different diseases, including relatively common diseases like tuberculosis, and a positive HIV test. In the United States about 65% of recent AIDS diagnoses have been based on a low CD4 immune cell count alone in HIV positive people with no illness; but this does not apply in Canada. (CDC 1999) (CCDR 1993) AIDS is 5-10 times more prevalent (per capita) in the United States than in Canada — even though Canada and the U.S. have very similar demographics and almost unrestricted traffic between them.

In Africa, where a positive HIV test is not required, merely having cough, diarrhea and/or a fever for a month qualifies an African as having AIDS. (WHO 1994)

Although it has been noted that HIV-positive people in Africa are more likely to get Kaposi's sarcoma, it is generally accepted that Kaposi's sarcoma is not caused by HIV. (Gallo 1998) Such a reversal in what was originally considered the signature disease of AIDS would be shocking if such reversals were not so commonplace in HIV "science". It is also notable that virologists are now trying to claim a different virus as the cause of Kaposi's sarcoma even though the disease has completely failed to show an infectious pattern. This virus, dubbed "Kaposi's Sarcoma Herpes Virus", was formerly known by the less exciting name of human herpes virus 8. It has been found in over 50% of Egyptian schoolchildren, yet this cancer represents less than 1% of all cancers diagnosed, and even is a minority of skin tumors:

HHV-8 antibodies are highly prevalent in Egyptian children, suggesting that, in developing countries, HHV-8 infection may be acquired early in life through routes other than sexual transmission. The lower seroprevalence of HHV-8 relative to that of the other herpes viruses suggests that HHV-8 is less transmissible than other common herpes viruses. (Andreoni 1999)

Vladimir Koliadin Ph.D., a Senior Research Scientist at The State Aerospace University in the Ukraine and a member of the American Mathematical Society, has some interesting observations about the data in Nunn et al. (7) In an earlier report from this British-funded study,(Mulder 1994) it was found that mortality in young (13-44) adults in Uganda is 60 times higher for HIV-seropositives than for seronegatives. Mainstream AIDS scientists present these results as strong evidence that HIV is the cause of AIDS. Such arguments are very persuasive to the public and most scientists, even though they are essentially flawed. Careful analysis shows the results don't confirm, but rather refute the official HIV-causes-AIDS hypothesis, and they are in agreement with predictions of the alternative hypotheses advanced by AIDS dissidents.

Koliadin observes that the death rate in the HIV-seronegative Ugandans in this study is lower than the usual (not related to HIV) death rate typical to this region. This is in perfect agreement with predictions of the alternative hypotheses which regard HIV-seropositivity as only a marker of deteriorated health and diseases usual to this region; and this contradicts predictions of the official HIV-causes-AIDS theory. (Koliadin 1998)

This reasoning suggests that the HIV test is a non-specific test that can identify a large proportion of the sick people in any group. Tragically, it sweeps them all into the AIDS basket. In Africa where medications can be rationed out to the hopeful prospects, the "HIV-positive" stigma may lead to deadly neglect.

As with any other chronic infection, various factors have a role in determining the risk of disease

     As with any other chronic infection, various factors have a role in determining the risk of disease. People who are malnourished, who already suffer other infections or who are older, tend to be more susceptible to the rapid development of AIDS following HIV infection. However, none of these factors weakens the scientific evidence that HIV is the sole cause of the AIDS epidemic.

COMMENT: If co-factors, like malnutrition and the presence of other infections, are important, then evidence is needed to prove that HIV is necessary and that the "co-" factors are not sufficient by themselves to cause AIDS, especially in Africa where much lower standards are required to give the diagnosis. A coherent theory must explain HIV-negative AIDS cases.

In this global emergency, prevention of HIV infection must be our greatest world-wide public-health priority

     In this global emergency, prevention of HIV infection must be our greatest world-wide public-health priority. The knowledge and tools to prevent infection are available. The sexual spread of HIV can be stopped by mutual monogamy, abstinence or by using condoms. Blood transmission can be prevented by screening blood products and by not reusing needles. Mother-to-child transmission can be reduced by half or more by short courses of antiviral drugs. (12) (13)

COMMENT: By reducing mother-to-child transmission of HIV with antiviral drugs the cure may kill the patients. See APPENDIX: Concerns about AZT

Limited resources and the crushing burden of poverty in many parts of the world constitute formidable challenges to the control of HIV infection

     Limited resources and the crushing burden of poverty in many parts of the world constitute formidable challenges to the control of HIV infection. People already infected can be helped by treatment with life-saving drugs, but the high cost of these drugs puts these treatments out of reach for most of the world. it is crucial to develop new antiviral drugs that are easier to take, have fewer side effects and are much less expensive, so that millions more can benefit from them.

COMMENT: Limited resources and the crushing burden of poverty are at the root of the AIDS-like conditions devastating impoverished nations. If these countries choose to administer drugs like AZT or other "anti-HIV" drugs — which have never been proven to save lives, and inflict side effects often indistinguishable from the symptoms of AIDS — we can expect further misery and death. The cost of providing these drugs on a large scale will wipe out the budgets of health departments in cash poor nations and turn them into client bureaucracies of international pharmaceutical corporations.

There are many ways of communicating the vital information on HIV/AIDS

     There are many ways of communicating the vital information on HIV/AIDS, and what works best in one country may not be appropriate in another. But to tackle the disease, everyone must first understand that HIV is the enemy. Research, not myths, will lead to the development of more effective and cheaper treatments, and, it is hoped, a vaccine. But for now, emphasis must be placed on preventing sexual transmission.

COMMENT: Given the evidence cited and quoted in this paper refuting nearly every aspect of conventional beliefs about AIDS, one could ask whether the popular beliefs about HIV and AIDS are myths.(Fumento 1993)

There is no end in sight to the AIDS pandemic

     There is no end in sight to the AIDS pandemic. But, by working together, we have the power to reverse its tide. Science will one day triumph over AIDS, just as it did over smallpox. Curbing the spread of HIV will be the first step. Until then, reason, solidarity, political will and courage must be our partners.

COMMENT: It is ironic that the phrase "by working together" should appear in a document designed to silence opposing views. Until HIV's role in AIDS causation is proven, examining all ideas about the causes of AIDS must become a priority. For science to triumph, the principles of open inquiry must be respected and adhered to. Surely all AIDS patients deserve the benefits of the widest possible search for greater understanding of this tragic illness and, ultimately, its cure.

The declaration has been signed by over 5000 people

The declaration has been signed by over 5000 people, including Nobel prizewinners, directors of leading research institutions, scientific academies and medical societies …

COMMENT: The widespread media attention that this letter received stands in stark contrast to the lack of coverage of a similar letter, written ten years ago, that called for a scientific reappraisal of the causes of AIDS. This letter has also been signed by thousands of people including Nobel Prizewinners and hundreds of Ph.D.'s and/or M.D.'s. (Philpott 1999) In an effort to solicit signatures to the "Durban Declaration," this remark was in the message that was sent out:

"Many of you will say that HIV/AIDS is not your area. However over the years you have heard enough of the arguments to understand the association." (Wain-Hobson 2000)

This fact demonstrates clearly that this is a political document with little or no effort to examine the scientific claims made by scientists who support reappraisal of the causes of AIDS.

The Group for the Scientific Reappraisal of the HIV-AIDS Hypothesis has been nearly universally censored for almost a decade. This is an international group of distinguished scientists (including Nobel Laureates), doctors, researchers, academics and other professionals who have signed on to the statement which was mentioned above:

"It is widely believed by the general public that a retrovirus called HIV causes the group of diseases called AIDS. Many biochemical scientists now question this hypothesis. We propose that a thorough reappraisal of the existing evidence for and against this hypothesis be conducted by a suitable independent group. We further propose that critical epidemiological studies be devised and undertaken."

Although the scientific press and mainstream media are all too eager to publicize the highly political but scientifically insignificant "Durban Declaration," the initial signatories (in June of 1991) to the above statement were unable to convince the editors of Nature, Science, The Lancet and The New England Journal of Medicine to publish their letter. Each of these leading scientific journals outright REFUSED to publish it. [RA Editorial Note: Science did eventually publish the letter in 1995.]

The list of signatories:

Updated as of November 2005

Where to go from here?

A logical response to the dialogue President Mbeki initiated, would be to design studies which can establish what role, if any, HIV has in AIDS. These studies should have been started 12 years ago when many scientists began questioning the HIV/AIDS hypothesis. As suggested at the meeting of President Mbeki's advisory panel, Helene Gayle of the CDC and Duesberg/Bialy along with an impartial group of scientists should undertake rigorously designed studies to sort the facts from popular consensus on HIV. Other parties as well may have compelling hypotheses worth testing. Here are a few examples, and certainly many more could be suggested:

1) Perform HIV tests (ELISA AND Western Blot) on a large sample of Africans who were diagnosed with AIDS without the use of such tests.
2) It is very curious that ELISA and Western blot tests are performed on heavily diluted serum, unlike other antibody tests. An excellent test of their true specificity would be to take serum that was "HIV-negative" when diluted and run the tests again without diluting it. This is best done on people suffering from one of the 30 or so "AIDS indicator" diseases.
3) Perform viral loads on a large sample of people who are HIV-negative by the antibody tests but who suffer from AIDS-indicator illnesses and symptoms.
4) Compare two groups of people diagnosed "HIV positive". One group who does not believe that HIV causes AIDS and who refuses to take medications to reduce "viral load", and the other group who actively participates in conventional beliefs and drug management. Members of HEAL and other similar organizations could serve as the first group. If this study is promising, a larger, better controlled study could be undertaken.

About the authors

  1. Robert Johnston is a co-founder of HEAL Toronto, and has been HIV-positive since 1985 yet has suffered no unusual illness since that time. He attributes his good health to not taking any anti-HIV medications and to not believing that his positive antibody test has much significance.
  2. Matt Irwin, MD is a family practice physician in Washington and is a co-founder of HEAL Washington DC.
  3. David Crowe is the president of the Alberta Reappraising AIDS Society and is also president of the Alberta Greens Party.


We are grateful to Carl Strygg, Harvey Bialy, John Fowler, Alison Maclean and David Gierak for suggestions and assistance preparing this document.

Durban Declaration References

  1. Joint United Nations Programme on HIV/AIDS (UNAIDS) Report on the Global HIV/AIDS Epidemic, June 2000 (UNAIDS, Geneva, 2000).
  2. Hahn, B. H. , Shaw, G. M. , De Cock, K. M. & Sharp, P. M. "AIDS as a zoonosis: scientific and public health implications". Science 287, 607–614 (2000).
  3. Weiss, R. A. & Jaffe, H. W. "Duesberg, HIV and AIDS". Nature 345, 659–660 (1990).
  4. NIAID. HIV as the Cause of AIDS
  5. O'Brien, S. J. & Goedert, J. J. "HIV causes AIDS: Koch's postulates fulfilled". Curr. Opin. Immunol. 8, 613– 618 (1996).
  6. Darby, S. C. et al. "Mortality before and after HIV infection in the complete UK population of haemophiliacs". Nature 377, 79–82 (1995).
  7. Nunn, A. J. et al. "Mortality associated with HIV-1 infection over five years in a rural Ugandan population: cohort study". Br. Med. J. 315, 767–771 (1997).
  8. Sperling, R. S. et al. "Maternal viral load, zidovudine treatment, and the risk of transmission of human immunodeficiency virus type 1 from mother to infant". N. Engl. J. Med. 335, 1678– 1680 (1996).
  9. Centers for Disease Control and Prevention (CDC) HIV/AIDS Surveillance Report 1999 11, 1–44 (1999).
  10. Liska, V. et al. "Viremia and AIDS in rhesus macaques after intramuscular inoculation of plasmid DNA encoding full-length SIVmac239". AIDS Res. Hum. Retroviruses 15, 445–450 (1999).
  11. Sitas, F. et al. "Antibodies against human herpesvirus 8 in black South African patients with cancer". N. Engl. J. Med. 340, 1863–1871 (1999).
  12. Shaffer, N. et al. "Short course zidovudine for perinatal HIV-1 transmission in Bangkok Thailand: a randomised controlled trial". Lancet 353, 773–780 (1999).
  13. Guay, L. A. et al. "Intrapartum and neonatal single-dose nevirapine compared with zidovudine for prevention of mother-to-child transmission of HIV-1 in Kampala, Uganda: HIVNET 012 randomised trial". Lancet 354, 795–802 (1999).

Rebuttal References

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