User:Revolver/AIDS reappraisal

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The AIDS reappraisal movement (or AIDS dissident movement) is a loosely-connected group of activists, journalists, citizens, scientists, researchers, and doctors who deny, challenge, or question, in various ways, the prevailing scientific consensus that the human immunodeficiency virus (HIV) is the sole cause of acquired immune deficiency syndrome (AIDS).

Their challenges often take one or more of the following forms:

  • HIV does not exist
  • HIV is a harmless retrovirus, often associated with AIDS conditions.
  • HIV does exist, and might cause AIDS, but it hasn't been proven to cause AIDS
  • HIV does exist, and might cause AIDS, but only in combination with other factors
  • HIV does exist, but does not cause AIDS: other infectious factors cause AIDS
  • HIV does exist, but does not cause AIDS: AIDS is not a contagious disease
  • HIV does exist, but does not cause AIDS: a combination of other infectious and non-infectious factors causes AIDS
  • AIDS does not always lead to death.
  • AIDS illnesses are often treatable and curable
  • Much of what causes AIDS illnesses is not infectious.
  • AIDS is a complicated phenomenon with many valid causes and many valid treatments, and cannnot be reduced to a single cause.
  • Anti-AIDS drugs, employed throughout the AIDS era, like AZT, often destroy the immune system causing the very illnesses they were/are supposed to prevent or reduce.

These claims are met with resistance by, and often evoke frustration, censorship and hostility those invested in the HIV-causes-AIDS paradigm. Members of the AIDS mainstream accuse AIDS dissidents of ignoring evidence in favor of HIV's role in AIDS, and irresponsibly posing a dangerous threat to public health by their continued activity. Dissidents assert that the current mainstream approach to AIDS, based on HIV causation, has resulted in inaccurate diagnoses, psychological terror, toxic treatments, and a squandering of public funds.

The debate and controversy regarding this issue from the early 1980s to the present has provoked heated emotions and passions from both sides.


AIDS terminology

One component of the AIDS reappraisal debate centers around semantic issues related to labeling supporters of various perspectives, or in referring to various theories and ideas. While the disagreement over the cause of AIDS is concerns scientific theories, independent of the terminology used in that conflict, semantic disagreement nevertheless influences discussions about the AIDS reapraisal.

Some mainstream "HIV researchers" and activists have used the term AIDS denialist in referring to those who question HIV's role in AIDS, an analogy to Holocaust denial. Dissidents argue that there is no actual denial of AIDS on the part of AIDS dissidents. Dissidents claim the mainstream uses this language as a strategy to avoid discussion of the HIV-causes-AIDS paradigm, by suggesting any such discussion is offensive and absurd.

Some dissenters have refer to themselves as "realists", implying their perspective is more realistic than the prevailing view. In this article, the term "dissident" is used for those who question HIV's role in AIDS.

The two camps are often in conflict over terminology with regard to the notion that HIV causes AIDS. This notion is variously called the "HIV hypothesis" or "HIV theory." To dissidents, the notion that HIV causes AIDS is, and remains, merely a hypothesis. To mainstream scientists, it is an established fact. In this article, the term "HIV theory" is used; here, "theory" is meant in its most general scientific sense, and is not synonymous with "hypothesis." The phrase "the HIV theory of AIDS" means "the HIV model for understanding AIDS."

The AIDS Dissident Community

Dissident viewpoints are quite diverse, as delinated above. AIDS dissidents include nobel winning scientists like Kary Mullis (inventor of PCR, the technology that gave rise to what is called the viral load test) and Walter Gilbert, as well as the scientist who first isolated a cancer gene, Peter Duesberg. AIDS dissidents include Dr. David Rasnick, a research scientist with nine patents on Protease Inhibitors, a drug used to treat people who are HIV diagnosed. Another notable dissident is Dr. Rodney Richards, who helped create one of the original HIV antibody test. AIDS dissidents include HIV diagnosed persons, government employees, scientists, doctors, and activists from all over the world. A web site called VIrusMyth contains a statement calling for the reappraisal of AIDS. The statement contains signatures from literally hundreds of research scientists from around the world, and thousands of those affected by AIDS, who believe the hypothesis HIV-causes-AIDS should be reappraised.

The next section describes some of the arguments that are frequently made by AIDS dissidents, along with some counter-arguments made in response. The following are summarised from some major papers of Peter Duesberg and others.

Claim: orthodoxy suppresses open debate and is ignorant of AIDS dissident reasoning and evidence

AIDS dissidents claim that orthodox AIDS proponents prevent an open discussion or presentation of AIDS reappraiser or dissident positions. To AIDS dissidents, that observation illustrates the hallmarks of the AIDS orthodoxy. They claims these are primary reasons the HIV-causes-AIDS paradigm persists: that an open, neutral discussion is unacceptable; and that orthodox AIDS proponents often do not actually understand or truly investigate dissident claims.

Herbert Spencer said, "There is a principle which is a bar against all information, which is proof against all arguments and which can not fail to keep a man in everlasting ignorance-that principle is contempt prior to investigation." Dissidents claim it is this reality that characterizes most AIDS orthodox promoters.

One prominent AIDS dissident, Jason Nusbaum, said, "When I have been able to actually engage the scientists and activists who believe HIV causes AIDS in rational discussion, almost without exception I've found they actually do not understand the evidence and arguments made by AIDS dissidents. When I point this out to them, their response is usually something like 'Everyone knows HIV causes AIDS, so I don't have the time or the inclination to ponder something so stupid.' These scientists not only don't know what they don't know about AIDS, they don't want to know!"

Dissidents claim that it is not that the AIDS orthodoxy understands dissident arguments and rejects them. It is that most of those researchers involved in AIDS never actually questioned the HIV-causes-AIDS paradigm. Dissidents say the HIV-hypothesis was announced at a press conference prior to any papers presented in the peer-reviewed, scientific literature.

The few orthodox scientists who claim to have questioned the HIV-causes-AIDS paradigm misstate and mischaracterize AIDS dissident positions (Maddox 1994a). As a result, dissidents claim the AIDS orthdoxy often argues against positions dissidents don't actually hold.

Here are two common, simple examples of the AIDS orthodoxy mischaracterizing dissident positions in their "rebuttals" of dissident research: 1) The AIDS orthodoxy repeteadly call AIDS dissidents AIDS denialists, even though virtually no AIDS dissidents "deny AIDS." 2) AIDS orthodoxy promoters repeatedly accuse AIDS dissidents of promoting unsafe sex, even though most dissident reasoning would lead the reader to understand there are many kinds of reasons to have "safer sex," as all dissidents acknowledge that sexually tranmitted diseases run rampant in AIDS-risk populations.

As of today, January 18, 2006, this article contains numerous passages written AIDS orthodoxy promoters who do not actually understand AIDS dissident positons.

Claim: HIV does not exist

Orthodox scientists claim studies have found that HIV-1 and HIV-2 are the causes of AIDS in humans. Orthdox scientists claim isolates of both HIV-1 and HIV-2 have been isolated and genotyped. The dissident claim is usually not that HIV does not exist, but that HIV-1 has not been properly "proven" to exist. This claim is based on two ideas: That the method used to isolate and discover all previous microbes, and specifically retroviruses, does not work when applied to HIV. Luc Montagnier, who was a co-discoverer of HIV, claims that the reason the previous methods cannot be used to isolate HIV is because that process destroys HIV. Dissidents respond by stating that it is impossible to know if HIV is being destroyed or even if it exists if you cannot isolate it in the first place. Subsequently, the orthodoxy changed the requirements for the isolation and characterization of new microbes, specifically retroviruses, and now claim HIV can be isolated using these criteria. Dissidents, like The Perth Group of Scientists in Australia, claim that the new criteria are illogical and do not prove characterization and isolation of mircobes, because the replacement criteria do not actually lead to the literal isolation of a new microbe.

While density gradient centrifugation is often employed in preparing HIV-1 and other lentiviruses, superior methods (including the production of infectious molecular clones) have been developed since the early 1970s (Monti-Bragadin et al., 1972; Peebles et al., 1976; Canaai et al., 1980; Grisson et al., 2004; Tebit et al., 2003; Adachi et al., 1986). Sinoussi, for instance, failed to separate 3 virus types in his sample using the techniques of the 1970s, and it was only through molecular cloning in the 1980s that scientists proved replication-competent "helper viruses" are needed to grow the replication-defective oncoviruses.

However, AIDS dissident scientists assert that the origin of infectious molecular clones is impossible to determine unless you can actually isolate a viable entity causing the "infectious molecular clones." In other words, dissidents do not dispute you can use different procedures to reveal infectious phenomena. But some dissident scientists posit you cannot infer that this infectious phenomena is unique to a newly discovered virus unless you have logical criteria to eliminate all other possibilities. AIDS dissidents claim this criteria does not exist for HIV, and that the AIDS orthodoxy never seriously considered the initial "discovery" of HIV could have been false in the first place.

Dissidents assert that even if other methods exist for isolating and charactertizing new viruses, as a result of needing to come up with new ways to prove HIV existence, this is irrelevant to the reality that the methods used in the original papers by Gallo and Montangier claiming the proof of HIV were invalid. Those methods required only the presence of AIDS, the presence of reverse transcriptase activity, or the presence of a protein called p24. Since the authors of the original HIV discovery papers could not find HIV using the original criteria for isolation, they changed their standards and claimed these phenomena proved HIV existed because these phenomena were caused by HIV. Dissidents claim this is illogical and that the justification for HIV causing AIDS made no sense in the original papers by Gallo and Montagnier. However, standards are constantlt changing, and the standards for isolating HIV have since changed again.

Dissidents go further and point out that the criteria used to establish HIV caused AIDS in these original papers are invalid, regardless of whether HIV was isolated in other studies. This is because reverse transcriptase activity can be detected in all kinds of people who do not have AIDS. And there are all kinds of humans and animals who test positive for the protein p24. However, many people can be infected with HIV and not have AIDS, as AIDS is the final step in the manifestation of HIV infection.

Claim: AIDS does not fulfill Koch's postulates for infectious disease

In order for HIV to satisfy Koch's postulates as the cause of AIDS,

  • It must be found in all individuals with AIDS
  • It must be possible to isolate HIV from someone with AIDS
  • The isolated HIV should cause AIDS when introduced into a healthy person
  • It should be possible to isolate HIV from the newly infected individual

Ideally, and within the constraints of ethical experimentation, proof of the fulfillment of these postulates is considered a sufficient demonstration of the causality of a disease. According to dissidents, failure to satisfy these postulates may cast doubt on HIV as the cause of AIDS because these are the logical rules that can establish causation and eliminate confounding variables which may contribute to AIDS etiology. Not all individuals diagnosed with HIV infection have quantifiable amounts of HIV in their blood. Dissidents claim that Koch's postulates are not adequately fulfilled, because there are individual cases in which the virus could not be found or reisolated using the methods used for all other viruses prior to the HIV era [1]. Dr. Etienne de Harven worked in electron microscopy (EM), primarily on the ultrastructure of retroviruses throughout his professional career of 25 years at the Sloan Kettering Institute in New York and 13 years at the University of Toronto. He writes, "The most impressive developments of molecular genetics over the past 20 years do not make Robert Koch's postulates obsolete. The first of these postulates indicates that to be considered as pathogenic, a microorganism should be isolated in every single case of the disease. Still, according to E. Papadopulos et all and S. Lanka (2) isolation of HIV from fresh plasma of AIDS patients has never been achieved under any circumstances."[2]

Mainstream scientists claim that HIV does fulfill these postulates, and that the exceptions are due to the imperfect sensitivity of HIV testing, or imperfect isolation techniques, rather than the absence of the virus. Mainstream scientists also claim that cholera, typhoid and Hepatitis C (a flavivirus) do not fulfill all of Koch's postulates, but are the causes of certain diseases and symptoms. Koch disregarded three postulates for cholera and typhoid (Koch 1884; Koch 1893).

Specifically, with regard to Koch's postulates #1 and #2 above in respect to HIV-1, mainstream scientists claim modern culture techniques allow the isolation of HIV in virtually all AIDS patients, as well as in almost all HIV-seropositive individuals with both early- and late-stage disease. In addition, using the polymerase chain reaction (PCR), invented by Nobel Prize-winning AIDS dissident Dr. Kary Mullis, and other sophisticated molecular techniques, mainstream researchers claim they can prove presence of HIV genes in virtually all patients with AIDS, as well as in individuals in earlier stages of HIV disease. It is not found in HIV-negative patients that do not go onto seroconvert and progress to AIDS.

But the dissidents counter that in order to make the claim that one is "isolating" "HIV genes," one must have techniques that exclude the possibility the genetic material being amplified comes from somewhere else, and can only come from a unique retrovirus, in this case HIV. Paul Philpott, former editor of "Reappraising AIDS," expelled from the Florida State University's PhD Biology program for holding AIDS dissident views, writes, "Without true isolates of the objects declared "HIV," there really is no way to determine if they constitute what HIV is claimed to be: a retrovirus of exogenous origin (an autonomous entity unaccounted for by a person's inherent DNA library). There is no way to pull proteins and genetic material out of a heterogeneous sample and know that they came from one group of particular looking objects rather than another, or simply from the surrounding molecular soup." [3]

Dr. de Harven, "In conclusion, and after extensive reviewing of the current AIDS research literature, the following statement appears inescapable: neither electron microscopy nor molecular markers have so far permitted a scientifically sound demonstration of retrovirus isolation directly from AIDS patients. "[4][5][6]

The following section is written from mainstream POV:

Postulates #3 and #4 have been fulfilled in incidents involving three laboratory workers with no other risk factors who have developed AIDS or severe immunosuppression after accidental exposure to concentrated, cloned HIV in the laboratory. In all three cases, HIV was isolated from the infected individual, sequenced and shown to be the infecting strain of virus. In another incident, transmission of HIV from a Florida dentist to six patients has been documented by genetic analyses of virus isolated from both the dentist and the patients. The dentist and three of the patients developed AIDS and died, and at least one of the other patients has developed AIDS. Five of the patients had no HIV risk factors other than multiple visits to the dentist for invasive procedures (O'Brien and Goedert, 1996; O'Brien, 1997; Ciesielski et al. 1994).

In addition, through December 1999, the CDC had received reports of 56 health care workers in the United States with documented, occupationally acquired HIV infection, of whom 25 have developed AIDS in the absence of other risk factors. The development of AIDS following known HIV seroconversion also has been repeatedly observed in pediatric and adult blood transfusion cases, in mother-to-child transmission, and in studies of hemophilia, injection-drug use and sexual transmission in which seroconversion can be documented using serial blood samples (CDC. HIV AIDS Surveillance Report 1999; AIDS Knowledge Base, 1999). For example, in a 10-year study in the Netherlands, researchers followed 11 children who had become infected with HIV as neonates by small aliquots of plasma from a single HIV-infected donor. During the 10-year period, eight of the children died of AIDS. Of the remaining three children, all showed a progressive decline in cellular immunity, and two of the three had symptoms probably related to HIV infection (van den Berg et al., 1994).

Koch's postulates also have been fulfilled in animal models of human AIDS. Chimpanzees experimentally infected with HIV have developed severe immunosuppression and AIDS. In severe combined immunodeficiency (SCID) mice given a human immune system, HIV produces similar patterns of cell killing and pathogenesis as seen in people. HIV-2, a less virulent variant of HIV which causes AIDS in people, also causes an AIDS-like syndrome in baboons. More than a dozen strains of simian immunodeficiency virus (SIV), a close cousin of HIV, cause AIDS in Asian macaques. In addition, chimeric viruses known as SHIVs, which contain an SIV backbone with various HIV genes in place of the corresponding SIV genes, cause AIDS in macaques. Further strengthening the association of these viruses with AIDS, researchers have shown that SIV/SHIVs isolated from animals with AIDS cause AIDS when transmitted to uninfected animals (O'Neil et al., 2000; Aldrovandi et al. 1993; Liska et al. 1999; Locher et al. 1998; Hirsch et al. 1994; Joag et al. 1996).

Claim: AIDS does not behave like an infectious disease

Dissidents claim that AIDS has not behaved like a typical infectious disease. Typically, they claim, infectious diseases spread rapidly, even exponentially. AIDS has progressed relatively slowly in comparison with some other known infectious diseases; this is taken by dissidents to be evidence against AIDS being caused by an infectious agent. Dissidents also note that in North America and Western Europe, AIDS spreads non-randomly, affecting specific groups of people, and moreover, that it is fragmented into distinct sub-epidemics with exclusive AIDS-defining diseases. According to dissidents, AIDS in Africa looks completely different from the corresponding syndrome in North America and Western Europe; one example that has been cited is that in Africa AIDS affects roughly equal numbers of men and women, while in North America and Western Europe it affects more men than women. Another statistic that is sometimes cited is that AIDS is highly correlated with drug use in Western countries, while it is associated with malnutrition and poor living conditions in Africa. According to dissidents, these are indicators of a non-infectious cause of AIDS.

The consensus view of mainstream scientists is that the relatively slow spread of AIDS is due to HIV's long latency period, and to new treatments and prevention campaigns which have slowed the spread of AIDS. There are many well-known infectious diseases which develop slowly and spread slowly, such as Creutzfeldt-Jakob Disease or Hepatitis C. Indeed, the slow rate of development of AIDS does not imply that it is not infectious. Transmission via body fluid contact has been well demonstrated and is typical of infectious disease: HIV behaves exactly like other viruses in terms of its transmission through blood and breast milk. Prevalence and incidence rates enable accurate predictions based on the established notion that AIDS is infectious; the epidemiology is not in any way incompatible with infectious causation.

Also, AIDS spreads within biologically isolated groups such as injection drug users and gay men because it is infectious and is effectively transmitted by sex and shared needles. HIV is said to cause the condition of immune suppresion, which in turn causes specific diseases among specific groups of people, and thus it should be expected that AIDS manifests itself differently among different groups of people. For example, if there are two people with identical immune system suppression, and one has clean water and the other doesn't, one would obviously expect the person drinking contaminated water to be more likely to develop diarrhea despite the similarities in immune function.

There could be many explanations for AIDS' appearance in different groups on different continents, including the simple coincidence of first being introduced into different groups on different continents. Educational campaigns may have had a beneficial effect in Western countries, while those in Africa have not received such educational benefits. Sexual practices in the U.S. may also be different from those in Africa. According to the prevailing perspective, none of this changes the fact that HIV is the underlying cause among all these groups. Historically, the occurrence of AIDS in human populations around the world has closely followed the appearance of HIV. In the United States, the first cases of AIDS were reported in 1981 among homosexual men in New York and California, and retrospective examination of frozen blood samples from a U.S. cohort of gay men showed the presence of HIV antibodies as early as 1978, but not before then. Subsequently, in every region, country and city where AIDS has appeared, evidence of HIV infection has preceded AIDS by just a few years (MMWR 1981a; MMWR 1981b; Jaffe et al. 1985; U.S. Census Bureau). Also, the subtype of HIV which is prevalent in Africa is different to that in North America and Europe. This may also play an important role.

Claim: HIV is harmless

In addition to the claims regarding the variations in AIDS definition between North America, Western Europe, and Africa, another fact cited as supporting evidence that HIV is harmless is the fact that a small number of HIV-positive people remain relatively healthy 15 or 20 years after testing positive for HIV. Conversely, some HIV-seronegative people develop what would have been considered AIDS-defining diseases had they tested positive.

According to the mainstream perspective, the long period of HIV infection preceding AIDS manifestations is to be expected; they claim that HIV can take years to cause the immunosuppression necessary to permit opportunistic disease to occur. Before treatment was available, the mean duration between HIV infection and the development of AIDS was thought to be eight to ten years. This long period before the development of severe consequences does not, according to mainstream scientists, mean that the virus is harmless. By this measurement, Hepatitis C would also be a "harmless" virus, as its latent stage often runs longer than 20 years.

Regarding the individuals who have developed AIDS-defining diseases in the absence of HIV, mainstream scientists state that such individuals have had their immune system compromised in other ways, and that this fact has no bearing on the ability of HIV to cause immunosuppression. Non-HIV immune suppression can also be caused by recreational drugs, chemotherapy drugs, drugs designed to be immunosuppressive, blood donations, serious genetic defects, leukemia, and severe malnourishment.

Another statistic cited by skeptics is the level of HIV infection over time. HIV has remained prevalent at a relatively constant rate in the United States population the past 20 years, suggesting to dissidents that it has existed long before the outbreak of AIDS there in the early 1980s. Mainstream scientists reply that this suggests only that the number of new infections are approximately equal to the number of deaths; thus, the level of infection remains consistent. What the dissidents fail to realise or accept, is that HIV is a cytopathic virus, but one with a high degree of variability in the cytopathic effect between isolates. This same observation is found and accepted by scientists with other viruses such as the influenza virus. It is possible to correlate the cytopathic effect of HIV and the decline of CD4 T cells with the progression to AIDS. Indeed, there exists a switch in the type of virus (R5 → X4) associated with AIDS progression. R5 is relatively harmless, but when the virus switches to the X4 variant, this is associated with a cytokine imbalance and a decline in CD4 cells leading to AIDS. R5 virus is normally selected naturally in primo-infection, hence the long latency period. However, in some individuals, this does not happen, and the X4 virus is the predominant form. In these cases, we see rapid progression towards AIDS.

A sub-category of this claim is that all retroviruses are harmless. As the association of some T-cell leukemias and lymphomas with the RNA retrovirus Human T-lymphotropic virus type I (HTLV-1) has become widely known, this claim has become less frequent. In fact, HIV itself was originally thought to be a type of HTLV.

Claim: AIDS is inconsistently defined

Of substantial concern to AIDS dissidents is the use of HIV antibody or viral testing as part of the definition of AIDS. Some of the approximately 30 AIDS-defining diseases, including Kaposi's Sarcoma and Pneumocystis jiroveci pneumonia (formerly Pneumocystis carinii or PCP), are considered diagnostic of AIDS only when serologic evidence of HIV is present. In the absence of such evidence, these diseases are thought to be related to other immune problems, and are not diagnosed as AIDS. In other words, according to dissidents, the definition of AIDS is an example of circular logic: because diagnosis with AIDS requires the presence of HIV antibodies, there can be no AIDS without HIV, by definition.

AIDS dissidents assert the HIV criterion for AIDS diagnosis creates contradictions in AIDS terminology. For example, a patient's symptoms may include a severe chest infection and diarrhea. AIDS dissidents assert that physicians under the impression that the patient is HIV positive consider the symptoms to be the result of AIDS. However, they assert, physicians do not diagnose AIDS if the patient is not in a high-risk HIV group and is thought to be HIV-negative, and they thus choose an entirely different treatment, despite identicial symptoms. AIDS dissidents claim that a self-fulfilling prophecy in the United States results from the fact that orthodox scientists only diagnose AIDS in patients thought to have HIV and then state that there are no AIDS cases without HIV.

Moreover, say dissidents, many of the AIDS-defining diseases, such as cervical cancer, have only indirect connections to immune deficiency, and should not be considered part of the definition of AIDS. Cervical cancer, for example, is caused by the human papilloma virus, which causes genital warts, but it is usually kept under control by the immune surveillance and is not able to develop into cervical cancer. Its connection to AIDS is only that a compromised immune system is unable to keep the genital warts virus under control.

AIDS stands for 'acquired immunodeficiency syndrome' and describes the collection of symptoms and infections associated with acquired deficiency of the immune system due to infection with HIV. AIDS was originally defined without reference to HIV---by necessity, since AIDS was defined as a syndrome before HIV was discovered. Once the theory that HIV causes AIDS had become established, it was added to the definition of the syndrome. It is not uncommon in medical science for a disease to first be described in terms of its physical manifestations, and to later have its definition altered as its causes become more evident. For example, the syndrome of acute pericarditis was originally described in terms of its symptoms of chest pain, pericardial friction rub, and pericardial effusion; as its etiology was determined, it became possible to classify the syndrome according to etiology---infectious (viral, tubercuarl, fungal), rheumatic, and other non-infectious causes---and a diagnosis of "acute pericarditis" without etiology is now considered incomplete. As with any new syndrome, scientists' understanding of AIDS evolved gradually, with the most obvious and severe manifestations noticed first and rarer or subtler ones recognized later.

The first definition of AIDS by the CDC in September 1982 listed 13 diseases, "at least moderately predictive of a defect in cell-mediated immunity, occurring in a person with no known cause for diminished resistance to that disease."

HIV was discovered in 1984. A year later, after discussion with epidemiologists, the CDC changed its operational definition of AIDS to add a small additional number of conditions which would be considered AIDS-definining if (and only if) they occurred in conjunction with a positive HIV test. The original list of conditions continued to trigger an AIDS diagnosis with or without a positive HIV test.

As experience with the disease continued, it became clear that it was associated with a broader array of illnesses than those initially listed. In 1987 the CDC added some of these to the case definition, including encephalopathy and wasting syndrome. These had not been in the initial definition because they are not conditions that are recorded during epidemiological surveillance.

It became apparent, however, that the operational case definition did not adequately reflect clinical experience. There were patients who were HIV infected but who did not have AIDS-defining illnesses who were doing poorly, and others who had AIDS-defining illnesses (such as one Kaposi's sarcoma lesion) yet were doing well. In January, 1993, the definition in the USA was again changed, to trigger an AIDS diagnosis on the basis of a CD4 cell count below 200 or a CD4 percentage below 14, and adding additional indicator diseases based on epidemiological observation: invasive cervical cancer, pulmonary tuberculosis and recurrent pneumonia.


It is for these reasons that the changing AIDS definition is seen by mainstream scientists as merely a reflection of broadened understanding of the disease, rather than a "circular" definition requiring a specific etiology. They claim that there is, and always has been, a strong correlation between HIV and AIDS, and thus it is perfectly natural for the presence of HIV antibodies to be a defining characteristic of AIDS.

Dissidents claim there is no consistent definition of AIDS across political or international boundaries. One example they give is that in Africa, a laboratory test is not required for a diagnosis of AIDS---this is because impoverished nations consider the test too expensive for routine use. This leaves global AIDS epidemiology without clear standards or norms.

However, mainstream scientists counter by saying that the inconsistencies among the various definitions of AIDS do not detract from the fact that HIV causes AIDS, and that while these inconsistencies represent difficulties in comparing the prevalence and incidence of the disease, they are unrelated to the causation of the disease. Furthermore, this phenomenon is not confined to HIV/AIDS issues; definitions for "high cholesterol" and "anemia" and many other medical conditions vary across political boundaries or cultures.

Two major AIDS defining systems are used today, these are the WHO recommended system for use in resource limited settings, and the CDC system for use in developed countries.

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Claim: HIV testing is unreliable

Skeptics of the HIV theory of AIDS claim that the process of testing individuals for the presence of HIV is flawed. One commonly cited example is the possibility of encountering a false positive, which would falsely identify someone as HIV positive when in fact they were HIV negative, e.g. because of cross-reactions with malaria antibodies. Dissidents also claim that the presence of antibodies to HIV should be taken as an indicator that the HIV within the body are being neutralized by the body's immune system, rather than as an indicator of active HIV.

Orthodox scientists recognize that all tests have false positives and false negatives, and strive to develop tests with lower rates of each. In any case, scientists work with aggregate data, not individual data, so that any given false result does not unduly skew results. Indeed, diagnosis of infection using antibody testing is one of the best-established concepts in medicine. Though the orthodoxy claims HIV antibody tests exceed the performance of most other infectious disease tests in both sensitivity (the ability of the screening test to give a positive finding when the person tested truly has the disease ) and specificity (the ability of the test to give a negative finding when the subjects tested are free of the disease under study), the reality is very different. All current government-approved HIV antibody tests have sensitivity and specificity in excess of 96% (except the HIV-TEK G by Sorin Biomedica) and are therefore claimed to be reliable (WHO, 2004). And ALL approved tests have the disclaimer that there is no recognized standard for establishing the absence or presence of HIV in human blood.

But with regard to HIV testing, these reliability statistics rely on underlying assumptions and orthodox claims that HIV has been properly isolated, and that these isolates were used to create the antibody or genetic HIV testing kits in use in the United States. Dissidents claim this is not what historically occurred. Instead, improper standards were used to "discover" HIV. This culture material (in vitro) from the original invalid studies, so the dissidents claim, was then used to create all subsequent "HIV diagnostic" procedures and testing kits. So even if subsequent methods were developed that in fact would yield more sensitive, specific, reliable, and/or accurate HIV diagnoses, the test kits and procedures in use throughout the AIDS era in the United States originated from studies that did not actually isolate or characterize HIV. In more simple terms, dissidents claim that because of this, actual HIV prevalance in the United States in truly unknown because the vast majority of HIV testing procedures arose from flawed studies which did not actually characterize or isolate HIV.

With technology such as the polymerase chain reaction or branched DNA assays, now routinely used in all AIDS patients in developed nations, fragements of what is called HIV DNA or RNA is detectable in nearly all symptomatic AIDS patients. Orthodox scientists and activists confuse this with actual virus testing. Dissidents claim that detecting or counting DNA or RNA fragments of a virus never properly isolated is not the same as finding viable, isolatable, infectious virions. The orthodoxy claims testing for actual viral genetic material, antigens and the virus in body fluids and cells is far more sensitive and reliable than testing for HIV antibodies. They also claim that not all antibodies are neutralizing antibodies, and have elucidated many different antibodies that are elicited by HIV infection. While not widely used for routine testing due to high cost and requirements in laboratory equipment, the orthodoxy claims these direct testing techniques have confirmed the validity of the antibody tests (Jackson et al., 1990; Busch et al., 1991; Silvester et al., 1995; Urassa et al., 1999; Nkengasong et al., 1999; Samdal et al., 1996).

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AIDS treatment toxicity

Dissidents claim the treatments prescribed to AIDS patients often cause the very symptoms they are supposed to delay. For example, the package insert of Revtrovir, a medicaton given to thousands of AIDS patients in the United States, "It was often difficult to distinguish adverse events possibly associated with administration of Retrovir from underlying signs of HIV disease or intercurrent illnesses."

Here are a few examples from the medical literature that dissidents cite as evidence AZT harmed AIDS patients:

1) The observation that among male homosexuals, "HIV dementia among those reporting any antiretroviral use (AZT, ddI, ddC, or d4T) was 97% higher than among those not using this antiretroviral therapy" is interpreted by its authors with little concern for percentages: "This effect was not statistically significant" (117[7]).

2) The stunning results that HIV-positive hemophiliacs on AZT have 4.5-times more AIDS and have a 2.4-times higher mortality than untreated HIV-positive hemophiliacs, is excused by the NIH researcher James Goedert, the former proponent of the nitrite-AIDS hypothesis (see 3.), with the casual explanation, "probably because zidovudine was administered first to those whom clinicians considered to be at highest risk" (204[8]). But, although AZT apparently increased the morbidity and mortality of hemophiliacs significantly, Goedert et al. did not question the appropriateness of AZT therapy.

3) Darby et al. report in Nature in 1995 that the mortality of HIV-positive British hemophiliacs increased 10-fold since the introduction of AZT in 1987 (183[9]). The authors acknowledge that "treatment, by prophylaxis against Pneumocystis carinii pneumonia or with zidovudine [AZT] has been widespread" in HIV-positive hemophiliacs. But instead of even considering that these drugs could play a role in accelerating the deaths of hemophiliacs, they argued that "HIV-associated mortality has not been halted by these treatments" (183[10]). They failed to explain why HIV-associated mortality would have risen 10-fold only after the introduction of AZT and other anti-AIDS therapies in 1987, rather than in the two decades before 1985 when HIV was unknowingly transfused into hemophiliacs together with clotting factor (24[11]).

4) Saah et al. explain their observation that male homosexuals on AZT have a two- to four-fold higher risk of Pneumocystis pneumonia than untreated controls as follows: "Zidovudine was no longer significant after T-helper lymphocyte count was considered, primarily because nonusers had higher cell counts..." (201[12]). The fact that an inhibitor of DNA synthesis designed to kill human cells would reduce lymphocyte counts was not mentioned.

5) An evaluation of AIDS prophylaxis with AZT produced in 1994 the following results: "the average time with neither a progression of disease nor adverse event was 15.7, 15.6, and 14.8 months for patients receiving placebo, 500 mg zidovudine, and 1500 mg zidovudine, respectively. …After 18 months, the 500-mg group gained an average of 0.5 month without disease progression, as compared with the placebo group, but had severe adverse events 0.6 month sooner." On this basis the authors concluded that, "…a reduction in the quality of life due to severe side effects of therapy approximately equals the increase in the quality of life associated with a delay in the progression of HIV disease" (202[13]). It remains unclear, however, how one gains 0.5 months "without disease progression" while one has "severe adverse effects" 0.6 months sooner.

In view of this one wonders why since 1994 at least 220,000 mostly healthy, HIV-positive people continue to receive AZT, either by itself or combined with other drugs like protease inhibitors, all of which have no therapeutic value and cost the patient or tax payer over $12,000 per year (26[14]).

6) The blunt result that AZT prophylaxis reduced survival from 3 to 2 years, and caused "wasting syndrome, cryptosporidiosis, and cytomegalovirus infection ... almost exclusively" in AZT-treated AIDS patients, was interpreted like this: "The study of patients who progress from primary HIV infection to AIDS without receiving medical intervention gives insights into the effects of medical intervention on presentation and survival after developing an AIDS defining illness". But the nature of these "insights" was not revealed by the authors (203[15]).

7) The largest test of AIDS prophylaxis with AZT of its kind, the Concorde trial, found no prophylactic value, but instead revealed a 25% higher mortality in AZT recipients than in untreated controls (343[16]). In view of these awkward results Seligmann et al. reached the patronizing conclusion: "The results of Concorde do not encourage the early use of zidovudine [AZT] in symptom-free HIV-infected adults" (160[17]).

8) A study that treated HIV-positive, intravenous drug users from New York with AZT observed: "The rate of CD4 lymphocyte depletion did not appear to slow after the initiation of zidovudine therapy….". This led to the conclusion: "Our data failed to provide evidence for an effect of zidovudine on the depletion of CD4+ lymphocytes, but the direction of the modeling results suggested that zidovudine users in this sample may have experienced more rapid CD4+ cell depletion" (87[18]).

9) As of 1994 the American NIAID and the CDC promoted the prevention of maternal HIV transmission with AZT (45, 184, 185, 344). But the costs of the hypothetical triumph of reduced HIV transmission in terms of birth defects and abortions were omitted from the reports of the original trial (184[19], 185[20], 344-347[21]). However a study from outside the US reported 8 spontaneous abortions, 8 therapeutic abortions and 8 serious birth defects, including holes in the chest, abnormal indentations at the base of the spine, misplaced ears, triangular faces, heart defects, extra digits and albinism among the babies born to 104 AZT-treated women. But these bewildering results were interpreted as just "not proving safety, thus lending tenuous support to the use of this drug" (200[22]).

Indeed, "spontaneous" or therapeutic abortion as a result of AZT was not an unforseeable accident. A review in The Lancet on "non-surgical abortion" documents that chemotherapeutic drugs, like methotrexate, have been used to abort normal and ectopic pregnancies since 1952 (188[23]). The article concedes early "concerns over teratogenicity, but concludes: used correctly, the method could bring great benefits" (188[24]).

10) In 1996, the American National Institute of Child Health and Human Development reported the consequences of AIDS prophylaxis with AZT for HIV-positive babies: "In contrast with anecdotal clinical observations and other studies indicating that zidovudine favorably influences weight-growth rates, our analysis suggests the opposite. Because our analysis of zidovudine effect on standardized growth outcomes was based on limited numbers of patients (no more than 10 at any one visit with prior zidovudine use) and because we could not control for stage of HIV disease in the study design, the result indicating no effect or a negative effect of zidovudine on growth should be interpreted with caution. Presumably, zidovudine use is confounded by progression of HIV disease. The observation that standardized LAZs [length for age scores] were lower after the start of zidovudine therapy than before may suggest merely that sicker infants received zidovudine. However, our findings suggest that the widely held view that antiretroviral treatment improves growth in children with HIV disease needs further study" (205[25]). Thus AZT toxicity was shifted to HIV.

But if the lower health standards of AZT-treated babies were due to prior "HIV disease", it would have been necessary to conclude that AZT failed to reverse or even maintain the "HIV disease" of these babies. But that possibility was not mentioned nor apparently even considered by the AZT-doctors. Moreover, the likelihood that AZT was the cause of the babies’ diseases was obscured by averaging the diseases of AZT-treated with those of untreated HIV-positive babies (see 7.7.).

11) The disquieting observation that AZT increases the annual lymphoma risk of HIV-positives 50-fold, from 0.3 to 14.5%, per year was resolved by the NCI director, Samuel Broder and his collaborators, by claiming a victory for AZT: "Therefore, patients with profound immunodeficiency are living longer [on AZT], theoretically allowing more time for the development of non-Hodgkin lymphoma or other malignancies" (198[26]).

Toxicity of Protease Inhibitors

Dissidents claim protease inhibitors can cause the appearance of temporary CD4 cell increases by measuring blood plasma, by the sequestering of these immune cells in lymph nodes, as the body enters into "toxic shock," as it is poisoned by the prescribed pharmaceutical drugs. Dissidents claim that eventually, because protease is an enzyme required for life, AIDS medications in the class of protease inhibitors, will kill HIV diagnosed people, regardless of whether HIV is the cause of AIDS.

HAART is the therapy, composed of multiple "anti-HIV drugs," that is prescribed to many HIV diagnosed people, even before they develop symptoms of AIDS (and without considering that many will never develop these symptoms). The therapy usually includes one nucleoside analog (DNA chain terminator), one protease inhibitor and either a second nucleoside analog (“nuke”) or a non-nucleoside reverse transcription inhibitor (NNRTI).

Protease inhibitors are like nucleoside analog drugs such as AZT in that they produce dysfunctional substitutes that interrupt or prevent normal processes of enzymes. While manufacturers of protease inhibitors claim that the drugs specifically target HIV protease, dissidents claim the growing list of side effects contradicts their assertions [27]. Nucleoside analogs such as AZT, once promoted as specifically targeting HIV, have been shown to block the construction of vital human DNA as effectively as they block the formation of HIV DNA[28]. It is now known that AZT, ddI and other nucleoside analogs block the DNA inside mitochondria, the subcellar particles that produce the energy required for the life of all cells[29].

The necessity for lifelong therapy with protease inhibitor cocktails was described as absolute for many years, although drug manufacturers often state in advertising that "the long-term effects of protease inhibitors are unknown."

According to Dr. David Rasnick, a protease expert working outside the AIDS system, the theory of resistant HIV protease is completely unfounded. Rasnick, a pioneer in the development of protease inhibitors points out, "no one has ever published data on a resistant HIV protease found in any patient. The only inhibitor-resistant HIV proteases ever examined have been produced in the lab using genetic engineering."[30]

Here are a few examples from the mainstream medical literature that dissidents claim indicate protease inhibitors increase morbidity and mortality in HIV diagnosed people:

“Our results show that a single oral dose of the HIV PI [Protease Inhibitor] indinavir induced insulin resistance [precursor to diabetes] in healthy HIV negative volunteers. The onset of insulin resistance was rapid and occurred at plasma concentrations of indinavir approximating steady-state levels observed in HIV-infected patients maintained on standard clinical doses. ” Noor MA et al. Indinavir acutely inhibits insulin-stimulated glucose disposal in humans: A randomized, placebo-controlled study. AIDS. 2002;16:F1-8.

“Participants who initiated therapy with a protease inhibitor were 2.02 times more likely to die than those who did not start therapy with this class of drug ” Hogg R et al. Rates of Disease Progression by Baseline CD4 Cell Count and Viral Load After Initiating Triple-Drug Therapy. JAMA. 2001 Nov 28;286(20):2568-77.

“[In this study on 55 healthy, uninfected, volunteers taking various combinations of the Protease Inhibitors Amprenavir (AVP) and Ritonavir (RTV) for 2 weeks]...the most common drug-related adverse events...were diarrhea, nausea, and oral paresthesia [prickling or tingling sensations in the mouth] in [treatment group 1]; nausea/vomiting, headache and dizziness in [treatment group 2] and diarrhea, nausea/vomiting, headache, and oral paresthesia in [treatment group 3, with double the dose of AVP]. In [treatment group 1] 1 individual withdrew from the study with [treatment group 2] 2 participants withdrew from the study, 1 due to rash...and 1 due to rash and [treatment group 3] 3 participants [16%] withdrew from the study, 1 due to nausea after the first dose of APV, one due to oral/perioral numbness, rash, edema of the face, ocular swelling and pruritis [itching] during APV/RTV, and 1 due to lightheadedness after RTV alone followed by vomiting and oral lesions. [Note that people diagnosed with AIDS have to take similar drugs for a lifetime, not 2 weeks, and usually in common with nucleoside analogs that are at least as toxic as protease inhibitors] ” Sadler BM et al. Pharmacokinetics and safety of amprenavir and ritonavir following multiple-dose, co-administration to healthy volunteers. AIDS. 2001 May 25;15(8):1009-18.

“A decrease in sexual interest was significantly more frequently reported by subjects (men and women) using HAART containing protease inhibitors (PI), compared with PI-naive patients ” Schrooten W et al. Sexual dysfunction associated with protease inhibitor containing highly active antiretroviral treatment. AIDS. 2001 May 25;15(8):1019-23.

“Indinavir is a protease inhibitor used for treating HIV-1. The drug is lithogenic and was thought to cause a 3% incidence of kidney stones...Our cohort study of the prevalence of indinavir nephrolitihiasis [kidney stone formation] included 155 patients with HIV for 5,732 patient-weeks...At 78 weeks 43.2% of patients had stones...The clinical prevalence of indinavir nephrolithiasis is much greater than initially reported. ” Saltel E et al. Increased prevalence and analysis of risk factors for Indinavir nephrolithiasis. J Urol. 2000 Dec;164:1895-7.

“This study demonstrates a higher than expected prevalence of premature carotid vessel lesions in the patient group treated with PI [Protease Inhibitors] for at least 12 months with respect to a patient cohort previously untreated with these drugs, thus confirming preliminary observations...The overwhelming difference between the percentage of acquired lesions reported for healthy individuals (6.7%) and our two seropositive groups including the PI-naive (14.9%) and PI-experienced (52.7%) patients indicates that HIV-1-positive patients have a much higher risk of endothelial damage which becomes quite remarkable in the case of the patients treated with PI-containing regimens for prolonged periods of time…drug abuse was not related to an increased risk of vascular lesions, nor was the viral load. ” Maggi P et al. Premature lesions of the carotid vessels in HIV-1-infected patients treated with protease inhibitors. AIDS. 2000 Nov 10;14:F123-8.

“It has previously been suggested that the metabolic and fat distribution abnormalities are a result of chronic HIV infection itself. Our results support those of others who have suggested that hyperlipidemia in the setting of HAART is a drug effect that reverses with drug withdrawal ” Hatano H et al. Metabolic and anthropometric consequences of interruption of highly active antiretroviral therapy. AIDS. 2000;14:1935-42.

“Osteopenia and osteoporosis [bone weakening disorders] are unique metabolic complications associated with protease inhibitor[PI]-containing potent antiretroviral regimens, that appear to be independent of adipose tissue maldistribution…Prior to the availability of PIs, low BMD [bone mineral density] was rarely observed in HIV-infected individuals ” Tebas P et al. Accelerated bone mineral loss in HIV-infected patients receiving potent antiretroviral therapy. AIDS. 2000 Mar 10;14(4):F63-7.

“Use of HIV-1 protease inhibitors is associated with endothelial dysfunction. The metabolic and phenotypic changes observed with these medications may predispose to atherosclerosis and increased vascular risk. ” Sosman JM et al. Endothelial Dysfunction Is Associated with the Use of Human Immunodeficiency Virus-1 Protease Inhibitors. 7th Conference on Retroviruses and Opportunistic Infections. 2000 Jan 30.

“Dr. Klein and her colleagues at the University of Wisconsin Medical School in Madison are conducting an ongoing pilot study with 21 HIV-infected patients who have received protease inhibitor therapy for more than 6 months and 7 HIV-infected controls...Flow-mediated vasodilation was impaired in all of the patients receiving protease inhibitors, but in none of the controls...These preliminary observations suggest that protease inhibitor use is associated with endothelial dysfunction, which may ...predispose to atherosclerosis and increased vascular risk. ” Reuters Health. 1999 Nov 9.

“Higher plasma levels of ritonavir are significantly associated with an increased risk of neurological or gastrointestinal side effects, Italian investigators report in [AIDS 1999; 13:2083-9] ” Reuters Health. 1999 Oct 18.

“We describe four men with HIV infection who sustained myocardial infarction (two of which were fatal) after 24 to 29 months of protease inhibitor therapy...Thus, AIDS, a fatal illness that is routinely and effectively managed with protease inhibitors, now seems to be presenting with potentially serious new risks associated with that therapy. ”

Flynn TE, Bricker LA. Myocardial Infarction in HIV-Infected Men Receiving Protease Inhibitors. Ann Intern Med. 1999 Oct 5. “British investigators have added two new cases to the growing list of reports of disfiguring striae [stretch-marks] in HIV-infected patients using protease inhibitors. "In both cases, the appearance of striae occurred within 3 months after the patient began treatment with the protease inhibitor indinavir," Dr. Amrit Darvay, now at St. Thomas’ Hospital in London, UK, and colleagues at Ealing Hospital report in the September issue of the Journal of the American Academy of Dermatology. ” Reuters Health. 1999 Oct 4.

“Adverse reactions to protease inhibitors occurred in 29% of the cohort...patients taking ritonavir were at increased risk for adverse drug reactions [particularly gastrointestinal disturbances] ” Lucas G et al. Highly Active Antiretroviral Therapy in a Large Urban Clinic: Risk Factors for Virologic Failure and Adverse Drug Reactions. Ann Intern Med. 1999 Jul 24;131:81-7.

“lipodystrophy [fat redistribution]…[was] reported by 83% of protease-inhibitor recipients and 4% of treatment-naive patients…Hyperlipidaemia [high lipid levels in the blood] at degrees associated with cardiovascular morbidity occurred in 74% of protease-inhibitor recipients.” Carr A et al. Diagnosis, prediction, and natural course of HIV-1 protease-inhibitor-associated lipodystrophy, hyperlipidaemia, and diabetes mellitus: a cohort study. Lancet. 1999 Jun 19;353(9170):2093-9.

“71% of the protease inhibitor-treated patients had hyperlipidemia compared with only 24% of the protease inhibitor-naive patients. Among the protease inhibitor-treated patients, 44% had isolated hypertriglyceridemia, 7% had type V hyperlipidemia, 37% had type IV hyperlipidemia, 36% had type IIb hyperlipidemia, and 18% had isolated hypercholesterolemia. ” Behrens G et al. Impaired glucose tolerance, beta cell function and lipid metabolism in HIV patients under treatment with protease inhibitors.. AIDS. 1999;13:F63-70.

“Despite biological plausibility, studies of protease inhibitors which evaluate survival benefit have not yet been carried out. The post-1996 AIDS conference hype that 'combination therapy including a protease inhibitor will make HIV a chronic, manageable disease just like diabetes' came back to haunt us. ” Carr A, Cooper DA. Gap between biology and reality in AIDS. Lancet. 1998 Dec 19;352(S5):16.

“Protease inhibitors can be associated with a non-ketosis-prone hyperglycaemia that occurs 1-7 months after starting treatment ” Dube MP et al. Protease inhibitor-associated hyperglycaemia. Lancet. 1997 Sep;350:713-4.

A brief history of the dissident movement

The dissident movement is often associated with one individual, a German American biochemist, Peter Duesberg, a professor of molecular and cell biology at the University of California, Berkeley. Duesberg has contributed more than any other dissident scientist to the debate. However, there were those who questioned the HIV theory before Duesberg. These include researchers in the NIH itself. Before 1984, many hypotheses were put forward to explain the new epidemic. Recreational and pharmaceutical drug abuse, multifactorial environmental models, infection with multiple STDs, behavioral models, and others were all posited by government researchers. As the cases of AIDS in transfusion recipients, hemophiliacs, sex partners of current AIDS cases, and other groups acumulated worldwide, the cause of AIDS was clearly transmissible via blood and sexual contact and the theory that HIV is the underlying cause of AIDS has been proven time and again (Cohen, 1994a; Horton, 1995).

However, one of the first people to question the role of HIV in AIDS was Casper Schmidt. In 1984 he wrote an article in the Journal of Psychohistory entitled "The Group-Fantasy Origins of AIDS" (Schmidt. 1984). In this manuscript, Schmidt posits that AIDS is an example of "epidemic hysteria" in which groups of people are subconsciously acting out social conflicts, and he compares it to documented cases of epidemic hysteria in the past, which were mistakenly thought to be infectious.

John Lauritsen, a former survey researcher and freelance journalist, also began publishing articles in the now defunct weekly, the New York Native, that were critical of the HIV theory and direction of research. He also began to develop his own ideas about recreational drug use as a cause of AIDS. His articles attracted some attention in the gay community, but remained little known among the general public.

It wasn't until 1987 that Peter Duesberg wrote his first major scientific paper questioning HIV in the journal Cancer Research; its title was "Retroviruses as Carcinogens and Pathogens: Expectations and Reality" (Duesberg, 1987). It attacked not only the virus-AIDS research program, but also the virus-cancer program. Duesberg's paper caused an immediate furor. The paper was published at just about the same time that major public health campaigns were being launched and AZT was being promoted as a treatment. A major publication, "Confronting AIDS", had been published in 1986, and this book set out an agenda for the public health sector in dealing with new epidemic. Many accused Duesberg of jeopardising public health by raising questions. During the same year, Lauritsen interviewed Duesberg, and his interview was published in the New York Native. Duesberg then followed up with a sequel in the highly respected Science and Proceedings of the National Academy of Sciences (Duesberg, 1989). However, from the outset, there were already obvious flaws in Duesberg’s publicly expressed HIV and AIDS opinion. He stated categorically that HIV is not the cause of AIDS (Duesberg, 1988). This was not possible to do, as on the basis of his analysis, all he could have reasonably claim was that it had not been proven that HIV causes AIDS. There then followed the epistemological problems. One such is what constitutes proof of causation in the biomedical sciences. Over the next several years, Duesberg continued to publish papers questioning HIV, and other scientists began to publicly voice their doubts.

Eleni Papadopulos-Eleopulos, a medical physicist based at Royal Perth Hospital in Australia, and her group have published since 1988, that HIV has never been fully isolated. They also stipulate that HIV has not been proven to exist as a distinct entity (Papadopulos-Eleopulos et al., 2004). Duesberg certainly agrees that HIV does exist, but he believes it is a harmless passenger virus as opposed to the causative agent in AIDS.

Orthodox scientists claim that HIV dissident scientists used their academic credentials and affiliations to generate interest, sympathy, and allegiances in lay audiences. Indeed, it was felt that they were not troubled about recruiting lay people—who were clearly unable to evaluate the scientific validity or otherwise of their views—to their cause.

Many dissidents claimed that their views were being "censored" by the established scientific community. Indeed, dissident views and their rebuttals were evaluated with active participation from both sides in mainstream medical journals such as Science, Cancer Research, Proceedings of the National Academy of Sciences, AIDS Forschung and Genetica. For instance, in 1991, twelve scientists, researchers, and doctors under the name Group for the Scientific Reappraisal of the HIV-AIDS Hypothesis submitted a short letter to various journals. It was finally accepted and published by the editor of Science (Baumann et al., 1995). It read:

"In 1991, we, the Group for the Scientific Reappraisal of the HIV/AIDS Hypothesis, became dissatisfied with the state of the evidence that the human immunodeficiency virus (HIV) did, in fact, cause AIDS.

Specifically, we have proposed that researchers independent of the HIV establishment should audit the Centers for Disease Control's records of AIDS cases, bearing in mind that the correlation of HIV with AIDS, upon which the case for HIV causation rests, is itself an artefact of the definition of AIDS. Since 1985, exactly the same diseases or conditions have been defined as "AIDS" when antibodies are present, and as "non-AIDS" when HIV and antibodies are absent. Independent professional groups such as the Society of Actuaries should be invited to nominate members for an independent commission to investigate the following question: How frequently do AIDS-defining diseases (or low T cell counts) occur in the absence of HIV? Until we have a definition of AIDS that is independent of HIV, the supposed correlation of HIV and AIDS is mere tautology.

Other independent researchers should examine the validity of the so-called "AIDS tests," especially when these tests are used in Africa and Southern Asia, to see if they reliably record the presence of antibodies, let alone live and replicating virus.

The bottom line is this: the skeptics are eager to see the results of independent scientific testing. Those who uphold the HIV "party line" have so far refused. We object."

In 1990, Lauritsen published "Poison By Prescription: The AZT Story", a book that was highly critical of the studies demonstrating the efficacy and safety of AZT in the treatment of AIDS. In 1992, Duesberg published a lengthy paper (76 pages) in Pharmacology and Therapeutics promoting his own alternative causation theory of AIDS -- the "drug-AIDS hypothesis" (Duesberg, 1992). He claimed that the majority of AIDS cases in North America and Western Europe were the result of recreational and pharmaceutical drug abuse. His arguments mirrored many that had been put forward by Lauritsen earlier. In 1993, Lauritsen published his own manifesto, "The AIDS War", a collection of his writings on AIDS from 1985 to 1992. Robert Root-Bernstein, an associate professor of physiology at Michigan State University and former MacArthur prize recipient, professed his own doubts about the HIV theory in his 1993 book "Rethinking AIDS: The Tragic Cost of Premature Consensus". In 1994, Neville Hodgikson and the London Sunday Times published a headline story on the dissidents, which attracted much media attention itself. On the 28 October of the same year, a medical doctor, Robert Wilner, held a press conference at a North Carolina hotel, during which, he jabbed his finger with a bloody needle he had just stuck into a man who said he was infected with HIV.

In 1995, 12 articles were published by dissidents in the journal Genetica. Three were written by Duesberg, two by Papadopulos-Eleopulos and two by Root-Bernstein.

In 1996, Duesberg published his manifesto in a new book, "Inventing the AIDS Virus", in which he put forward his arguments and positions to the general reader (Duesberg, 1996a). The same year "AIDS: Virus or Drug Induced?" was published (Duesberg, 1996b). It included articles and papers by Duesberg, mathematician Mark Craddock, NIDA researcher Harry Haverkos, Lauritsen, Nobel prize winner Kary Mullis (the creator of PCR), Yale math professor Serge Lang, public health professor Gordon Stewart, and journalist Celia Farber. Neville Hodgkinson wrote his own book detailing his journalistic efforts, entitled "AIDS: The Failure of Contemporary Science". An internet website was also launched during this time, and it immediately became a destination for dissidents around the world to exchange ideas and views.

As dissident scientists continued their questioning, a patient/activist branch of the movement had also begun to develop. Health Education AIDS Liaison (HEAL) was founded in New York in 1982 and it eventually became the most prominent activist organization in the dissident movement. Other groups have come into being since then, including Alive and Well. These groups have openly challenged the HIV theory.

The usenet newsgroup was founded by James Scutero, as a place to debate dissident views.

In 1997, Lauritsen and Ian Young co-published a collection of articles on the psychological aspects of AIDS, entitled "The AIDS Cult: Essays on the Gay Health Crisis". In this book, they posit a sociopsychological aspect of the epidemic based on hysteria, fear, and forced conformity. One article which appears was written by the doctor Casper Schmidt in 1984 in the Journal of Psychohistory, entitled "The Group-Fantasy Origins of AIDS" (Schmidt. 1984). In this manuscript, Schmidt posits that AIDS is an example of "epidemic hysteria" in which groups of people are subconsciously acting out social conflicts, and he compares it to documented cases of epidemic hysteria in the past, which were mistakenly thought to be infectious. Other essays in the collection condemn the psychological aspects of AIDS education which equate sex and an HIV diagnosis with death.

Dissidents continue to campaign and publish. They have protested at recent World AIDS Conferences and other international meetings. Quite recently, dissidents attracted their first real endorsement from a major political figure, Thabo Mbeki, president of South Africa. Mbeki has openly questioned the HIV theory, and he has invited dissident scientists such as Duesberg and David Rasnick to South Africa to debate the nature of AIDS with mainstream scientists. Mbeki has suffered considerable political fallout over these actions.

The increased visibility has lead to increased response from mainstream scientists and from physicians. For many years most AIDS doctors and scientists had considered the dissidents to be a fringe movement that would disappear if ignored. They are now concerned that refusal to answer is a mistake, as they believe the theories put forth by dissidents have real-world life-and-death patient-care consequences. They believe that the dissident's notions that HIV is harmless or doesn't exist, and that AIDS is not contagious, suggest that no sexual or body fluid precautions are necessary, although many dissidents are quick to point out that this does not follow from their conclusions, and they stress that safe sexual practices are important to follow in any case. Consensus medical authorities also deplore the fact that dissidents advocate that individuals not take HIV tests or HIV drugs. They believe the proper response to this behavior is to step up their public educational efforts and thereby prevent the AIDS dissident movement from doing serious damage to worldwide efforts to control the pandemic.


  • "If there is evidence that HIV causes AIDS, there should be scientific documents which either singly or collectively demonstrate that fact, at least with a high probability. There is no such document." -- Kary Mullis, 1993 Nobel Prize in Chemistry (Sunday Times (London) 28 Nov 1993)
  • "Epidemiology is like a bikini: what is revealed is interesting; what is concealed is crucial." -- Peter Duesberg (Proceedings of the National Academy of Sciences, Feb 1991)
  • "If ever there was a rush to judgment with its predictable disastrous results, it has been the HIV-AIDS hypothesis and its aftermath." -- Dr. Richard Strohman, emeritus professor of molecular and cell biology, UC Berkeley (preface to Inventing the AIDS Virus, 1995)
  • "It is the rare person who gets up and strips himself of his personal agenda and articulates what we really do not know, because by saying that, they would diminish the impact of their own work, which is their agenda." -- Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases (NY Times, 30 Jan 2001)
  • "If I saw a man get hit by a truck and run over, and you asked, "Did you get the proof? Did the truck do it?" OK, it comes to something like that. Silly." -- Robert Gallo (Spin, Feb 1988)
  • "Last century there was a sharp difference of opinion between those, such as Koch and Pasteur, who proposed that disease could be caused by invisible microbes, and others who held that epidemics are the result of evil vapours (mal'aria). Arguments that AIDS does not have an infectious basis are as quaint as those of the miasmalists." -- Weiss and Jaffe (Nature, June 1990)
  • "(Duesberg )...has built a case on what to some looks like possible misinterpretation, misuse of statistics, and highly selective cherry-picking of the data while contrary evidence is ignored." Martin Delaney (Science, p. 314, Vol. 267, No. 5196, Jan. 20, 1995)

Mainstream Rebuttal

In 1994, the journal Science conducted a 3-month investigation to discredit dissident claims. [31] The eight page Science editorial was written two years prior to Duesberg's 700 page, referenced book called "Inventing the AIDS Virus.[32]" They interviewed many orthodox HIV-causes-AIDS supporters, a few AIDS dissidents, examined some AIDS literature, and a small fraction of Duesberg’s publications. The Science editorial claimed “...although the Berkeley virologist raises provocative questions, few researchers find his basic contention that HIV is not the cause of AIDS persuasive. Mainstream AIDS researchers argue that Duesberg’s arguments are constructed by selective reading of the scientific literature, dismissing evidence that contradicts his theses, requiring impossibly definitive proof, and dismissing outright studies marked by inconsequential weaknesses.” The Science editorial also claimed that although Duesberg and the dissident movement have garnered support from prominent mainstream scientists, including Nobel Prize winners, most of this support is related to Duesberg’s right to hold a dissenting opinion, rather than support of his claims that HIV does not cause AIDS.

"Science" did not call for any of Duesberg's hypotheses to be tested and did not conduct any experiments. Dissidents claim that the Science article failed to address most of Duesberg's central claims, for example, the validity, reliability or accuracy of HIV testing. Dissidents also claim that Science refused to allow Duesberg or any of his colleagues the right to reply to many of the articles claims. The editorial was written by a reporter, not a scientist, and it was not peer-reviewed for accuracy.

The Science editorial failed to mention the reality that the AIDS reappraisal movement is diverse, including hundreds of scientists from all over the world[33]. Dissident scientists like Valendar Turner, PhD, state that even if Duesberg's claims were all disproved, there would still be many other scientists who did not agree HIV has been isolated or proven to cause AIDS. These scientists arguments are based on evidence not presented or considered in the "Science" editorial, for example [34] "Science" failed to present claims and evidence from anyone besides Duesberg. Respected logician, mathematician and Yale Professor Serge Lang, PhD, author of many articles and a book on scientific controversies, claimed the editorial misrepresented many of Duesberg's claims, ignored most of the evidence he says support his claims, and then argued against positions he doesn't actually take [35]. Lang wrote, "the article completely omitted mention of dissenters such as Bialy and Haverkos, as well as many points raised by dissenters. For example, the NIDA meeting of May [1994], the position of Harry Haverkos on nitrite inhalants, the situation in Africa, the fact that malaria, tuberculosis, leprosy, and influenza, test false positive on the HIV antibodies test, were still not mentioned in the "Science" article."

See also



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  • Baumann E, Bethell T, Bialy H, Duesberg PH, Farber C, Geshekter CL, Johnson PE, Maver RW, Schoch R, Stewart GT, et al. (1995) AIDS proposal. Group for the Scientific Reappraisal of the HIV/AIDS Hypothesis. Science 267, 945-946 PMID 7863335
  • Busch MP, Eble BE, Khayam-Bashi H, Heilbron D, Murphy EL, Kwok S, Sninsky J, Perkins HA, Vyas GN. (1991) Evaluation of screened blood donations for human immunodeficiency virus type 1 infection by culture and DNA amplification of pooled cells. N Engl J Med 325, 1-5 PMID 2046708
  • Canaani E, Tronick SR, Robbins KC, Andersen PR, Dunn CY, Aaronson SA. (1980) Cellular origin of the transforming gene of Moloney murine sarcoma virus. Cold Spring Harb Symp Quant Biol. 44 Pt 2, 727-734 PMID 6253207
  • Ciesielski CA, Marianos DW, Schochetman G, Witte JJ, Jaffe HW. (1994) The 1990 Florida dental investigation. The press and the science. Ann Intern Med 121, 886-888 PMID 7978703
  • Cohen J. (1994) The Duesberg phenomenon. Science 266, 1642-1644 PMID 7992043
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de:Aids-Dissident eo:Aidoso-retaksado pt:Reavaliação da AIDS zh:艾滋病重估运动