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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.
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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]).
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