Document:Drug Consumption 3
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Criteria of Infectious and Noninfectious Disease
The correct hypothesis explaining the cause of AIDS must predict the fundamental differences between the two main AIDS epidemics and the bewildering heterogeneity of the 25 AIDS diseases. In addition, the cause of American/European AIDS should make clear why – in an era of ever-improving health parameters, population growth and decreasing mortality (The Software Toolworks World Atlas™, 1992; Anderson and May, 1992) – suddenly a subgroup of mostly 20- to 45-year-old males would die from diverse microbial and nonmicrobial diseases. The mortality from all infectious diseases combined has been reduced to less than 1% in the Western World (Cairns, 1978) through advanced sanitation and nutrition (Section 6) (McKeown, 1979; Moberg and Cohn, 1991; Oppenheimer, 1992). Further, 20- to 45-year-olds are the least likely to die from any disease (Mims and White, 1984). Their relative immunity to all diseases is why they are recruited as soldiers. The correct AIDS hypothesis would also have to explain why only a small group of about 20,000 Africans have developed AIDS diseases annually since 1985 (Table 1), during a time in which Central Africa enjoyed the fastest population growth in the world, i.e. 3% (The Software Toolworks World Atlas™, 1992).
The sudden appearance of AIDS could signal a new microbe, i.e. infectious AIDS. Yet the suddenness of AIDS could just as well signal one or several new toxins, such as the many new psychoactive drugs that have become popular in America and Europe since the Vietnam War (Section 4).
Based on common characteristics of all orthodox infectious diseases, infectious AIDS would be predicted to:
- Spread randomly between the sexes. This is just as true for venereal as for other infectious diseases (Judson et al., 1980; Haverkos, 1990).
- Cause primary disease within weeks or months after infection, because infectious agents multiply exponentially in susceptible hosts until stopped by immunity. They are self-replicating, and thus fast acting toxins. (Although “slow” viruses are thought to be pathogenic long after neutralization by antiviral immunity (Evans, 1989c), slow pathogenicity by a neutralized virus has never been experimentally proven (Section 6.1).)
- Coincide with a common, active and abundant microbe in all cases of the same disease. (Inactive microbes or microbes at low concentrations are harmless passengers, e.g. lysogenic bacteriophages, endogenous and latent retroviruses (Weiss et al., 1985), latent herpes virus or latent ubiquitous Pneumocystis and Candida infections (Freeman, 1979; Pifer, 1984; Williford Pifer et al., 1988). Hibernation is a proven microbial strategy of survival, which allows indefinite coexistence with the host without pathogenicity.)
- Coincide with a microbe that lyses or renders nonfunctional more cells than the host can spare or regenerate.
- Generate a predictable pattern of symptoms.
By contrast non-infectious AIDS, caused by toxins, would be predicted to:
- Spread nonrandomly, according to exposure to toxins. For example, lung cancer and emphysema were observed much more frequently in men than in women 20 years ago, because men consumed much more tobacco than women 30–40 years ago (Cairns, 1978).
- Follow intoxication after variable intervals as determined by lifetime dosage and personal thresholds for disease. These intervals would be considerably longer than those between microbes and disease, because microbes are self-replicating toxins. For example, lung cancer and emphysema are “acquired” only after 10–20 years of smoking, and liver cirrhosis is “acquired” only after 10–20 years of alcoholism.
- Manifest toxin-specific and intoxication site-specific diseases, e.g. cigarettes causing lung cancer and alcohol causing liver cirrhosis.
AIDS Not Compatible with Infectious Disease
All direct parameters of AIDS are incompatible with classical criteria of infectious disease:
- Unlike conventional infectious diseases, including venereal diseases (Judson et al., 1980), American/European AIDS is nonrandomly (90%) restricted to males, although no AIDS disease is male-specific (Table 1).
- The long and unpredictable intervals between infection and “acquiring” primary AIDS symptoms – averaging two years in infants and 10 years in adults, and termed “latent periods of HIV” – stand in sharp contrast to the short intervals of days or weeks between infection and primary disease observed with all classical viruses, including retroviruses (Duesberg, 1987; Duesberg and Schwartz, 1992). These short intervals reflect the time periods, that all exponentially growing microbes with generation times of half-hours, and viruses including HIV (Clark et al., 1991; Daar et al., 1991) with generation times of 8–48 hr need to reach immunogenic and thus potentially pathogenic concentrations (Fenner et al., 1974; Freeman, 1979; Mims and White, 1984). Once stopped by immunity, conventional viruses and microbes are no longer pathogenic. Thus long latent periods between immunity against a microbe and a given disease are incompatible with conventional microbial causes, including HIV (Section 3.5.14). The discrepancy of eight years between the hypothetical “latent periods of HIV” in infants and adults presents a secondary paradox.
Nevertheless, HIV could possibly play a role in AIDS if it were consistently reactivated by an “acquired immunodeficiency” – 10 years after it was neutralized by antibodies (Section 3.4.2) – just as Candida, Pneumocystis and cytomegalovirus play roles in AIDS if they are activated by “acquired immunodeficiency.” However, HIV is nearly always inactive even during acquired immunodeficiency (Sections 3.3.1 and 3.5.6). In the absence of HIV reactivation during AIDS, long hypothetical latent periods are simply statistical artifacts. They are conceived to link HIV with AIDS and to buy time for the real causes of AIDS to generate AIDS-defining diseases.
- There is no active microbe common to all AIDS patients, and no common group of target cells are lysed or rendered nonfunctional (Sections 3.3 and 3.5.10).
- There is no common, predictable pattern of AIDS symptoms in patients of different risk groups. Instead, different risk groups have characteristic AIDS diseases (Sections 2.1.3, 3.4.4 and 3.4.5).
Thus AIDS does not meet even one of the classical criteria of infectious disease. In a recent response to these arguments, Goudsmit, a proponent of the HIV-AIDS hypothesis, confirmed that “AIDS does not have the characteristics of an ordinary infectious disease. This view is incontrovertible” (Goudsmit, 1992). Likewise, the epidemiologists Eggers and Weyer conclude that “the spread of AIDS does not behave like the spread of a disease that is caused by a single sexually transmitted agent” (Eggers and Weyer, 1991) and hence have “simulated a cofactor [that] cannot be identified with any known infectious agent” (Weyer and Eggers, 1990). Anderson and May (1992) had to invent “assortative scenarios” for different AIDS risk groups to reconcile AIDS with infectious disease. Indeed, AIDS would never have been accepted as infectious without the numerous unique assumptions that have been made to accommodate HIV as its cause (Sections 3.5 and 6.1).
No Proof for the Virus-AIDS Hypothesis
Despite research efforts that exceed those on all other viruses combined and have generated over 60,000 papers on HIV (Christensen, 1991), it has not been possible to prove that HIV causes AIDS. These staggering statistics illustrate that the virus-AIDS hypothesis is either not provable or is very difficult to prove.
Proof for pathogenicity of a virus depends either on (1) meeting Koch’s classical postulates, (2) preventing pathogenicity through vaccination, (3) curing disease with antiviral drugs or (4) preventing disease by preventing infection. However, the HIV-hypothesis fails all of these criteria.
Virus Hypothesis Fails to Meet Koch’s Postulates
Koch’s postulates may be summarized as follows: (i) the agent occurs in each case of a disease and in amounts sufficient to cause pathological effects; (ii) the agent is not found in other diseases; and (iii) after isolation and propagation in culture, the agent can induce the disease anew (Merriam-Webster, 1965; Weiss and Jaffe, 1990).
But:
(i) HIV is certainly not present in all AIDS patients, and even antibody against HIV is not found in all patients who have AIDS-defining diseases. HIV is not even present in all persons who die from multiple indicator-diseases plus general immune system failure – the paradigm AIDS cases (Sections 3.4 and 4.5). In addition, HIV is never present “in amounts sufficient to cause pathological effects” based on the following evidence:
- On average only 1 in 500 to 3000 T-cells, or 1 in 1500 to 8000 leukocytes of AIDS patients are infected by HIV (Schnittman et al., 1989; Simmonds et al., 1990). (About 35% of leukocytes are T-cells (Walton et al., 1986).) A recent study, relying on in situ amplification of a proviral HIV DNA fragment with the polymerase chain reaction, detects HIV DNA in 1 of 10 to 1 of 1000 leukocytes of AIDS patients. However, the authors acknowledge that the in situ method cannot distinguish etween intact and defective proviruses and may include false-positives, because it does not characterize the amplified DNA products (Bagasra et al., 1992). Indeed the presence of 1 provirus per 10 or even 100 cells is exceptional in AIDS patients. This is why direct hybridization with viral DNA, a technique that is capable of seeing 1 provirus per 10 to 100 cells, typically fails to detect HIV DNA in AIDS patients (Duesberg, 1989c). According to one study, “The most striking feature...is the extremely low level of HIV provirus present in circulating PBMCs (peripheral blood mononuclear cells) in most cases” (Simmonds et al., 1990).
Since on average only 0.1% (1 out of 500 to 3000) of T-cells are ever infected by HIV in AIDS patients, but at least 3% of all T-cells are regenerated (Sprent, 1977; Guyton, 1987) during the two days it takes a retrovirus to infect a cell (Duesberg, 1989c), HIV could never kill enough T-cells to cause immunodeficiency. Thus even if HIV killed every infected T-cell (Section 3.5.10), it could deplete T-cells only at 1/30 of their normal rate of regeneration, let alone activated regeneration. The odds of HIV causing T-cell deficiency would be the same as those of a bicycle rider trying to catch up with a jet airplane.
- It is also inconsistent with a common pathogenic mechanism that the fraction of HIV-infected leukocytes in patients with the same AIDS diseases varies 30- to 100-fold. One study reports that the fraction of infected cells ranges from 1 in 900 to 1 in 30,000 (Simmonds et al., 1990), and another reports that it ranges from 1 in 10 to 1 in 1000 (Bagasra et al., 1992). In all conventional viral diseases the degree of pathogenicity is directly proportional to the number of infected cells.
- It is entirely inconsistent with HIV-mediated pathogenicity that there are over 40 times more HIV-infected leukocytes in many healthy HIV carriers than in AIDS patients with fatal AIDS (Simmonds et al., 1990; Bagasra et al., 1992). Simmonds et al. report that there are from 1 in 700 to 1 in 83,000 HIV-infected leukocytes in healthy HIV carriers and from 1 in 900 to 1 in 30,000 in AIDS patients. Bagasra et al. report that there are from 1 in 30 to 1 in 1000 infected leukocytes in healthy carriers and from 1 in 10 to 1 in 1000 in patients with fatal AIDS. Thus there are healthy persons with 43 times (30,000:700) and 33 times (1000:30) more HIV-infected cells than in AIDS patients.
- In terms of HIV’s biological function, it is even more important that the levels of HIV RNA synthesis in AIDS are either extremely low or even nonexistent. Only 1 in 10,000 to 100,000 leukocytes express viral RNA in 50% of AIDS patients. In the remaining 50% no HIV expression is detectable (Duesberg, 1989c; Simmonds et al., 1990). The very fact that amplification by the polymerase chain reaction must be used to detect HIV DNA or RNA (Semple et al., 1991) in AIDS patients indicates that not enough viral RNA can be made or is made in AIDS patients to explain any, much less fatal, pathogenicity based on conventional precedents (Duesberg and Schwartz, 1992). The amplification method is designed to detect a needle in a haystack, but a needle in a haystack is not sufficient to cause a fatal disease, even if it consists of plutonium or cyanide.
- In several AIDS diseases, that are not caused by immunodeficiency (Section 3.5.8), HIV is not even present in the diseased tissues, e.g. there is no trace of HIV in any Kaposi’s sarcomas (Salahuddin et al., 1988) and there is no HIV in neurons of patients with dementia, because of the generic inability of retroviruses to infect nondividing cells like neurons (Sections 3.5.8 and 3.5.10) (Duesberg, 1989c).
As a result, there is typically no free HIV in AIDS patients (Section 3.5.6). Indeed, the scarcity of infectious HIV in typical AIDS patients is the reason that neutralizing antibodies, rather than virus, have become the diagnostic basis of AIDS. It is also the reason that on average 5 million leukocytes of HIV-positives must be cultured to activate (“isolate”) HIV from AIDS patients. Even under these conditions it may take up to 15 different isolation efforts (!) to get just one infectious virus out of an HIV carrier (Weiss et al., 1988). The scarcity of HIV and HIV-infected cells in AIDS patients is also the very reason for the notorious difficulties experienced by leading American (Hamilton, 1991a; Hamilton, 1991b; Crewdson, 1992) and British (Connor, 1991, 1992; Weiss, 1991) AIDS researchers in isolating, and in attributing credit for isolating HIV from AIDS patients.
(ii) HIV does not meet Koch’s second postulate, because it is found not just in one, but in 25 distinct diseases, many as unrelated to each other as dementia and diarrhea, or Kaposi’s sarcoma and pneumonia (Table 1, Section 2.1.2).
(iii) HIV also fails Koch’s third postulate, because it fails to cause AIDS when experimentally inoculated into chimpanzees which make antibodies against HIV just like their human cousins (Blattner et al., 1988; Institute of Medicine, 1988; Evans, 1989b; Weiss and Jaffe, 1990). Up to 150 chimpanzees have been inoculated since 1983 and all are still healthy (Duesberg, 1989c) (Jorg Eichberg, personal communication, see Section 1). HIV also fails to cause AIDS when accidentally introduced into humans (Duesberg, 1989c, 1991a).
There is, however, a legitimate limitation of Koch’s postulates, namely that most microbial pathogens are only conditionally pathogenic (Stewart, 1968; McKeown, 1979; Moberg and Cohn, 1991). They are pathogenic only if the immune system is low, allowing infection or intoxication of the large numbers of cells that must be killed or altered for pathogenicity. This is true for tuberculosis bacillus, cholera, influenza virus, polio virus and many others (Freeman, 1979; Mims and White, 1984; Evans, 1989c).
However, even with such limitations HIV fails the third postulate. The scientific literature has yet to prove that even one health care worker has contracted AIDS from the over 206,000 American AIDS patients during the last 10 years, and that even one of thousands of scientists has developed AIDS from HIV, which they propagate in their laboratories and companies (Section 3.5.16) (Duesberg, 1989c, 1991a). AIDS is likewise not contagious to family members living with AIDS patients for at least 100 days in the same household (Friedland et al., 1986; Sande, 1986; Hearst and Hulley, 1988; Peterman et al., 1988). However the CDC has recently claimed that seven health care workers have developed AIDS from occupational infection (Centers for Disease Control, 1992c). But the CDC has failed to provide any evidence against nonoccupational causation, such as drug addiction (see Section 4). Indeed thousands of health care workers, e.g. 2586 by 1988 (Centers for Disease Control, 1988), have developed AIDS from nonprofessional causes. In addition the CDC has failed to report the AIDS diseases of the seven patients and those of their putative donors, has failed to report their sex (see next paragraph) and whether these patients developed AIDS only after AZT treatment (see Section 4) (Centers for Disease Control, 1992c). The failure of HIV to meet the third postulate is all the more definitive since there is no antiviral drug or vaccine. Imagine what would happen if there were 206,000 polio or viral hepatitis patients in our hospitals and no health care workers were vaccinated!
Contrary to expectations that health care workers would be the first to be affected by infectious AIDS, the AIDS risk of those health care workers that have treated the 206,000 American AIDS patients is in fact lower than that of the general population, based on the following data. The CDC reports that about 75% of the American health care workers are females, but that 92% of the AIDS patients among health care workers are males (Centers for Disease Control, 1988). Thus the AIDS risk of male health care workers is 35 times higher than that of females, indicating nonprofessional AIDS causes.
Moreover, the CDC reports that the incidence of AIDS among health care workers is percentagewise the same as that in the general population, i.e. by 1988, 2586 out of 5 million health care workers, or 1/2000 had developed AIDS (Centers for Disease Control, 1988), by the same time 110,000 out of the 250 million Americans, or 1/2250, had developed AIDS (Centers for Disease Control, 1992b). Since health care workers are nearly all over 20 years old and since there is virtually no AIDS in those under 20 (Table 1), but those under 20 make up about 1/3 of the general population, it can be estimated that the AIDS risk of health care workers is actually 1/3 lower (1/3 times 1/2000) than that of the general population – hardly an argument for infectious AIDS.
In view of this, leading AIDS researchers have acknowledged that HIV fails Koch’s postulates as the cause of AIDS (Blattner et al., 1988; Evans, 1989a, b; Weiss and Jaffe, 1990; Gallo, 1991). Nevertheless, they have argued that the failure of HIV to meet Koch’s postulates invalidates these postulates rather than HIV as the cause of AIDS (Section 6.1) (Evans, 1989b, 1992; Weiss and Jaffe, 1990; Gallo, 1991). But the failure of a suspected pathogen to meet Koch’s postulates neither invalidates the timeless logic of Koch’s postulates nor any claim that a suspect causes a disease (Duesberg, 1989b). It only means that the suspected pathogen cannot be proven responsible for a disease by Koch’s postulates – but perhaps by new laws of causation (Section 6).
Anti-HIV Immunity Does Not Protect Against AIDS
Natural antiviral antibodies, or vaccination, against HIV—which completely neutralize HIV to virtually undetectable levels—are consistently diagnosed in AIDS patients with the “AIDS test.” Yet these antibodies consistently fail to protect against AIDS diseases (Section 3.5.11) (Duesberg, 1989b, c, 1991a; Evans, 1989a, b). According to Evans, “The dilemma in HIV is that antibody is not protective” (Evans, 1989a).
By contrast, all other viral diseases are prevented or cured by antiviral immunity. Indeed, since Jennerian vaccination in the late 18th century, antiviral immunity has been the only protection against viral disease. In view of this HIV researchers have argued that antibodies do not neutralize this virus (Section 3.5.11) instead of considering that HIV may not be the cause of AIDS.
Antiviral Drugs Do Not Protect Against AIDS
All anti-HIV drugs fail to prevent or cure AIDS diseases (Section 4).
All AIDS-defining Diseases Occur in the Absence of HIV
The absence of HIV does not prevent AIDS-defining diseases from occurring in all AIDS risk groups, it only prevents their diagnosis as AIDS (Sections 3.4.4, 4.5 and 4.7).
Thus, there is no proof for the virus-AIDS hypothesis – not even that AIDS is contagious. Instead, the virus-AIDS hypothesis is based only on circumstantial evidence, including epidemiological correlations and anecdotal cases (Sections 3.4 and 3.5).
Noncorrelations Between HIV and AIDS
Leading AIDS researchers acknowledge that correlations are the only support for the virus-AIDS hypothesis. For example, Blattner et al. state, “...overwhelming seroepidemiologic evidence (is) pointing toward HIV as the cause of AIDS... Better methods...show that HIV infection is present in essentially all AIDS patients” (Blattner et al., 1988). According to an editorial in Science, Baltimore deduces from studies reporting an 88% correlation between antibodies to HIV and AIDS: “This was the kind of evidence we are looking for. It distinguishes between a virus that was a passenger and one that was the cause” (Booth, 1988). The studies Baltimore relied on are those published by Gallo et al. in Science in 1984 that are the basis for the virus-AIDS hypothesis (Gallo et al., 1984; Sarngadharan et al., 1984), but their authenticity has since been questioned on several counts (Beardsley, 1986; Schupach, 1986; Connor, 1987; Crewdson, 1989; Hamilton, 1991a; Hamilton 1992b; Crewdson, 1992). Weiss and Jaffe concur that “the evidence that HIV causes AIDS is epidemiological...” (Weiss and Jaffe, 1990), although Gallo concedes that epidemiology is just “one hell of a good beginning” (Gallo, 1991). In view of correlations it is argued that “persons infected with HIV will develop AIDS and those not so infected will not” (Evans, 1989a), or that “HIV...is the sine qua non for the epidemic” (Gallo, 1991).
But correlations are only circumstantial evidence for a hypothesis. According to Sherlock Holmes, “Circumstantial evidence is a very tricky thing. It may seem to point very straight to one thing, but if you shift your point of view a little, you may find it pointing in an equally uncompromising manner to something entirely different” (Doyle, 1928). The risk in epidemiological studies is that the cause may be difficult to distinguish from noncausal associations. For example, yellow fingers are noncausally and smoking is causally associated with lung cancer. “In epidemiological parlance, the issue at stake is that of confounding” (Smith and Phillips, 1992). This is true for the “overwhelming seroepidemiologic evidence” claimed to support the virus-AIDS hypothesis on the following grounds.
Only about Half of American AIDS is Confirmed HIV-antibody-positive
In the U.S. antibodies against HIV are only confirmed in about 50% of all AIDS diagnoses; the remainder are presumptively diagnosed (Institute of Medicine, 1988; Selik et al., 1990). Several studies indicate that the natural coincidence between antibodies against HIV and AIDS diseases is not perfect, because all AIDS defining diseases occur in all AIDS risk groups in the absence of HIV (Section 4). Ironically, the CDC never records the incidence of HIV in its HIV/AIDS Surveillance Reports (Centers for Disease Control, 1992b).
It follows that the reportedly perfect correlation between HIV and AIDS is in reality an artifact of the definition of AIDS and of allowances for presumptive diagnoses (Centers for Disease Control, 1987; Institute of Medicine, 1988). Since AIDS has been defined exclusively as diseases occurring in the presence of antibody to HIV (Section 2.2), the diagnosis of AIDS is biased by its definition toward a 100% correlation with HIV. That is why “persons infected by HIV will develop AIDS and...those not so infected will not” (Evans, 1989a), and why HIV is the “sine qua non” of AIDS (Gallo, 1991).
Antibody-positive, but Virus-negative AIDS
The correlations between AIDS and HIV are in fact not correlations with HIV, but with antibodies against HIV (Sarngadharan et al., 1984; Blattner et al., 1988; Duesberg, 1989c). But antibodies signal immunity against viruses, signal neutralization of viruses, and thus protection against viral disease – not a prognosis for a future disease as is claimed for antibodies against HIV. For example, antibody-positive against polio virus and measles virus means virus-negative, and thus protection against the corresponding viral diseases. The same is true for antibodies against HIV: antibody-positive means very much virus-negative. Residual virus or viral molecules are almost undetectable in most antibody-positive persons (Sections 3.3 and 3.5.6). Thus antibodies against HIV are not evidence for a future or current HIV disease unless additional assumptions are made (Section 3.5.11).
HIV: Just One of Many Harmless Microbial Markers of Behavioral and Clinical AIDS Risks
In addition to antibodies against HIV, there are antibodies against many other passenger viruses and microbes in AIDS risk groups and AIDS patients (Sections 2.3 and 4.3.2). These include cytomegalovirus, hepatitis virus, Epstein-Barr virus, Human T-cell Leukemia Virus-I (HTLVI), herpes virus, gonorrhea, syphilis, mycoplasma, amoebae, tuberculosis, toxoplasma and many others (Gallo et al., 1983; Sonnabend et al., 1983; Blattner et al., 1985; Mathur-Wagh et al., 1985; Darrow et al., 1987; Quinn et al., 1987; Messiah et al., 1988; Stewart, 1989; Goldsmith, 1990; Mills and Masur, 1990; Root-Bernstein, 1990a, c; Duesberg, 1991a; Buimovici-Klein et al., 1988). In addition, there are between 100 and 150 chronically latent retroviruses in the human germ line (Martin et al., 1981; Nakamura et al., 1991). These human retroviruses are in every cell, not just in a few like HIV, and have the same genetic structure and complexity as HIV and all other retroviruses (Duesberg, 1989c). According to Quinn et al., “Common to African patients with AIDS and outpatient controls and American patients with AIDS and homosexual men was the finding of extremely high prevalence rates of antibody to CMV (range, 92–100%), HSV (range, 90–100%), hepatitis B virus (range, 78–82%), hepatitis A virus (range, 82–95%), EBV capsid antigen (100%), syphilis (11–23%), and T. gondii (51–74%). In contrast, the prevalence of antibody to each of these infectious agents was significantly lower among the 100 American heterosexual men...” (Quinn et al., 1987). Thus, the incidence of many human parasites, both rare and common, is high in typical AIDS patients and in typical AIDS risk groups (Sections 2.3 and 5). However, none of these microbes are fatal and nearly all are harmless to a normal immune system ([Document:Drug Consumption 2#Alternative Infectious Theories of AIDS|Section 2.3]]).
Most of these parasites, including HIV, have been accumulated by AIDS risk behavior and by clinical AIDS risks (Blattner et al., 1985; Institute of Medicine, 1988; Stewart, 1989). Such behavior includes the long-term injection of unsterile, recreational “street” drugs and large numbers of sexual contacts promoted by oral and injected aphrodisiac drugs (Section 4) (Dismukes et al., 1968; Darrow et al., 1987; Des Jarlais et al., 1987; Espinoza et al., 1987; Moss, 1987; Moss et al., 1987; van Griensven et al., 1987; Des Jarlais et al., 1988; Messiah et al., 1988; Chaisson et al., 1989; Weiss, S.H., 1989; Deininger et al., 1990; McKegney et al., 1990; Stark et al., 1990; Luca-Moretti, 1992; Seage et al., 1992). Clinical risk groups, such as hemophiliacs, accumulate such viruses and microbes from occasionally contaminated transfusions (Section 3.4.4).
It follows that a high correlation between AIDS and antibodies against one particular virus, such as HIV, does not “distinguish between a virus that was a passenger and one that was a cause” (Baltimore, see above) (Booth, 1988). It is an expected consequence or marker of behavioral and clinical AIDS risks, particularly in countries where the percentage of HIV carriers is low (Duesberg, 1991a). In addition to HIV, many other microbes and viruses which are rare and inactive, or just inactive, in the general population, such as hepatitis virus, are “specific” for AIDS patients, and thus markers for AIDS risks (Sections 2.2, 2.3 and 4.3.2). For example, 100% of AIDS patients within certain cohorts, not just 50% as with HIV (Section 2.2), were shown to have antibodies against, or acute infections of, cytomegalovirus (Gottlieb et al., 1981; Francis, 1983; van Griensven et al., 1987; Buimovici-Klein et al., 1988). A comparison of 481 HIV-positive with 1499 HIV-negative homosexual men in Berlin found that the HIV-positives were “significantly more often carriers of antibodies against hepatitis A virus, hepatitis B virus, cytomegalovirus, Epstein-Barr virus and syphilis” (Deininger et al., 1990). And the frequent occurrence of antibodies against hepatitis B virus in cohorts of homosexual AIDS patients, termed “hepatitis cohorts,” was a precedent, that helped to convince the CDC to drop the “lifestyle” hypothesis of AIDS in favor of the “hepatitis analogy” (Francis et al., 1983; Centers for Disease Control, 1986; Oppenheimer, 1992) (Section 2.2).
The higher the consumption of unsterile, injected drugs, the more sexual contacts mediated by aphrodisiac drugs and the more transfusions received, the more accidentally contaminating microbes will be accumulated (Sections 3.4.4.5, 4.3.2 and 4.5). In Africa antibodies against HIV and hepatitis virus are poor markers for AIDS risks, because millions carry antibodies against these viruses (Table 1) (Quinn et al., 1987; Evans, 1989c; Blattner, 1991). Thus it is arbitrary to consider HIV the AIDS “driver” rather than just one of the many innocent microbial passengers of AIDS patients (Francis, 1983), because it is neither distinguished by its unique presence nor by its unique biochemical activity.
Annual AIDS Risks of Different HIV-infected Risk Groups, Including Babies, Homosexuals, Drug Addicts, Hemophiliacs and Africans, Differ over 100-fold
If HIV were the cause of AIDS the annual AIDS risks of all infected persons should be similar, particularly if they are from the same country. Failure of HIV to meet this prediction would indicate that HIV is not a sufficient cause of AIDS. The occurrence of the same AIDS-defining diseases in HIV-free controls would indicate that HIV is not even necessary for AIDS.
Table 2
| HIV-infected group | Annual AIDS in percent | Group-specific diseases |
| American recipients of transfusions | 50 | pneumonia, opportunistic infections |
| American babies | 25 | dementia, bacterial |
| Male homosexual using sexual stimulants | 4-6 | Kaposi's sarcoma |
| Intravenous drug users | 4-6 | tuberculosis, wasting |
| American hemophiliacs | 2 | pneumonia, opportunistic infections |
| German hemophiliacs | 1 | pneumonia, opportunistic infections |
| American teenagers | 0.16-1.7 | hemophilia-related |
| American general population | 0.1-1 | opportunistic infections |
| Africans | 0.3 | fever, diarrhea, tuberculosis |
| Thais | 0.05 | tuberculosis |
*Based on controlled studies, it is proposed that the health risks of all HIV-infected AIDS risk groups are the same as those of matched HIV-free controls (Sections 3.4.4, 4 and 5). The virus hypothesis simply claims the specific morbidity of each of these groups for HIV.
Critically Ill Recipients of Transfusions
The annual AIDS risk of HIV-infected American recipients of transfusions (other than hemophiliacs) is about 50%, as half of all recipients die within one year after receiving a transfusion (Table 2) (Ward et al., 1989).
Since the AIDS risk of transfusion recipients is much higher than the national 3–4% average, nonviral factors must play a role (Table 1). Indeed, about 50% of American recipients of transfusions without HIV also die within 1 year after receiving a transfusion (Hardy et al., 1985; Ward et al., 1989), and over 60% within 3 years (Bove et al., 1987). Moreover, the AIDS risk of transfusion recipients increases 3–6 times faster with the volume of blood received than their risk of infection by HIV (Hardy et al., 1985; Ward et al., 1989). This indicates that the illnesses that necessitated the transfusions are responsible for the mortality of the transfusion recipients. Yet the virus hypothesis claims the relatively high mortality of American transfusion patients for HIV without considering HIV-free controls. The hypothesis also fails to consider that the effects of HIV on transfusion mortality should be practically undetectable in the face of the high mortality of transfusion recipients and its postulate that HIV causes AIDS on average only 10 years after infection.
HIV-infected Babies
The second highest annual AIDS risk is reported for perinatally infected American babies, whose health has been compromised by maternal drug addiction or by congenital diseases like hemophilia (Section 2.1.3). They develop AIDS diseases on average two years after birth (Anderson and May, 1988; Blattner et al., 1988; Institute of Medicine, 1988; Blattner, 1991). This corresponds to an annual AIDS risk of 25% (Table 2).
Since the AIDS risk of babies is much higher than the national average of 3–4% (Table 1), nonviral factors must play a role in pediatric AIDS. Based on correlations and controlled studies documenting AIDS-defining diseases in HIV-free babies, it is proposed below that maternal drug consumption (Section 4) and congenital diseases, like hemophilia (Section 3.4.4.5), are the causes of pediatric AIDS. Indeed, before AIDS surfaced, many studies had shown that maternal drug addiction was sufficient to cause AIDS-defining diseases in newborns (Section 4.6.1). In accord with this proposal it is shown that HIV is naturally a perinatally transmitted retrovirus – and thus harmless (Section 3.5.2).
HIV-positive Homosexuals
The annual AIDS risk of HIV-infected male homosexuals with hundreds of sex partners, who frequently use aphrodisiac drugs (Section 4), was originally estimated at about 6% (Mathur-Wagh et al., 1985; Anderson and May, 1988; Institute of Medicine, 1988; Lui et al., 1988; Moss et al., 1988; Turner et al., 1989; Lemp et al., 1990; van Griensven et al., 1990; Blattner, 1991). As more HIV-positives became identified, lower estimates of about 4% were reported (Table 2) (Rezza et al., 1990; Biggar and the International Registry of Seroconverters, 1990; Munoz et al., 1992).
Since the annual AIDS risk of such homosexual men is higher than the national average, group-specific factors must be necessary for their specific AIDS diseases. Based on correlations with drug consumption and studies of HIV-free homosexuals, it is proposed here that the cumulative consumption of sexual stimulants and psychoactive drugs determines the annual AIDS risk of homosexuals (Sections 4.4 and 4.5). Indeed, all AIDS-defining diseases were observed in male homosexuals from behavioral risk groups before HIV was discovered and have since been observed in HIV-free homosexuals from AIDS risk groups (Sections 4.5 and 4.7).
In the spirit of the virus-AIDS hypothesis, many of these HIV-free homosexual AIDS cases have been blamed on various retrovirus-like particles, papilloma viruses, other viruses and microbes by researchers who have not investigated drug use, particularly not oral drug use. These cases include 153 immunodeficient HIV-free homosexuals with T4/T8-cell ratios below 1 (Drew et al., 1985; Weber et al., 1986; Novick et al., 1986; Collier et al., 1987; Bartholomew et al., 1987; Buimovici-Klein et al., 1988) and 23 HIV-free Kaposi’s sarcomas (Afrasiabi et al., 1986; Ho et al., 1989b; Bowden et al., 1991; Safai et al., 1991; Castro et al., 1992; Huang et al., 1992) (see also Note added in proof).
HIV-positive Intravenous Drug Users
Application of the annual AIDS risk of male homosexual risk groups led to valid predictions for the annual AIDS risk of intravenous drug users (Lemp et al., 1990). Therefore the annual AIDS risk of HIV-infected intravenous drug users was originally estimated to be 6% (Table 2) (Lemp et al., 1990; Blattner, 1991; Goudsmit, 1992). More recent studies have concluded that the annual AIDS risk of intravenous drug users is about 4% (Table 2) (Rezza et al., 1990; Munoz et al., 1992).
These findings argue against a sexually transmitted cause, because sexual transmission predicts a much higher AIDS risk for homosexuals with hundreds of sexual partners than for intravenous drug users (Section 4) (Weyer and Eggers, 1990; Eggers and Weyer, 1991). Indeed, numerous controlled studies have indicated that the morbidity and mortality of intravenous drug users is independent of HIV (Sections 4.4, 4.5 and 4.7). On the basis of such studies it is proposed that the lifetime dose of drug consumption determines the annual AIDS risk of intravenous drug users (Section 4).
HIV-positive Hemophiliacs
The hemophiliacs provide the most accessible group to test the virus hypothesis, because the time of infection can be estimated and because the role of other health risks can be controlled by studying HIV-free hemophiliacs.
About 15,000, or 75% of the 20,000 American hemophiliacs have HIV from transfusions received before the “AIDS test” was developed in 1984 (Tsoukas et al., 1984; Hardy et al., 1985; Institute of Medicine, 1986, 1988; Stehr-Green et al., 1988; Goedert et al., 1989; Koerper, 1989). Based on limited data and antibodies against selected viral antigens, it is generally estimated that most of these infections occurred between 1978 and 1984 (Evatt et al., 1985; Johnson et al., 1985; McGrady et al., 1987; Goedert et al., 1989). This high rate of infection reflects the practice, developed in the 1960s and 1970s, of preparing factor VIII from blood pools collected from large numbers of donors (Johnson et al., 1985; Aronson, 1988; Koerper, 1989). Since only about 300 of the 15,000 HIV-infected American hemophiliacs have developed AIDS annually over the last 5 years (Morgan et al., 1990; Centers for Disease Control, 1992a, b), the annual AIDS risk of HIV-infected American hemophiliacs is about 2% (Table 2). Data from Germany extend these results: about 50% of the 6000 German hemophiliacs are HIV-positive (Koerper, 1989), and only 37 (1%) of these developed AIDS-defining diseases during 1991 and 303 (1% annually) from 1982 until 1991 (Bundesgesundheitsamt (Germany), 1991; Leonhard, 1992). An international study estimated the annual AIDS risk of adult hemophiliacs at 3% and that of children at 1% over a 5-year period of HIV-infection (Biggar and the International Registry of Seroconverters, 1990).
According to the virus-AIDS hypothesis, one would have expected that by now (about one 10-year-HIV-latent-period after infection) at least 50% of the 15,000 HIV-positive American hemophiliacs would have developed AIDS or died from AIDS. But the 2% annual AIDS risk indicates that the average HIV-positive hemophiliac would have to wait for 25 years to develop AIDS diseases from HIV, which is the same as their current median age. The median age of American hemophiliacs has increased from 11 years in 1972, to 20 years in 1982 and to over 25 years in 1986, despite the infiltration of HIV in 75% (Johnson et al., 1985; Institute of Medicine, 1986; Koerper, 1989). Thus, one could make a logical argument that HIV, instead of decreasing the lifespan of hemophiliacs, has in fact increased it.
Considering the compromised health of many hemophiliacs compared to the general population, it is also surprising, that the 1–2% annual AIDS risk of HIV-infected hemophiliacs is lower than the 3–4% risk of the average HIV-infected, nonhemophilic European or American (Table 1). There is even a bigger discrepancy between the annual AIDS risks of hemophiliacs and those of intravenous drug users and male homosexuals, which are both about 4–6% (Table 2). In an effort to reconcile the relatively low annual AIDS risks of hemophiliacs with that of homosexuals, the hematologists Sullivan et al. (1986) noted “The reasons for this difference remain unclear.” And Biggar and colleagues (1990) noted that “AIDS incubation...was significantly faster” for drug users and homosexuals than for hemophiliacs.
In view of the many claims that HIV causes AIDS in hemophiliacs, it is even more surprising that there is not even one controlled study from any country showing that the morbidity or mortality of HIV-positive hemophiliacs is higher than that of HIV-negative controls.
Instead, controlled studies show that immunodeficiency in hemophiliacs is independent of HIV, and that the lifetime dosage of transfusions is the cause of AIDS-defining diseases of hemophiliacs. Studies describing immunodeficiency in HIV-free hemophiliacs are summarized in Table 3 (Tsoukas et al., 1984; AIDS Hemophilia French Study Group, 1985; Ludlam et al., 1985; Gill et al., 1986; Kreiss et al., 1986; Madhok et al., 1986; Sullivan et al., 1986; Sharp et al., 1987; Matheson et al., 1987; Antonaci et al., 1988; Mahir et al., 1988; Aledort, 1988; Jin et al., 1989; Jason et al., 1990; Lang, et al., 1989; Becherer et al., 1990). One of these studies even documents an AIDS-defining disease in an HIV-free hemophiliac (Kreiss et al., 1986). Immunodeficiency in these studies is typically defined by a T4 to T8-cell ratio of about 1 or less than 1, compared to a normal ratio of 2.
Table 3
in HIV-negative and -positive Hemophiliacs*
| Study | HIV-negative | HIV-positive |
| 1. Tsoukas et al. (1984) | 6/14 | 9/15 |
| 2. Ludlam et al. (1985) | 15 | — |
| 3. French Study Group (1985) | 33 | 55 |
| 4. Sullivan et al. (1986) | 28 | 83 |
| 5. Madhok et al. (1986) | 9 | 10 |
| 6. Kreiss et al. (1986) | 6/17 | 22/24 |
| 7. Gill et al. (1986) | 8/24 | 30/32 |
| 8. Sharp et al. (1987) | 5/12 | — |
| 9. Matheson et al. (1987) | 5 | 3 |
| 10. Mahir et al. (1988) | 6 | 5 |
| 11. Antonaci et al. (1988) | 15 | 10 |
| 12. Aledort (1988) | 57 | 167 |
| 13. Jin et al. (1989) | 12 | 7 |
| 14. Lang et al. (1989) | 24 | 172 |
| 15. Becherer et al. (1990) | 74 | 136 |
| 16. Jason et al. (1990) | 31 | — |
| 17. de Biasi et al. (1991) | — | 10/20 |
*In a normal immune system, the T4 to T8 T-cell ratio is about 2, in immunodeficient persons and in many AIDS patients it is about 1 or below 1. Studies which list the fraction of immunodeficient hemophiliacs in HIV-positive and HIV-negative groups indicate, that HIV-positives are more likely to be immunodeficient. This is because HIV is a marker for the number of transfusions received and transfusion of foreign proteins causes immune deficiency. The study by de Biasi et al. (1991) showed that among 20 HIV-positive hemophiliacs only those 10 who received commercially purified factor VIII, but not those who received further purified factor VIII developed immunodeficiency over a period of two years. See text for references.
Most of the studies listed in Table 3 and additional ones conducted before HIV had been discovered have concluded or noted that immunodeficiency is directly proportional to the number of transfusions received over a lifetime (Menitove et al., 1983; Kreiss et al., 1984; Johnson et al., 1985; Hardy et al., 1985; Pollack et al., 1985; Prince, 1992; Ludlum et al., 1985; Gill et al., 1986). According to the hematologists Pollack et al. (1985) “derangement of immune function in hemophiliacs results from transfusion of foreign proteins or a ubiquitous virus rather than contracting AIDS infectious agent.” The “ubiquitous virus” was a reference to the virus-AIDS hypothesis but a rejection of HIV, because in 1985 HIV was extremely rare in blood concentrates outside the U.S., but immunodeficiency was observed in Israeli, Scottish and American hemophiliacs (Pollack et al., 1985). Madhok et al. also arrived at the conclusion that “clotting factor concentrate impairs the cell mediated immune response to a new antigen in the absence of infection with HIV” (Madhok et al., 1986). Aledort observed that “chronic recipients...of factor VIII, factor IX and pooled products...demonstrated significant T-cell abnormalities regardless of the presence of HIV antibody” (Aledort, 1988). Even those who claim that clotting factor does not cause immunodeficiency show that immunodeficiency in hemophiliacs increases with both the age and the cumulative dose of clotting factor received during a lifetime (Becherer et al., 1990).
One controlled study showed directly that protein impurities of commercial factor VIII, rather than factor VIII or HIV, were immunosuppressive among factor VIII-treated, HIV-positive hemophiliacs. Over a period of two years the T-cells of HIV-positive hemophiliacs treated with commercial factor VIII declined two-fold, while those of matched HIV-positive controls treated with purified factor VIII remained unchanged (Table 3) (de Biasi et al., 1991).
Before AIDS, a multicenter study investigating the immune systems of 1551 hemophiliacs treated with factor VIII from 1975 to 1979 documented lymphocytopenia in 9.3% and thrombocytopenia in 5% (Eyster et al., 1985). Accordingly, AIDS-defining opportunistic infections, including 60% pneumonias a