Document:Drug Consumption 3

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AIDS Acquired by Drug Consumption and Other Noncontagious Risk Factors
Pharmacology & Therapeutics 55: 201–277, 1992
Part 3: Discrepancies Between AIDS and Infectious Disease
by Peter Duesberg


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Contents

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:


  1. Spread randomly between the sexes. This is just as true for venereal as for other infectious diseases (Judson et al., 1980; Haverkos, 1990).

  2. 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).)

  3. 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.)

  4. Coincide with a microbe that lyses or renders nonfunctional more cells than the host can spare or regenerate.

  5. Generate a predictable pattern of symptoms.


By contrast non-infectious AIDS, caused by toxins, would be predicted to:


  1. 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).

  2. 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.

  3. 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:


  1. 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).

  2. 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.

  3. 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).

  4. 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:


  1. 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.

  2. 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.

  3. 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.

  4. 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.

  5. 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
TABLE 2

Annual AIDS Risks of HIV-infected Groups*

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
TABLE 3

Immunosuppression (T4/T8 about or less than 1)
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 and 20% tuberculosis, have been recorded in hemophiliacs between 1968 and 1979 (Johnson et al., 1985). These transfusion-acquired immunodeficiencies could more than account for the 2% annual incidence of AIDS-defining diseases in HIV-positive hemophiliacs recorded now (Centers for Disease Control, 1992b). An American hematologist who recorded opportunistic infections in hemophiliacs occurring between 1968 and 1979, including 2 candidiasis and 66 pneumonia deaths, commented in 1983 “...it seems possible that many of the unspecified pneumonias in hemophiliacs in the past would be classified today as AIDS” (Aronson, 1983).

It follows that long-term transfusion of foreign proteins causes immunodeficiency in hemophiliacs with or without HIV. The virus hypothesis has simply claimed normal morbidity and mortality of hemophiliacs for HIV, by ignoring HIV-free controls.

Nevertheless several investigators comparing HIV-negative to HIVpositive hemophiliacs have noted that immunodeficiency is more often associated with HIV-positives (Table 3), and have observed that HIV correlates with the number of transfusions received (Tsoukas et al., 1984; Kreiss et al., 1986; Sullivan et al., 1986; Koerper, 1989; Becherer et al., 1990). According to Kreiss et al. “seropositive hemophiliac subjects, on average, had been exposed to twice as much concentrate...as seronegative[s]” (Kreiss et al., 1986). And according to Goedert et al. “the prevalence of HIV-1 antibodies was directly associated with the degree of severity (of hemophilia)” (Goedert et al., 1989). Thus HIV appears just to be a marker of the multiplicity of transfusions, rather than a cause of immunodeficiency.

The conclusion that long-term transfusion of foreign proteins causes immunodeficiency makes three testable predictions:


  1. It predicts that hemophiliacs with “AIDS” would be older than average hemophiliacs. Indeed, the median age of hemophiliacs with AIDS in the U.S. (Evatt et al., 1984; Koerper, 1989; Stehr-Green et al., 1989), England (Darby et al., 1989) and other countries (Biggar and the International Registry of Seroconverters, 1990; Blattner, 1991) is significantly higher (about 34 years in the U.S.; Johnson et al., 1985; Koerper, 1989; Becherer et al., 1990) than the average age of hemophiliacs (20–25 years in the U.S., see above). Goedert et al. reported that the annual AIDS risk of 1- to 17-year-old hemophiliacs was 1.5%, that of 18- to 34-year-old hemophiliacs was 3% and that of 64-year-old hemophiliacs was 5% (Goedert et al., 1989). This confirms that the cumulative dose of transfusions received is the cause of AIDS-defining diseases among hemophiliacs. According to the hematologist Koerper, “this may reflect lifetime exposure to a greater number of units of concentrate...” and to Evatt et al., “This age bias may be due to differences in duration of exposure to blood products...” (Evatt et al., 1984; Koerper, 1989).

    By contrast, AIDS caused by an autonomous infectious pathogen would be largely independent of the age of the recipient. Even if HIV were that pathogen, the hemophiliac population with AIDS should have the same age distribution as the hemophiliac population over 10 years, because HIV is thought to take 10 years to cause AIDS and nearly all hemophiliacs were infected about 10 years ago (Johnson et al., 1985; [http://documents.aidswiki.net/PHDDC/MCG.PDF McGrady et al., 1987; Koerper, 1989).

  2. Foreign protein-mediated immunodeficiency further predicts that all AIDS diseases of hemophiliacs are opportunistic infections. If hemophilia AIDS were due to HIV only 62% of their AIDS diseases would be opportunistic infections, because 38% of all American AIDS patients have diseases, that are not dependent on, and not consistently associated with, immunodeficiency (Table 1, Section 3.5.8). These include wasting disease (19%), Kaposi’s sarcoma (10%), dementia (6%) and lymphoma (3%) (Table 1).

    The AIDS pathology of hemophiliacs confirms the prediction of the foreign protein-hypothesis exactly. In America 99% of the hemophiliacs with AIDS have opportunistic infections, of which about 70% are fungal and viral pneumonias, and less than 1% have Kaposi’s sarcoma (Evatt et al., 1984; Selik et al., 1987; Stehr-Green et al., 1988; Goedert et al., 1989; Koerper, 1989; Becherer et al., 1990). The small percentage of Kaposi’s sarcoma is due to the nitrite inhalants used by male homosexual hemophiliacs as sexual stimulants (Section 4). There are no reports of wasting disease and dementia in hemophiliacs.

  3. If hemophilia AIDS is due to transfusion of foreign proteins, the wives of hemophiliacs should not contract AIDS from their mates. But if it were due to a parenterally or sexually transmitted virus, hemophilia AIDS would be sexually transmissible. Indeed, AIDS researchers claim that the wives of hemophiliacs develop AIDS from sexual transmission of HIV (Lawrence et al., 1990; Weiss and Jaffe, 1990; Centers for Disease Control, 1992b). For example AIDS researcher Fauci asks: “How about the 60-year-old wife of a hemophiliac who gets infected? Is she cruising, too?” (Booth, 1988).

    However, (a) statistical scrutiny and (b) a controlled study unconfirm the hypothesis that hemophilia AIDS is sexually transmissible: (a) The CDC reports that 94 wives of hemophiliacs have been diagnosed with unnamed AIDS diseases since 1985 (Centers for Disease Control, 1992b). If one considers that there have been 15,000 HIV-positive hemophiliacs in the U.S. since 1985 and assumes that a third are married, then there are 5000 wives of HIV-positive hemophiliacs. About 13 of these women have developed AIDS annually during the 7 years (94:7) from 1985 to 1991 (Centers for Disease Control, 1992b). By contrast, at least 80 of these women would be expected to die per year, considering the human lifespan of about 80 years and that on average at least 1.6% of all those over 20 years of age die annually. Thus, until controls show that among 5000 HIV-negative wives of hemophiliacs only 67 (80–13) die annually, the claim that wives of hemophilics die from sexual transmission of HIV is unfounded speculation.

    Moreover, it has been pointed out that all AIDS-defining diseases of the wives of hemophiliacs are typically age-related opportunistic infections, including 81% pneumonia (Lawrence et al., 1990). Kaposi’s sarcoma, dementia, lymphoma and wasting syndrome are not observed in wives of hemophiliacs (Lawrence et al., 1990). Thus the virus-AIDS hypothesis seems to claim, once more, normal morbidity and mortality of the wives of hemophiliacs for HIV.

    (b) To test the hypothesis that immunodeficiency of hemophiliacs is sexually transmissible the T4 to T8 cell-ratio of 41 spouses and female sexual partners of immunodeficient hemophiliacs were analyzed (Kreiss et al., 1984). Twenty-two of the females had relationships with hemophiliacs with T-cell ratios below 1 and 19 with hemophiliacs with ratios of 1 and greater. The mean duration of relationships was 10 years, the mean number of sexual contacts was 111 during the previous year, and only 12% had used condoms (Kreiss et al., 1984). Since the T-cell ratios of all spouses were normal, averaging 1.68 – exactly like those of 57 normal controls, the authors concluded that “there is no evidence to date for heterosexual or household-contact transmission of T-cell subset abnormalities from hemophiliacs to their spouses...” (Kreiss et al., 1984).


It follows that the foreign protein-hypothesis, but not the HIV-hypothesis, correctly predicts (1) the pathology, (2) the age bias, (3) the noncontagiousness of hemophilia AIDS and (4) HIV-free immunodeficiency in hemophiliacs. It also explains the discrepancies between the annual AIDS risks of hemophiliacs and other risk groups (Table 2).

Since the virus hypothesis has become totally dominant in 1988, no new studies have described HIV-free immunodeficient hemophiliacs (Table 3) and the question whether HIV-free immunodeficient hemophiliacs ever developed AIDS-defining diseases became a taboo. The study by Jason et al. described data collected in the mid 1980s, the studies by Jin et al. and Becherer et al. collected data before 1988 and the one by de Biasi et al. compared the effects of purified to unpurified factor VIII only in HIV-positive hemophiliacs (Table 3).

In response to the argument that hemophiliacs only began to develop AIDS diseases when HIV appeared (Centers for Disease Control, 1986; Oppenheimer, 1992), it is proposed that “new” AIDS-defining diseases among hemophiliacs are an indirect consequence of extending their life with factor VIII treatment. Long-term treatment with factor VIII has prolonged the median life of hemophiliacs from 11 in 1972 to 25 in 1986. But contaminating foreign proteins received over periods of 10 years of treatment have also caused immunodeficiencies, and various viral and microbial contaminants have caused infections in some, and HIV infection in 75%. HIV has been a marker for the number of transfusions and factor VIII treatments received, just like hepatitis virus infection was a marker of the number of transfusions received until it was eliminated from the blood supplies (Anonymous, 1984; Koerper, 1989). Prior to factor VIII therapy most hemophiliacs died as adolescents from internal bleeding (Koerper, 1989).

HIV-positive Teenagers

The annual AIDS risk of HIV-infected American teenagers can be calculated as follows: There are about 30 million American teenagers, of which 0.03% (10,000) (Burke et al., 1990) to 0.3% (100,000) (St Louis et al., 1991) are HIV-positive. Since only 160 developed AIDS in 1991 and only 170 in 1990 (Centers for Disease Control, 1992b), their annual AIDS risk is between 0.16% and 1.7% (Table 2).

Thus the AIDS risk of teenagers with HIV is less than the national average of 3–4%. There are no statistics to indicate that the annual risk for AIDS-defining diseases of the HIV-infected teenage population is higher than that of HIV-free controls (Section 3.5.2). Since most American teenagers with AIDS are either hemophiliacs (38%), intravenous drug users (25%) or male homosexuals (25%) (Section 2.1.3), it is proposed that the associated risk factors, rather than HIV, are the cause of teenage AIDS (Sections 3.4.4.5 and 4).

HIV-positive General U.S. Population

The CDC reports that 3% of all American AIDS cases are from the general population, corresponding to 900–1200 of the 30,000~40,000 annual AIDS cases (Table 1) (Centers for Disease Control, 1992b). Since at least 0.03% to 0.3%, or 80,000 to 800,000, of the general American population of 250 million are infected (Section 3.5.2) (U.S. Department of Health and Human Services, 1990; Burke et al., 1990; Morgan et al., 1990; St Louis et al., 1991), the annual AIDS risk of the general population must be between 0.1% and 1% (Table 2). Thus the annual AIDS risk of HIV-infected Americans of the general population is similar to that of teenagers.

There are no statistics to indicate that the annual AIDS risk of the general HIV-infected population is higher than the annual risk for AIDS-defining diseases in HIV-free controls. Because the incidence of AIDS in the general population is exceedingly low, it is proposed again that it reflects the normal, low incidence of AIDS-defining diseases, rather than HIV-mediated diseases.

HIV-positive Africans

The annual AIDS risks of HIV-infected Africans is only 0.3% (Tables 1 and 2), because 6 million HIV carriers generated 129,000 AIDS cases from 1985 to the end of 1991 (Table 1). There are no controlled studies indicating that the risk for AIDS-defining diseases of HIV-infected Africans differs from that of HIV-negative controls.

Since the annual AIDS risk of HIV-infected Africans is (1) 10-times lower than the average American and European risk, (2) up to 100-fold less than that of American/European risk groups, (3) the same for both sexes unlike that in America and Europe and (4) very low considering that the annual mortality in Africa is around 2% and that AIDS includes the most common African diseases, it is proposed that African AIDS is just a new name for indigenous African diseases (Section 2.1.2).

Instead of a new virus, malnutrition, parasitic infections and poor sanitary conditions have all been proposed as causes of African AIDS-defining diseases (Editorial, 1987; Konotey-Ahulu, 1987, 1989; Rappoport, 1988; Adams, 1989). Further, it has been proposed that the incidence of tuberculosis, diarrhea, fever and other African AIDS-defining diseases may be the same in Africans with and without HIV (Editorial, 1987). And prior to the discovery of HIV, protein malnutrition was identified by the AIDS researchers Fauci et al. as the world’s leading cause of immunodeficiency, particularly in underdeveloped countries (Seligmann et al., 1984).

Indeed, recent studies document that only 2168 out of 4383 (49.5%) African AIDS patients with slim disease, tuberculosis and other Africa-specific diseases, who all met the WHO definition of AIDS, were infected by HIV. These patients were from Abidjan, Ivory Coast (De Cock et al., 1991; Taelman et al., 1991), Lusaka, Zambia and Kinshasa, Zaire (Taelman et al., 1991). Another study reports 135 (59%) HIV-free AIDS patients from Ghana out of 227 diagnosed by clinical criteria of the WHO. These patients suffered from weight loss, diarrhea, chronic fever, tuberculosis and neurological diseases (Hishida et al., 1992). An earlier study documents 116 HIV-negatives among 424 African patients that meet the WHO definition of AIDS (Widy-Wirski et al., 1988). According to an African AIDS doctor, “Today, because of AIDS, it seems that Africans are not allowed to die from these conditions any longer” (Konotey-Ahulu, 1987). Another asks “What use is a clinical case definition for AIDS in Africa?” (Gilks, 1991).

The 10-fold difference between the average annual AIDS risks of Africans and Americans/ Europeans (Table 1) can thus be resolved as follows:


  1. The high AIDS risk of HIV-positive Americans and Europeans is the product of the low absolute numbers of HIV carriers in the U.S. and Europe compared to Africa (Table 1) and of the concentration of HIV in AIDS risks groups, e.g. consumers of recreational drugs and the antiviral drug AZT (Section 4) and recipients of transfusions (Section 3.4.3).

  2. The low AIDS risk of Africans is a product of large absolute numbers of HIV carriers and their relatively low, spontaneous and malnutrition-mediated AIDS risks.


HIV-positive Thais

Given that there have been only 123 Thai AIDS cases in the last 1–2 years and an estimated 300,000 HIV carriers in Thailand (Weniger et al., 1991), the annual AIDS risk of HIV-infected Thais can be calculated to be less than 0.05% (Table 2). Since most of these 123 were either intravenous drug users or “sex workers” (Section 2.1.3), it is proposed that these specific health risks are their cause of AIDS (Section 4), rather than the HIV that they share, unspecifically, with 300,000 healthy Thais.

The over 100-fold range in the annual AIDS risks of different AIDS risks groups, summarized in Table 2, clearly indicates that HIV is not sufficient to cause AIDS. It confirms and extends an earlier CDC conclusion: “The magnitude of some of the differences in rates is so great that even gross errors in denominator estimates can be overcome” (Hardy et al., 1985). Moreover, analysis of the specific health risks of each risk group has identified nonviral health risks that are necessary and sufficient causes of AIDS (Table 3 and Section 4.5).

Specific AIDS Diseases Predetermined by Prior Health Risks

If HIV were the cause of AIDS, every AIDS case should have the same risk of having one or more of the 25 AIDS diseases. However, the data listed above (Section 2.1) and in Table 2 indicate that per AIDS case different risk groups have very specific AIDS diseases:


  1. Male homosexuals have 20 times more Kaposi’s sarcoma than all other American and European AIDS risk groups.

  2. Hemophiliacs and other recipients of transfusions have fungal and viral pneumonia and other opportunistic infections, and practically no Kaposi’s sarcoma or dementia.

  3. The AIDS diseases of the “general population” are either spontaneous, hemophilia- or age-related opportunistic infections. Typical examples are cited below (Section 3.5.16).

  4. Babies exclusively have bacterial infections (18%) and a high rate of dementia (14%), compared to adults (6%) (Table l).

  5. Africans develop Africa-specific AIDS diseases 10 times more and Kaposi’s sarcoma 10 times less often than Americans or Europeans.


The epidemiological data summarized in Section 3.4 indicate that HIV is sufficient to determine neither the annual AIDS risk, nor the type of AIDS disease an infected person may develop. Instead, prior health risks including drug consumption, malnutrition and congenital diseases like hemophilia and their treatments and even the country of residence, predetermine AIDS diseases. The correlations between HIV and AIDS that are claimed to support the virus-AIDS hypothesis are not direct, not complete, not distinctive and, above all, not controlled. Controlled studies indicate that the incidence of AIDS-defining diseases in intravenous drug users, male homosexuals practicing risk behavior and hemophiliacs is independent of HIV.

Therefore, it is proposed that various group-specific health risk factors, including recreational and antiviral drugs (Section 4) and malnutrition, are necessary and sufficient causes of AIDS. The existence of risk group-specific AIDS-defining diseases in the absence of HIV confirms this conclusion (Sections 3.4.4 and 4.5).

Assumptions and Anecdotal Cases that Appear to Support the Virus-AIDS Hypothesis

The following assumptions and anecdotal cases are frequently claimed to prove the virus-AIDS hypothesis. Despite the popularity of these claims they are either uncontrolled for alternative explanations or they are natural coincidences between HIV infection and naturally-occurring diseases.

HIV is Presumed New Because AIDS is New

HIV is presumed new in all countries with AIDS, because AIDS is new ({{PHDDCPDFlink|author=Blattner et al., 1988|link=BLAT4; Gallo and Montagnier, 1988; Weiss and Jaffe, 1990). The presumed newness of HIV is used as a primary argument for the virus-AIDS hypothesis: "...the time of occurrence of AIDS in each country is correlated with the time of introduction of HIV into that country; first HIV is introduced, then AIDS appears" (Blattner et al., 1988) or: “In every country and city where AIDS has appeared, HIV infection preceded it just by a few years” (Weiss and Jaffe, 1990).

However, according to Farr’s law, the age of a microbe in a population is determined by changes in its incidence over time (Bregman and Langmuir, 1990). If a microbe is spreading from a low to a high incidence it is new; however, if its incidence in a population is constant, it is old (Figure 1) (Freeman, 1979; Duesberg, 1991a). Figure 1 shows the incidences of long established microbes in the U.S. population, i.e. Candida and Pneumocystis each at about 100% (Freeman, 1979; Pifer, 1984; Williford Pifer et al., 1988), and cytomegalovirus and herpes virus at about 50% and 40%, respectively (Evans, 1989c). In addition, it shows the typical exponential rise and subsequent fall of a hypothetical epidemic by a new influenza virus strain (Freeman, 1979).

Figure 1

DrugConsumptionFigure1.jpg
Figure 1: Determination of the age of a microbe in a population based on Farr’s law. Farr’s law holds that a microbe entering a population spreads exponentially until a susceptible pool is saturated. Subsequently those microbes that are incompatible with long term survival of the host are eliminated exponentially, to generate a bell-shaped curve. The rise and fall of a hypothetical flu epidemic caused by a new strain of influenza virus is an example. But microbes that can coexist with their host become established. Examples are Candida, Pneurnocystis (Freeman, 1979), cytomegalovirus, herpes virus (Evans, 1989c) and HIV (see text), these are shown at the percentages at which they are established in the American population.


Ever since antibodies against HIV were first detected by the “AIDS test” in 1985, the number of antibody-positive Americans has been fixed at a constant population of 1 million, or 0.4% (Section 2.2 and Table 1). The U.S. Army also reports that from 1985 to 1990 an unchanging 0.03% of male and female applicants have been HIV-positive (Burke et al., 1990). This is the predicted distribution of a long established virus (Figure 1). Since there are over 250 million uninfected Americans, and since there is no antiviral vaccine or drug to stop the spread of HIV, the non-spread of HIV in the U.S. in the last 7 years is an infallible indication that the American “HIV epidemic” is old. The Central African HIV epidemic has also remained fixed at about 10% of the population since 1985 (Section 2.2). Likewise, HIV has remained fixed at 500,000 Europeans since 1988 (World Health Organization, 1992a). The nonspread of HIV confirms exactly the conclusion reached below that HIV behaves in a population as a quasi-genetic marker (Section 3.5.2). Hence, the assumption that HIV is new in the U.S. or in Africa is erroneous.

Indeed HIV existed in the U.S. long before its fictitious origin in Africa (Gallo, 1987; Gallo and Montagnier, 1988; Anderson and May, 1992) and its fictitious entry into this country in the 1970s (Shilts, 1987). For example, in the U.S. in 1968 an HIV-positive, male homosexual prostitute died from Kaposi’s sarcoma and immunodeficiency (Garry et al., 1988), and 45 out of 1129 American intravenous drug users were found to be HIV-positive in 1971 and 1972 (Moore et al., 1986).

The putative novelty of HIV is an anthropocentric interpretation of new technology that made it possible to discover HIV and many other latent retroviruses like HTLV-I (Duesberg and Schwartz, 1992). Indeed, the technology to detect a latent virus like HIV only became available around the time AIDS appeared. Given a new virus-scope, the assertion that HIV is new is just like claiming the appearance of “new” stars with a new telescope. Thus the claims that “...first HIV is introduced, then AIDS appears” (Blattner et al., 1988) and that “HIV...preceded it [AIDS]” (Weiss and Jaffe, 1990) are ironically more true than the proponents of the virus hypothesis had anticipated. HIV preceded AIDS by many, perhaps millions, of years.

HIV – Assumed to be Sexually Transmitted – Depends on Perinatal Transmission for Survival

AIDS is said to be a sexually transmitted disease, because HIV is thought to be a sexually transmitted virus (Section 2.2). However, HIV is not by nature a sexually transmitted virus. Sexual transmission of HIV is extremely inefficient. Based on studies measuring heterosexual and homosexual transmission, it depends on an average of 1000 heterosexual contacts and 100–500 homosexual contacts with antibody-positive people (Rosenberg and Weiner, 1988; Lawrence et al., 1990; Blattner, 1991; Hearst and Hulley, 1988; Peterman et al., 1988). According to Rosenberg and Weiner, “HIV infection in non-drug using prostitutes tends to be low or absent, implying that sexual activity alone does not place them at high risk” (Rosenberg and Weiner, 1988). Moreover, unwanted pregnancies and venereal diseases, but not HIV infections, have increased significantly in the U.S. since HIV has been known (Institute of Medicine, 1988; Aral and Holmes, 1991). This argues directly against sexual transmission of HIV.

Sexual transmission is so inefficient because there is no free, nonneutralized HIV anywhere in antibody-positive persons, particularly not in semen (Section 3.3). In a group of 25 antibody-positive men, only one single provirus of HIV could be found in over 1 million cells of semen in one of the men and no HIV at all was found in the semen of the other 24 (Van Voorhis et al., 1991). Likewise, HIV could only be isolated or reactivated from ejaculates of 9 out of 95 antibody-positive men by cocultivation with 2 million phytohemagglutinin-activated leukocytes (Anderson et al., 1992). No virus or microbe could survive if it depended on a transmission strategy that is as inefficient as 1 in 1000 contacts.

Indeed, HIV depends on perinatal, instead of sexual, transmission for survival – just like other animal and human retroviruses. Therefore, the efficiency of perinatal transmission must be high. This appears to be the case. Based on HIV-tracking via the “AIDS test,” perinatal transmission from the mother is estimated to be 13–50% efficient (Blattner et al., 1988; Blattner, 1991; Duesberg, 1991a; Institute of Medicine, 1988; European Collaborative Study, 1991). This number does not include paternal HIV transmission to the baby via semen, for which there are currently no data. The real efficiency of perinatal transmission must be higher than the antibody-tests suggest, because in a fraction of recipients HIV only becomes immunogenic when its hosts are of an advanced age (Quinn et al., 1986; St Louis et al., 1991). During the antibody-negative phase, latent HIV can be detected by the polymerase chain reaction (Rogers et al., 1989, European Collaborative Study, 1991). This is also true for other perinatally transmitted human (Blattner, 1990; Duesberg, 1991a) and animal retroviruses (Rowe, 1973; Duesberg, 1987).

HIV survival via perinatal transmission leads to two predictions: (1) HIV cannot be inherently pathogenic – just like all other perinatally transmitted viruses and microbes (Freeman, 1979; Mims and White, 1984). No microbe-host system could survive if the microbe were perinatally transmitted and at once fatal. (2) HIV must function as a quasigenetic marker, because it is quasi-nontransmissible by sex, or other natural horizontal modes of transmission, just like known murine retrovirus prototypes (Freeman, 1979; Duesberg, 1987). Both predictions are confirmed:


  1. Overwhelming statistical evidence from the U.S. and Africa documents that the risk for AIDS-defining diseases for HIV-positive babies, in the absence of other risk factors (Sections 3.4.4 and 4), is the same as that of HIV-free controls:

    (a) “AIDS tests” from applicants to the U.S. Army and the U.S. Job Corps indicate that between 0.03% (Burke et al., 1990) and 0.3% (St Louis et al., 1991) of the 17- to 19-year-old applicants are HIV-infected but healthy. Since there are about 90 million Americans under the age of 20, there must be between 27,000 and 270,000 (0.03%–0.3% of 90 million) HIV carriers. In Central Africa there are even more, since 1–2% of healthy children are HIV-positive (Quinn et al., 1986).

    Most, if not all, of these adolescents must have acquired HIV from perinatal infection for the following reasons: sexual transmission of HIV depends on an average of 1000 sexual contacts, and only 1 in 250 Americans carries HIV (Table 1). Thus, all positive teenagers would have had to achieve an absurd 1000 contacts with a positive partner, or an even more absurd 250,000 sexual contacts with random Americans to acquire HIV by sexual transmission. It follows that probably all of the healthy adolescent HIV carriers were perinatally infected, as for example the 22-year-old Kimberly Bergalis (Section 3.5.16).

    The AIDS risk of perinatally infected babies of the general population can be estimated as follows. Between 27,000 and 270,000 Americans under the age of 20 carry HIV. But only about 4260 AIDS cases have been recorded in this age group in the last 10 years (Centers for Disease Control, 1992b). Therefore, between 85% and 98% of HIV-infected youths do not develop AIDS up to 20 years after perinatal infection (Section 2.1). Since the above number includes the AIDS babies from drug-addicted mothers (Sections 3.4.2 and 4), the AIDS risk of HIV-infected babies from mothers that don’t use drugs probably reflects normal infant mortality.

    (b) A controlled study from Africa compared 218 newborns from HIV-positive mothers to 218 from HIV-negative mothers, and the “rates of prematurity, low birth weight, congenital malformations and neonatal mortality were comparable in the two groups” (Lepage et al., 1991). The mothers were matched for age and parity and the “frequency of signs and symptoms was not statistically different in the two groups.”

  2. The incidence of HIV in American teenagers of different ethnic backgrounds is predictable on genetic grounds. It is about 10-fold higher in blacks than in whites, i.e. 0.3% compared to 0.03% (U.S. Department of Health and Human Services, 1990; Burke et al., 1990; Blattner, 1991; Palca, 1991; St Louis et al., 1991; Vermund, 1991). HIV was even 50-fold more common in black mothers in inner-city hospitals in New York (36%) than in whites (0.7%) (Landesmann et al., 1987). This reflects the 25- to 50-fold higher incidence of HIV in the blacks’ African ancestors (10%) compared to the whites’ European ancestors (0.2 to 0.4%) (Section 2.2, Table 1). Likewise, the different ethnic groups of the Caribbean reflect the distinct HTLV-I incidences of their ancestors in Africa, Europe and Japan, despite generations of coexistence on the Caribbean islands (Blattner, 1990). The unchanging incidence of HIV in the American population (Figure 1) also confirms the view that HIV is a quasi-genetic marker. Since there is virtually no horizontal transmission of retroviruses, murine retroviruses have functioned as classical genetic markers of mice that could only be distinguished from cellular genes by fastidious genetic crosses (Rowe, 1973).


Thus the assumption that AIDS is sexually transmitted by HIV is not consistent with the natural perinatal mode of HIV transmission. If natural transmission of HIV caused a disease, AIDS would be a pediatric disease. Instead, HIV is merely a marker of either an average of 1000 sexual contacts and thus of many other possible AIDS risks associated with very high sexual activity or of long-term intravenous drug use (Sections 3.4.3 and 5).

AIDS Assumed to be Proportional to HIV Infection

The incidence of AIDS is assumed to be proportional to the incidence of HIV via a constant factor. For example, a 10-fold higher incidence of AIDS in American and European males compared to females is assumed to reflect a 10-fold higher incidence of HIV in men (Blattner et al., 1988; Blattner, 1991; Goudsmit, 1992).

However, there is no evidence that the incidence of HIV is 10 times higher in males than in females of the general American and European population, although this is the case for AIDS (Table l). Indeed, the most recent claim for a 90% bias of HIV for males of the general population (Blattner, 1991) is only supported by a reference to an editorial (Palca, 1991), which itself provides nothing more than an unreferenced cartoon showing global patterns of HIV infection. According to a CDC epidemiologist, estimates of how HIV is distributed between the sexes of the general population are “approximations” based on the distribution of AIDS (Tim Dondero, CDC, personal communication; see also Anderson and May, 1992) – a tautology.

Proportionality between HIV and AIDS via a constant is also incompatible with the following statistics. The U.S. Army (Burke et al., 1990) and the U.S. Job Corps (St Louis et al., 1991) report, based on millions of tests, that HIV has been equally distributed between the sexes among 17- to 21-year-olds of the general population over the last five years for which data were available (Sections 3.5.1 and 3.5.2). Since testing 17- to 19-year-olds annually for 5 years is equivalent to testing 17- to 24- year-olds, the U.S. Army data predict that among 17- to 24-year-olds, AIDS risks should be distributed equally between the sexes. However, the CDC documents that 85% of the AIDS cases among 17- to 24-year-olds were males (Centers for Disease Control, 1992b).

In response to this, some proponents of the virus-AIDS hypothesis have speculated that teenage homosexuals exclude themselves from the Army. However, Randy Shilts, a homosexual writer, reports that just the opposite is true (Shilts, 1991). Moreover, most teenagers are not as yet aware of a definite homosexual persuasion and are not likely to understand the implications nor to fear the consequences of a positive “AIDS test.”

The over 100-fold discrepancies between the AIDS risks of different HIV-infected risk groups also disprove the claim that the incidence of AIDS is proportional via a constant to the incidence of HIV (Table 2). The proportionality between HIV and AIDS only holds if the analysis is restricted to groups with the same AIDS risks. In groups with the same percentage of HIV but with different AIDS risks, AIDS segregates specifically with nonviral AIDS risks, e.g. illicit recreational drugs, the antiviral drug AZT (Section 4) and frequent transfusions (Section 3.4.4).

AIDS Assumed to be Homosexually Transmitted in the U.S. and Europe

In view of a sexually transmitted AIDS virus, it is paradoxical that AIDS is 90% male in America and 86% male in Europe (Sections 3.1 and 3.2). Therefore it is assumed that “the virus first got its footing in the U.S.” in male homosexuals (Booth, 1988) and has remained with homosexuals because it is transmitted preferentially by anal intercourse and because homosexuals have no sex with heterosexuals (Centers for Disease Control, 1986; Shilts, 1987; Blatter et al., 1988; Institute of Medicine, 1988; Blattner, 1991; Bardach, 1992; Project Inform, 1992).

However, this assumption is inconsistent with the fact that about 10% of all males and females prefer anal intercourse (Bolling and Voeller, 1987; Turner et al., 1989) and that American and European heterosexuals have sufficient access to HIV. The females would be infected by HIV-positive, heterosexual intravenous drug users, hemophiliacs, and bisexual males. Thus, if HIV were transmitted by anal intercourse, about the same percentage of women as men should develop AIDS, particularly since the efficiencies of transmission of anal and vaginal intercourse are approximately the same, e.g. between 1 to 100 and 1 to 500 for anal and 1 to 1000 for vaginal intercourse (Blattner, 1991) (see also Section 3.5.2). Yet, despite widespread alarm, this has not occurred in the last 10 years in the U.S. (Table 1), although the first women with AIDS had been diagnosed as early as in 1981 (Centers for Disease Control, 1986; Guinan and Hardy, 1987). The risk of women for both HIV infection and AIDS is the same for those who practice anal intercourse as for those who practice other types of intercourse (Guinan and Hardy, 1987).

The preferred anal-transmission hypothesis is also incompatible with the sexually equal distribution of HIV and AIDS in Africa. Since it is postulated that HIV appeared in America and Africa at about the same time 10–20 years ago (Institute of Medicine, 1986; Blattner et al., 1988; Gallo and Montagnier, 1988), HIV should have reached the same equilibria between the sexes in all countries.

Instead it is shown below that the male bias for AIDS in America and Europe reflects male-specific behavior, including the facts that over 75% of all intravenous drug users are males and that long-term consumption of sexual stimulants, like amylnitrite and ethylchloride inhalants, is almost entirely restricted to male homosexuals (Section 4). HIV is just a marker of the many sexual stimulants used to achieve 500–1000 sexual contacts (Section 4). The difference between the AIDS risks of men in America and Europe, namely drugs, and those of Africans, namely country-specific, but not sex-specific, risk factors (Section 3.4.4.8) resolves the paradox between the different sexual distributions of AIDS in these countries.

AIDS Assumed to be Heterosexually Transmitted by African “Life-style”

AIDS in Africa is assumed to affect both genders equally, because HIV is distributed equally between the sexes by “prostitution” (Institute of Medicine, 1988), lack of “circumcision” (Klein, 1988; Marx, 1989; Blattner, 1991), African “lifestyle” (Quinn et al., 1987; Blattner et al., 1988; Goodgame, 1990) and “voodoo rituals” (Gallo, 1991). These assumptions are compatible with the sexually equal distributions of HIV and AIDS in Africa.

However, AIDS in Africa is hard to reconcile with the known efficiency of sexual transmission of HIV. Since it takes 1000 HIV-positive sexual contacts to transmit HIV and about 10% of all Central Africans, or 6 million, are HIV-positive (Section 2.2), 6 million Africans would have had to achieve on average at least 10,000 sexual contacts with random Africans to pick up HIV. Since this is highly improbable, it is also highly improbable that sexual transmission of HIV is the cause of AIDS in Africa. The true reason for the sexually equal distribution of HIV in Africa is perinatal transmission of HIV (Section 3.5.2). Nonsexual, country-specific risk factors are the reason for the “sexually” equal distribution of AIDS in Africa (Section 3.4.4.8).

HIV Claimed to be Abundant in AIDS Cases

HIV is said to be abundant or viremic in AIDS patients (Baltimore and Feinberg, 1989; Coombs et al., 1989; Ho et al., 1989a; Semple et al., 1991) and thus compatible with orthodox viruses which cause disease only at high titers (Duesberg and Schwartz, 1992). In other words HIV is assumed to meet Koch’s first postulate (Section 3.3). The assumption is based on two papers which reported HIV titers of 102 to 103 infectious units per mL of blood in 75% of AIDS patients and in 25–50% of asymptomatic HIV carriers (Coombs et al., 1989; Ho et al., 1989a). The authors and an accompanying editorial, "HIV Revealed, Toward a Natural History of the Infection" (Baltimore and Feinberg, 1989), concluded that these findings established HIV viremia as an orthodox criterion of viral pathogenicity. Viremia of similar titers was recently also implied in some AIDS patients and asymptomatic carriers based on an indirect assay that amplifies HIV RNA in vitro (Semple et al., 1991).

However, several arguments cast doubt on the claim that HIV viremia is relevant for AIDS:


  1. Since viremia was observed in 25–50% of asymptomatic HIV carriers (Coombs et al., 1989; Ho et al., 1989a; Semple et al., 1991), it cannot be sufficient for AIDS.

  2. Since no viremia was observed in 25% of the AIDS cases studied by two groups (Coombs et al., 1989; Ho et al., 1989a), it is not necessary for AIDS.

  3. Viremia initiated from a previously suppressed virus and observed years after infection is a classical consequence, rather than the cause of immunodeficiency. Indeed, many normally latent parasites become activated and may cause chronic “opportunistic infections” in immunodeficient persons, as for example Candida, Pneumocystis, herpes virus, cytomegalovirus, hepatitis virus, tuberculosis bacillus, toxoplasma (Sections 2.3 and 3.4.3) – and sometimes even HIV. It is consistent with this view that HIV viremia is observed more often in AIDS patients than in asymptomatic carriers (Duesberg, 1990c).

  4. The HIVs that make up the “viremias” are apparently not infectious in vivo, because only a negligible fraction of leukocytes, on average only 1 in 1500 to 8000, of AIDS patients are infected (Section 3.3). The probable reason is that the “viremias” consist of viruses that are neutralized by the antiviral antibodies of “seropositive” AIDS patients (Duesberg, 1992d). Since viruses, as obligatory cellular parasites, can only be pathogenic by infecting cells, these noninfectious viremias cannot be relevant to the cause of AIDS. If assayed in vitro, in the absence of free antiviral antibodies, antibodies may dissociate from neutralized viruses and thus render the virus infectious for cells in culture. This explains the discrepancy between the noninfectious “viremias” in vivo and the relatively high infectivity recorded in vitro (Coombs et al., 1989; Ho et al., 1989a).


Thus HIV viremia is a rare, predictable consequence of immunodeficiency rather than its cause.

HIV to Depend on Cofactors for AIDS

Conceding that HIV is not sufficient to cause AIDS, it is assumed to depend on cofactors. Montagnier (Goldsmith, 1990; Lemaitre et al., 1990; Balter, 1991) and Lo (Lo et al., 1991) have proposed mycoplasmas that were discovered in their laboratories; Gallo has proposed two viruses, herpes virus-6 and HTLV-I, which were both discovered in his laboratory (Cotton, 1990; Gallo, 1990, 1991; Lusso et al., 1991). Others have proposed cytomegalovirus, Epstein-Barr virus (Quinn et al., 1987; Evans, 1989a; Root-Bernstein, 1990c), “age” (Evans, 1989a; Goedert et al., 1989; Weiss and Jaffe, 1990; Biggar and the International Registry of Seroconverters, 1990), unidentified “coagents” (Weyer and Eggers, 1990; Eggers and Weyer, 1991), “clinical illness promotion factors” (Evans, 1989b, 1992) and even “pre-existing immune abnormalities” (Ludlam et al., 1985; Marion et al., 1989; Ludlam, 1992) as cofactors of HIV.

However, cofactor hypotheses only replace HIV-specific AIDS problems with the following HIV-plus-cofactor-specific AIDS problems:


  1. Since HIV is extremely rare and dormant in most antibody-positive AIDS patients (Sections 2.2 and 3.3), it is hard to imagine how its various AIDS-allies could benefit from their dormant “cofactor” HIV.

  2. Since HTLV-I is just as dormant and unable to kill cells as HIV (Duesberg, 1987; Blattner, 1990; Duesberg and Schwartz, 1992), it is even harder to imagine how one dormant virus could help another dormant virus to generate the biochemical activity that would be necessary to cause a fatal disease.

  3. Since mycoplasma (Freeman, 1979; Cotton, 1990; Goldsmith, 1990; Balter, 1991), herpes virus-6 (Cotton, 1990; Lusso et al., 1991), cytomegalovirus and Epstein-Barr virus (Mims and White, 1984; Evans, 1989c) are each very common, if not ubiquitous, parasites (Freeman, 1979; Froesner, 1991), AIDS should develop in most people as soon as they are infected by HIV. Likewise, “aged” people should develop AIDS as soon as they are infected by HIV. Yet not more than 3–4% of HIV antibody-positive Americans or Europeans and 0.3% of antibody-positive Africans develop AIDS per year (Tables 1 and 2).

    Moreover, if infectious cofactors helped HIV to cause AIDS, the AIDS risk of Africans would be expected to be higher than that of Americans. This is because the incidence of hypothetical, microbial cofactors in Africans without AIDS was found to be the same as in those with AIDS, while the incidence of microbial cofactors in Americans without AIDS risks was significantly lower than in those with AIDS (Section 3.4.3) (Quinn et al., 1987). Even the cofactor HIV was present in 6% of African AIDS-free controls (Quinn et al., 1987). Yet the annual AIDS risk of HIV-infected Africans is 10-times lower than that of Americans (Table 1).

  4. Contrary to the claims that “age” is an AIDS cofactor of HIV, the virus-AIDS hypothesis postulates that the latent period for HIV is longer in adults (10 years) than in children (2 years) (Section 2.2). However, the proposal that “age” is a cofactor for HIV becomes more compelling the more the hypothetical “latent period” of HIV grows. Clearly, if a 70-year-old will be infected by a virus with a “latent period” of 10 years, “age” will be a predictable cofactor (see, for example, hemophiliacs, Section 3.4.4.5 and Paul Gann, Section 3.5.16).

  5. The claims that HIV depends on “clinical illness promotion factors” (Evans, 1992) or on a “pre-existing immune abnormality” (Marion et al., 1989; Ludlam, 1992) for AIDS are euphemisms for saying that HIV cannot cause AIDS until something else does (Duesberg, 1989b). The additional hypothesis that a “pre-existing immune abnormality” (Ludlam, 1992) or a “prior immune dysfunction” (Marion et al., 1989) makes a subject more susceptible to HIV is erroneous, because a pre-existing immune deficiency only affects the progression of an infection, but not the risk of infection.


In view of this, I share Gallo’s concerns about cofactors of HIV, which he expresses with a quotation from Lewis Thomas: “Multifactorial is multi-ignorance. Most factors go away when we learn the real cause of a disease” (Gallo, 1991). The “cofactor” HIV may be no exception. Until any one of these hypothetical cofactors is actually shown to depend on HIV to cause AIDS, HIV must be considered just one of many innocent bystanders found in AIDS patients (Section 3.4.3).

All AIDS Diseases to Result from Immunodeficiency

All AIDS diseases are said to reflect a primary immunodeficiency (Coffin et al., 1986; Institute of Medicine, 1986; Blattner et al., 1988).

However, immunodeficiency is not a common denominator of all AIDS diseases. About 38% of all AIDS diseases, i.e. dementia, wasting disease, Kaposi’s sarcoma and lymphoma (Table 1), are neither caused by, nor necessarily associated with, immunodeficiency. Cancer is not a consequence of immunodeficiency (Stutman, 1975; Duesberg, 1989c). Indeed, Kaposi’s sarcoma frequently has been diagnosed in male homosexuals in the absence of immunodeficiency. For example, the immune systems of 20 out of 37 HIV-positive homosexuals with Kaposi’s sarcoma were normal when their disease was first diagnosed (Spornraft et al., 1988). Another study also describes 19 male homosexual Kaposi’s sarcoma patients with normal immune systems (Murray et al., 1988). Likewise, Kaposi’s sarcomas have been diagnosed in HIV-free male homosexuals with normal immune systems (Afrasiabi et al., 1986; Archer et al., 1989; Friedman-Kien et al., 1990; Marquart et al., 1991).

Dementia and wasting disease also are not consequences of immunodeficiency (Duesberg, 1989c, 1991a). Thus, the assumption that all AIDS diseases are caused by immunodeficiency is erroneous.

HIV to Induce AIDS via Autoimmunity and Apoptosis

In view of the extremely low number of HIV-infected cells in AIDS patients (Section 3.3), HIV has recently been proposed to cause AIDS by inducing autoimmunity (Hoffmann, 1990; Maddox, 1991a; Mathé, 1992) or apoptosis (Laurent-Crawford et al., 1991; Goudsmit, 1992). According to these new ideas HIV is assumed either to confuse the immune system into attacking itself or to persuade the immune cells to commit suicide, termed apoptosis. The autoimmune hypothesis postulates homology between HIV and human cells, and currently relies only on mouse and monkey models (Hoffmann, 1990; Maddox, 1991a), and on precedents for autoimmunity induced in humans as a consequence of graft rejection and blood transfusions (Root-Bernstein, 1990a, Root-Bernstein, R.S. b; Mathé, 1992). One autoimmunologist claims that “each of Duesberg’s paradoxes might be understood in the context of the model without sacrificing the idea that HIV is usually involved in pathogenesis” (Hoffmann, 1990). This strategy of crediting me rather than the virus-AIDS hypothesis for its paradoxes shifts the discussion from a problem with science to a problem with a scientist (Booth, 1988; Weiss and Jaffe, 1990).

However, both the autoimmune and the apoptosis hypotheses are incompatible with human AIDS on several grounds:


  1. Autoimmunity or apoptosis cannot account for all those AIDS diseases that are not caused by immunodeficiency, e.g. Kaposi’s sarcoma, dementia, wasting disease and lymphoma (Section 3.5.8).

  2. Autoimmunity or apoptosis fail to explain risk group-specific AIDS diseases (Section 2.1.3, Tables 1 and 2).

  3. Autoimmunity and apoptosis fail to explain the long average intervals, “latent periods,” from conventional immunity against HIV, detected by the “AIDS test,” to hypothetical autoimmunity 10 years later (Section 3.2).

  4. Autoimmunity and apoptosis fail to explain the over 100-fold discrepancies between the annual AIDS risks of different HIV-infected groups (Table 2).

  5. HIV-induced autoimmunity or apoptosis fail to explain the consistent 90% bias of American/European AIDS for males (Section 2.1, Table 1).

  6. In view of the autoimmunity or apoptosis hypothesis, it is paradoxical that 80% of antibody-positive Americans (1 million minus the 206,000 who have developed AIDS) and 98% of antibody-positive Africans (6 million minus the 129,000 who have developed AIDS) have not developed AIDS since 1984 (Table 1). Obviously, these figures are not even corrected for the normal and drug-induced incidence of AIDS-defining diseases in those groups (Section 3.4.4, Table 2).

  7. There is no sequence homology between HIV and human DNA detectable by hybridization to predict autoimmunity (Shaw et al., 1984). Therefore, autoimmunologists argue that antibodies against those antibodies, which are directed at the viral proteins that bind to cellular receptors, would also react with cellular receptors and thus cause AIDS (Hoffmann, 1990). However, if this were true, all viruses should cause AIDS.


Thus the HIV-autoimmunity and apoptosis hypotheses of AIDS are (a) not compatible with essential parameters of human AIDS and (b) arbitrary, because they are not based on an autoimmunogenic or apoptogenic property of HIV that is distinct from all other viruses.

HIV Assumed to Kill T-cells

Based on an early observation by Gallo et al. HIV is assumed to cause immunodeficiency by specifically killing T-cells (Gallo et al., 1984; Weiss and Jaffe, 1990). Gallo’s observation was restricted to primary T-cells (Gallo et al., 1984) but not to established T-cell lines (Rubinstein, 1990). However, according to Montagnier, the discoverer of HIV, “In a search for a direct cytopathic effect of the virus on (primary) T-lymphocytes, no gross changes could be seen in virus-producing cultures, with regard to cell lysis or impairment of cell growth” (Montagnier et al., 1984). Others have confirmed that HIV does not kill infected, primary T-cells in vitro (Hoxie et al., 1985; Anand et al., 1987; Langhoff et al., 1989; Duesberg, 1989c). Moreover HIV-infected primary T-cells are considered the natural “reservoir” of HIV in vivo (Schnittman et al., 1989).

Thus Gallo’s controversial observation probably reflects the notorious difficulties experienced by his laboratory in maintaining primary blood cells alive in culture instead of a genuine cytocidal function of HIV (Crewdson, 1989; Culliton, 1990; Rubinstein, 1990; Hamilton, 1991a). Gallo showed in a later study from his laboratory that about 50% of uninfected T-cells died within 12 days in culture (Gallo, 1990).

Indeed, the assumption that HIV is cytocidal is incompatible with generic properties of retroviruses and with specific properties of HIV:


  1. The hallmark of retrovirus replication is to convert the viral RNA into DNA and to deliberately integrate this DNA as a parasitic gene into the cellular DNA (Weiss et al., 1985). This process of integration depends on mitosis to succeed, rather than on cell death (Rubin and Temin, 1958; Duesberg, 1989c). The resulting genetic parasite can then be either active or passive, just like other cellular genes (Duesberg, 1987). Transcription of viral RNA from chromosomally integrated proviral DNA also only works if the cell survives infection, because dying cells are not transcriptionally active. Thus, this strategy of replication depends entirely on the survival of the infected cell.

    Noncytocidal replication is the reason that retroviruses were all considered potential carcinogens before AIDS (Weiss et al., 1985; Duesberg, 1987). For example, Gallo’s first candidate for an AIDS virus is called Human T-cell Leukemia Virus-I (Gallo et al., 1983), and Gallo’s second candidate for an AIDS virus was originally described at a press conference in April 1984 by Gallo and the Secretary of Health and Human Services as “a variant of a known human cancer virus called HTLV III” (Crewdson, 1989; Rubinstein, 1990). It used to be called Human T-cell Leukemia Virus-III by Gallo (Gallo et al., 1984; Shaw et al., 1984) before it was renamed HIV in 1986 (Coffin et al., 1986).

  2. Limited cytotoxicity of HIV has been observed soon after infection of cells in vitro (Duesberg, 1989c; Bergeron and Sodroski, 1992). Therefore, it has been proposed that multiple copies of unintegrated proviral DNA, generated by multiple infections before all cellular receptors are blocked by newly replicated viruses, could kill T-cells (Bergeron and Sodroski, 1992). However, cells infected by every retrovirus, including HIV (Bergeron and Sodroski, 1992), survive multiple unintegrated proviral DNAs during the early phase of the infection (Weiss et al., 1985). Rare cell death during this phase of infection is a consequence of cell fusion, which is mediated by viruses on the surface of infected cells binding to receptors of uninfected cells. In some conditions retrovirus-mediated fusion occurs so reliably that it has been used to quantitate retroviruses in tissue culture. However, virus-mediated fusion is blocked by antiviral antibodies and thus not relevant to the loss of T-cells in persons with antibodies against HIV (Duesberg, 1989c).

    Alternatively, it has been proposed that HIV proteins are directly toxic because of structural similarities with scorpion and snake poisons (Gallo, 1991; Garry et al., 1991; Garry and Koch, 1992). However, no such toxicity is observed in millions of asymptomatic HIV carriers, and there is no reason that it should occur, if it did, only after latent periods of 10 years.

  3. The propagation of HIV in indefinitely growing human T-cells for the “AIDS test” was patented by Gallo et al. in 1984 (Rubinstein, 1990) and was recently confirmed by Montagnier (Lemaître et al., 1990). It is totally incompatible with Gallo’s claim that HIV kills T-cells. Such HIV-producing T-cells have been growing in many laboratories and companies since 1984 producing virus at titers of up to 106 virus particles per mL, which is many orders of magnitude more than is ever observed in humans with or without AIDS (Duesberg, 1989c, 1991a).

    In view of this, Gallo postulates that T-cell lines in culture have all acquired resistance to HIV killing (Gallo, 1991). However, there is no precedent for this ad hoc hypothesis, as no other cytocidal virus has ever been observed that is cytocidal in vivo and in primary cells in vitro, but is noncytocidal in cell lines in culture. It is also implausible that a potentially life-saving cellular mutation, such as resistance to the hypothetical “AIDS virus,” would be restricted just to cells in culture, particularly if these mutations occur so readily that they are found in all T-cell lines. There is not even one T-cell line that is consistently killed by HIV.

  4. HIV, like all other retroviruses, does not specifically infect T-cells. It also infects monocytes, epithelial cells, B-cells, glial cells and macrophages, etc. and none of these are killed by HIV (Levy, 1988; Duesberg, 1991a). Most other retroviruses also infect T-cells, which is why so many of them are suspected “T-cell leukemia” viruses (Weiss et al., 1985); Duesberg, 1987; Blattner, 1990).


Thus, the assumption that HIV causes AIDS by killing T-cells is not tenable.

Antibodies Assumed not to Neutralize HIV

Antibodies against HIV, detected by a positive “AIDS test,” are claimed not to protect against AIDS because they do not neutralize HIV (Institute of Medicine, 1988; Evans, 1989a; Weiss and Jaffe, 1990; Gallo, 1991). “It is a test for anti-HIV antibodies and not, as Duesberg states, ‘neutralizing antibodies’” (Baltimore and Feinberg, 1990).

However, antiviral immunity completely neutralizes HIV and restricts it to undetectable levels in healthy HIV-carriers as well as in AIDS patients (Section 3.3.1) (Duesberg, 1989b, c). Indeed, two recent studies have just confirmed that HIV activity is “rapidly and effectively limited” by antiviral immunity (Clark et al., 1991; Daar et al., 1991) to less than 1 in 1000 T-cells (Section 3.3). By contrast, HIV replicates in the absence of antiviral immunity in human T-cells in culture to titers of 106 virus particles per mL (Section 3.5.10). Thus, the assumption that HIV causes AIDS because of inadequate antiviral immunity is unconfirmed. Baltimore’s, Feinberg’s and Evans’ paradox “that antibody is not protective” (Evans, 1989a) is their failure to recognize the non-role of HIV in AIDS (Section 3.3.2).

HIV Claimed to Cause AIDS in 50% Within 10 Years

All HIV-infected persons are said to die from AIDS after a medium latent period of 10 years (Anderson and May, 1988; Institute of Medicine, 1988; Moss et al., 1988; Lemp et al., 1990; Blattner, 1991; Duesberg, 1991a).

However, according to statistics from the CDC, only about 30,000–40,000, or 3–4%, of a reservoir of 1 million HIV-infected Americans develop AIDS annually (Table 1). Likewise, 3% of infected Europeans develop AIDS per year (Table 1). Accordingly, 50% of HIV-infected Americans and Europeans would have to wait 12–16 years and 100%, 24–33 years to develop AIDS. During this time, many would die from other causes. Since only 0.3% of infected Africans develop AIDS diseases annually (Tables 1 and 2), 50% of Africans would have to wait about 150 years and 100% would have to wait 300 years to develop AIDS.

Thus, it is presumptuous to claim that HIV causes AIDS in 50% of infected persons after median latent periods of 10 years, particularly since the virus has only been known for nine years.

HIV Said to Derive Pathogenicity from Constant Mutation

During its long latent periods, HIV is claimed to acquire pathogenicity by mutation, for example by generating variants that escape immunity (Hahn et al., 1986; Levy, 1988; Eigen, 1989; Gallo, 1990; Weiss and Jaffe, 1990; Anonymous, 1992; Anderson and May, 1992) or by generating defective variants (Eigen, 1989; Haas, 1989; Weiss, R.A., 1989).

However, a recent study just demonstrated that the replicative and functional properties of HIVs from AIDS patients are the same as those from asymptomatic carriers (Lu and Andrieu, 1992). Indeed, most essential structural and replicative proteins of a virus cannot be mutated without eliminating its viability. Functionally relevant mutations of any virus are also severely restricted by the necessity to remain compatible with the host (Duesberg, 1990b). Moreover, there is no precedent for an immune system that has been able to neutralize a virus completely and is then unable to catch up with an occasional subsequent mutation. If viruses in general could evade the immune system by mutation, the immune system would be a useless burden to the host.

Likewise, the proposals that defective HIVs could generate pathogenicity is untenable. Defective viruses are only viable in the presence of nondefective helper viruses and thus unlikely to survive in natural transmission from host to host at low multiplicity of infection, particularly with helper viruses that never achieve high titers like HIV (Duesberg, 1989a).

There are, however, examples of new antigenic variants of retroviruses (Beemon et al., 1974) or influenza viruses (Duesberg, 1968), that have arisen upon rare double infection by two antigenically distinct virus strains via genetic recombination. Yet antigenically new variants of HIV have never been observed in American and European AIDS patients, as all HIV strains diagnosed to date crossreact with the very same standard HIV-1 strain that is patented in America and Europe for the “AIDS test” (Connor, 1991, 1992; Palca, 1991; Weiss, 1991).

Moreover, if recombination or spontaneous mutation could generate pathogenic HIV mutants from nonpathogenic strains, one would expect all those who are infected by HIV from AIDS patients to develop AIDS within weeks after infection. Such HIV mutants should be pathogenic just as soon as conventional, nonpathogenic HIV strains are immunogenic. But this is not observed.

Thus, the assumption that HIV acquires pathogenicity by mutation during the course of the infection is not tenable.

HIV Assumed to Cause AIDS with Genes Unique Among Retroviruses

AIDS researchers assert that HIV causes AIDS with unique genetic information that all other animal and human retroviruses lack and that these unique genes would regulate HIV down during the “latent period” and up during AIDS (Gallo and Montagnier, 1988; Haseltine and Wong-Staal, 1988; Institute of Medicine, 1988; Eigen, 1989; Temin, 1990; Fauci, 1991; Gallo, 1991). Further, it is claimed that HIV-infected cells export factors encoded by these genes that promote neoplastic growth of uninfected cells to cause, for example, Kaposi’s sarcoma (Salahuddin et al., 1988; Ensoli et al., 1990; Gallo, 1990); at the same time such genes are said to export “scorpion poison”-related toxins that kill uninfected neurons to cause dementia (Gallo, 1991; Garry et al., 1991; Garry and Koch, 1992). By contrast, all other known bacterial, animal and human viruses, including retroviruses, are only able to kill or alter those cells they infect, because viruses are manufactured inside cells and would not benefit from proteins released to uninfected cells.

However, the claims of unique retroviral HIV genes with unique control functions raises several unresolvable problems:


  1. Despite its presumed unique properties HIV has the same genetic complexity, i.e. 9000 nucleotides, and the same genetic structure as all other retroviruses (Beemon et al., 1974; Wang et al., 1976; Institute of Medicine, 1988). It shares with other retroviruses the three major genes gag-pol-env, which are linked in this order in all animal and human retroviruses (Wang et al., 1976). Although “novel” genes that overlap with the major retroviral genes have been discovered in HIV by computerized sequence analysis, and by new protein detection technology (Varmus, 1988), such genes have also been found with the same technology in other retroviruses that do not cause AIDS, such as HTLV-I, other human retroviruses, bovine retroviruses, simian retroviruses and sheep retroviruses (Varmus, 1988; Weiss, 1988; Duesberg, 1989c; Palca, 1990). Thus there is no unique genetic material and no uncommon genetic structure in HIV RNA that could indicate where this unique AIDS-specific information of HIV is hiding.

  2. Since all retroviral genes share just one common promoter, it would be impossible to differentially activate one HIV gene while the others are latent. Thus the idea that different viral genes would regulate latency and virulence, as with lambda phage, is not compatible with HIV (Haseltine and Wong-Staal, 1988; Eigen, 1989; Temin, 1990; Fauci, 1991). Since all HIV genes share the same promotor, latent HIV can only be activated by the host – just like all other latent retroviruses. In addition HIV cannot make specific AIDS factors, while its major genes are dormant. Since viral RNA synthesis in vivo is only detectable in 1 out of 10,000 to 100,000 leukocytes and then only in half of all AIDS patients (Section 3.3), HIV cannot make Kaposi’s sarcomagenic and neurotoxic factors in amounts sufficient to cause fatal tumors and dementias. This is why such factors have not been detectable in vivo (Weiss and Jaffe, 1990; Gallo, 1991).


Thus, based on the structure, information and function of its RNA, HIV is a profoundly conventional retrovirus. It does not contain unique genes that distinguish it from other retroviruses, nor can its genes be differentially regulated at the transcriptional level.

Simian Retroviruses to Prove that HIV Causes AIDS

Animal retroviruses may cause diseases in experimental animals that overlap with the wide spectrum of AIDS diseases. Such systems are now studied for analogies to gain experimental support for the virus-AIDS hypothesis (Blattner et al., 1988; Weiss and Jaffe, 1990; Goudsmit, 1992). For example, a retrovirus isolated from macaques (Fultz et al., 1990), termed simian immunodeficiency virus (SIV), that is 40% related to HIV, is said to cause AIDS-like diseases in rhesus monkeys (Kestler et al., 1990; Temin, 1990). According to an editorial in Science, “if SIV infection is all that is needed to cause simian AIDS, that’s one more indication that HIV is all that is needed to cause human AIDS” (Palca, 1990).

However, the presumed role of SIV in the diseases of infected monkeys is very different from that of HIV in human AIDS:


  1. According to one study, about half of the infected monkeys developed diseases within several months to one year after infection (Kestler et al., 1990). By contrast only 3–4% of HIV-infected Americans or Europeans and 0.3% of infected Africans develop AIDS annually (Table 1).

  2. In the same study, the absence of antiviral antibodies predicted the incidence of diseases in monkeys, while the opposite is claimed for humans infected with HIV. Another study has confirmed that the monkey’s risk of disease is directly proportional to the titer of SIV (Fultz et al., 1990).

  3. The simian retroviruses barely reduce the T-cell levels of ill monkeys (Kestler et al., 1991), while HIV is claimed to deplete T-cells in humans.

  4. The spectrum of diseases observed in the SIV-infected monkeys is different from AIDS, including bacteremia and lacking, among others, Kaposi’s sarcoma and dementia (Kestler et al., 1990; Fultz et al., 1990).

  5. In follow-up studies, SIV failed to cause disease in rhesus and mangabey monkeys despite extensive sequence variation which is thought to enhance pathogenicity of the virus (Fultz et al., 1990; Burns and Desrosiers, 1991; Villinger et al., 1991).

  6. Since SIV has never caused any disease in wild monkeys, although about 50% are naturally infected (Duesberg, 1987, 1989c; Blattner et al., 1988; Fultz et al., 1990; Burns and Desrosiers, 1991; Villinger et al., 1991), SIV is not an appropriate model for the hypothesis that HIV causes AIDS in naturally infected humans.


It would appear that SIV causes disease in monkeys like all viruses cause disease soon after infection and in the absence of effective immunity. This is not a model for the hypothesis that HIV causes AIDS 10 years after it is neutralized by antibodies. Indeed, in the vast literature on retroviruses there is not even one proven example of a latent retrovirus that, in the presence of antiviral immunity, has ever caused a disease in any animal, including chickens, mice, cattle, and monkeys (Weiss et al., 1985; Duesberg, 1987, 1989c).

Moreover, the observation that a retrovirus that is 60% unrelated to HIV causes disease in monkeys cannot prove that HIV causes AIDS in humans, even if all parameters of infection were completely analogous. It can only prove that under analogous conditions other retroviruses may also cause disease, which has been demonstrated with numerous avian and murine retroviruses long ago (Weiss et al., 1985).

Anecdotal AIDS Cases from the General Population

Rare AIDS cases occurring outside the major risk groups are claimed to prove that HIV alone is sufficient to cause AIDS in persons with no other AIDS risks (Blattner et al., 1988; Booth, 1988; Baltimore and Feinberg, 1989; Weiss and Jaffe, 1990). Four examples illustrate this point:


  1. Ryan White, an 18-year-old hemophiliac, was said to have died from AIDS in April 1990. However, information from the National Hemophilia Foundation revealed that White had died from unstoppable internal bleeding and had also been treated for an extended period with the cytotoxic DNA chain terminator AZT prior to his death (Duesberg and Ellison, 1990). It appears that hemophilia and AZT (Section 4) would each be sufficient causes of death, and certainly a combination of both would be more than adequate to explain the death of Ryan White. Thus there is no convincing evidence that White died from HIV.

    To prove that HIV played a role in White’s death, it would be necessary to compare mortality of matched hemophiliacs with and without HIV. To prove that AZT contributed to his death, matched HIV-positive hemophiliacs with and without AZT must be compared. Without such evidence the HIV-death of White is just a hypothesis. Yet White was generally described as an innocent victim of HIV (practicing no risk behavior), which is why the U.S. Senate approved the Ryan White Comprehensive AIDS Resources Act for over $550 million in aid to hospitals for AIDS emergencies and treatment of children (Anonymous, 1990).

  2. In 1989 the California tax-reformer Paul Gann was reported to have died from AIDS at the age of 77 after receiving HIV from a blood transfusion. However, a close examination of Gann’s case reveals that he had 5-bypass heart surgery for blocked arteries in 1982, when he may have received the blood transfusion with HIV. In 1983 he needed further bypass surgery for blocked intestinal arteries. In 1989, at the age of 77, he was hospitalized again for a broken hip. While recovering from the hip fracture, Gann was immobilized for weeks and developed a pneumonia from which he died (Folkart, 1989). This is a rather typical death for a 77-year-old man in poor health.

    To determine whether HIV played any role at all in his death, a controlled study would be necessary showing that the mortality of HIV-positive 77-year-old bypass patients with broken hips is higher than that of HIV-negative counterparts. No such study exists.

  3. Kimberly Bergalis, a 22-year-old woman, developed candidiasis and a transient pneumonia 17 and 24 months, respectively, after the extraction of two molars (Centers for Disease Control, 1990). After her dentist had publicly disclosed that “he had AIDS,” she was tested for HIV, although Bergalis was a virgin and did not belong to an AIDS risk group (Breo and Bergalis, 1990). Since she was HIV-antibody-positive the CDC concluded that she had contracted AIDS from her dentist (Centers for Disease Control, 1990), who was a homosexual with Kaposi’s sarcoma (Ou et al., 1992).

    Clearly prior to the virus-AIDS hypothesis, the story of a doctor transmitting his Kaposi’s sarcoma in the form of a yeast infection to his client via a common infectious cause would have hardly made The New York Times and certainly not the scientific literature (Lambert, 1991). But since the two entirely unrelated diseases are both labeled AIDS and because of the tremendous popularity of the virus-AIDS hypothesis, the paradoxical story became a case célèbre for AIDS in the general population.

    Once diagnosed for AIDS Bergalis was treated with the cytotoxic DNA chain terminator AZT, which is prescribed to inhibit HIV, until she died in December 1991 with weight loss (15 kg), hair loss, uncontrollable candidiasis, anemia and muscle atrophy (requiring a wheelchair) (Breo and Bergalis, 1990; Anonymous, 1991; Lauritsen, 1991) – the symptoms of chronic AZT toxicity (Section 4). It is not clear whether her AZT therapy started before or after her pneumonia, since it was only mentioned in an edited interview conducted for the American Medical Association (Breo and Bergalis, 1990) and in some newspapers (Anonymous, 1991), but not in a single one of several scientific reports (Centers for Disease Control, 1990; Witte and Wilcox, 1991; Ou et al., 1992; Palca, 1992a, b) and not in The New York Times (Lambert, 1991). Since her fatal condition was attributed to HIV, she received $1 million in compensation from her dentist’s, rather than from her AZT doctor’s (Section 4), malpractice insurance (Palca, 1992a).

    In view of the celebrity of the case and the fear it inspired among patients, 1100 further patients of the dentist came forward to be tested for HIV (Ou et al., 1992; Palca, 1992a). Seven of these, including Bergalis, tested positive. Four or 5 of these, including Bergalis and another woman, did not belong to an AIDS risk group, but 2 or 3 did. At least three of those who did not belong to a risk group received $1 million settlements from the dentist’s malpractice insurance (Palca, 1992b). However, a plausible mechanism of HIV transmission from the dentist to his 4–5 positive clients without AIDS risks was never identified, and there is no consensus as to whether the viruses of the three carriers studied by the CDC and the insurance companies were sufficiently related to claim a common source (Palca, 1992a, b).

    Statistically, it can be shown that the incidence of HIV-infections among the dentist’s clients reflects, almost to the decimal point, the national incidence of the virus in the U.S. The national incidence of HIV-positives among all Americans is 0.4% (1 out of 250) (Table 1), the incidence of HIV-positives among 1100 patients of the Florida dentist was 0.4% (4 to 5 out of 1100) and the incidence among 15,795 patients from 32 HIV-positive doctors, determined by the CDC for the Bergalis case, was 0.5% (84 out of 15,795). Thus the incidence of HIV in patients from HIV-positive doctors reflects the national incidence of HIV. This suggests noniatrogenic and, most likely, perinatal infection as the source of HIV in these patients, particularly in the case of the virgin Bergalis (Section 3.5.2). In addition, it identifies a rich source of insurance income for 0.4% of American patients of HIV-positive doctors!

    To determine whether HIV had contributed to Bergalis’ death, a controlled study would be necessary comparing the mortality of women with yeast infections, with and without antibodies against HIV, and with and without AZT therapy. Since such a study is not available, the assumption that Bergalis died from HIV is pure speculation.

  4. A doctor, presumably infected with HIV from a needle stick in 1983 (Aoun, 1992), described himself in a letter to the New England Journal of Medicine as an AIDS patient (Aoun, 1989). He was diagnosed HIV-positive in 1986 (Aoun, 1992). His only AIDS symptom at that time was a weight loss of 4.5 kg (Aoun, 1989). In 1991, then 8 years after the presumed date of the infection, the doctor described his case again in a speech “From the eye of the storm...” published in the Annals of Internal Medicine (Aoun, 1992). The speech did not describe any current AIDS symptoms. This case has been cited as an example that HIV is sufficient to cause AIDS (Baltimore and Feinberg, 1989).

    However, the weight loss diagnosed in 1986 could have been the result of the anxiety that HIV infection causes in believers of the HIV-AIDS hypothesis, rather than the work of HIV. This interpretation is consistent with the fact that since 1985 at least 800,000 Americans (1 million minus the 206,000 AIDS cases recorded by the end of 1991; see Table 1) have not lost weight or developed other AIDS diseases (Duesberg, 1991a). Likewise, 6 million Central Africans (minus the 129,000 with AIDS) have been healthy HIV-carriers since at least 1985 (Table 1).


Thus, there are no convincing anecdotal cases to prove that HIV causes AIDS in persons outside the major risk groups. The use of the above assumptions and anecdotal cases as proof for the virus-AIDS hypothesis is misleading, although they may provide valuable clues for future research.

Consequences of the Virus-AIDS Hypothesis

Despite the lack of proof and numerous discrepancies with orthodox criteria of infectious disease, the virus-AIDS hypothesis has remained since 1984 the only basis for all efforts in predicting, preventing, investigating and even treating AIDS. AIDS prevention is based entirely on preventing the spread of HIV. This includes promotion of safe sex (Booth, 1988; Institute of Medicine, 1988; Weiss and Jaffe, 1990; Mann and the Global AIDS Policy Coalition, 1992; Anderson and May, 1992), clean injection equipment for intravenous drugs (National Commission on AIDS, 1991) and the exclusion of HIV antibody-positive blood donations from transfusions (Vermund, 1991; Duesberg and Schwartz, 1992).

The Food and Drug Administration mandated in 1985 that the 12 million plus annual blood donations in the U.S. (Williams et al., 1990) are tested for HIV-1, and as of 1992 also for HIV-2, although there is as yet only one single American AIDS patient infected by HIV-2 (O’Brien et al., 1992). Since 1985 over 2 million tests have also been performed annually by the U.S. Army (Burke et al., 1990). By 1986 already over 20 million “AIDS tests” were performed in the U.S. (Institute of Medicine, 1986), at a minimum cost to the client of $12 to $70 (Irwin Memorial Blood Bank, San Francisco, personal communication) or $45 (U.S. Immigration Service). The former U.S.S.R. conducted 20.2 million “AIDS tests” in 1990 and 29.4 million in 1991 to detect 112 and 66 antibody-positives, respectively (Voevodin, 1992).

The detection of antibodies in healthy persons is interpreted as a 50% certain prognosis for AIDS within 10 years (Section 3.5.12). Therefore, a positive “AIDS test” is psychologically toxic (Grimshaw, 1987; Albonico, 1991b) and often the basis for the physiologically toxic antiviral therapy with AZT (Section 4) (Duesberg, 1992b, d). A negative test for HIV is a condition for admission to the U.S. Army (Burke et al., 1990), for admission to health insurance programs, for residence in many countries and even for travel into the U.S. and China. Currently, over 50 countries restrict one or more classes of entrants based on positive antibody-tests for HIV (Duckett and Orkin, 1989). Antibody-positive Americans who had sex with antibody-negatives have been convicted of “assault with a deadly weapon” (Duesberg, 1991c; McKee, 1992). In communist Cuba about 600 antibody-positive persons are quarantined in the name of the virus-AIDS hypothesis (Scheper-Hughes and Herrick, 1992; Treichler, 1992).

Based on the assumption that HIV had either originated recently or spread recently from isolation to its current levels, at the same rates as AIDS had spread in the risk groups in the U.S. and Europe, and on the assumption that AIDS would follow the presumed spread of HIV with a hiatus of 10 years, epidemiologists have made apocalyptic predictions about an AIDS epidemic that has raised fears and funding to unprecedented levels (Heyward and Curran, 1988; Mann et al., 1988; Mann and the Global AIDS Policy Coalition, 1992; Anderson and May, 1992).

Above all, over 180,000 antibody-positives, with and without AIDS, are currently treated indefinitely with the cytotoxic DNA chain terminator AZT in an effort to inhibit HIV (Section 4.4).

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