Infectious AIDS - Stretching the Germ Theory Beyond Its Limits

By Peter Duesberg
Department of Molecular and Cell Biology, University of California, Berkeley, Calif., USA

Original Publication
Int Arch Allergy Immunol
1994; 103: 118-126

Abstract

The hypothesis that human immunodeficiency virus (HIV) causes AIDS was advanced in 1984, based only on circumstantial evidence. To this date, the primary evidence are correlations between the presence of antibody against HIV and AIDS. But these correlations are biased by proponents of the HIV hypothesis in favour of HIV. They ignore HIV-free AIDS and they base correlations on selected studies because there are no national HIV-AIDS statistics. The HIV-AIDS hypothesis has made the following predictions: (1) AIDS would 'explode' from the original risk groups into the general population via sexual transmission of HIV. (2) Health care workers would contract AIDS from their patients, scientists from propagating HIV, and prostitutes from their clients. (3) The 150 chimpanzees that have been experimentally inoculated with HIV, and the 15,000 American hemophiliacs who have been iatrogenically inoculated before 1984, would develop AIDS. (4) immunity and vaccines would protect against AIDS. (5) HIV would cause AIDS by killing T-cells. (6) AIDS would occur only in people infected by HIV. But none of these predictions proved to be correct. Recent studies show that HIV is a passenger virus instead of the cause of AIDS: (1) AIDS occurs at unpredictable intervals after infection; (2) HIV may be active, passive, or totally absent from otherwise identical AIDS cases. Indeed, AIDS does not meet one of the classical criteria of infectious disease: (1) Equal distribution between the sexes; (2) disease following infection within days or weeks, the time microbes take to become either immunogenic or pathogenic or both; (3) the presence of a common active microbe. Therefore it is proposed that American and European AIDS is caused by the long-term consumption of recreational drugs and the anti-HIV drug AZT. This hypothesis is testable and provides a rational basis for AIDS control.

Introduction

In April 1984, the retrovirologist Robert Gallo from the National Institutes of Health in Bethesda and the American Secretary of Health and Human Services announced, at an international press conference in Washington, that the acquired immunodeficiency syndrome (AIDS) was caused by a retrovirus, now termed human immunodeficiency virus (HIV) [1]. The announcement was made before even one American study on HIV had appeared in the scientific literature. Gallo and his collaborators cited antibodies against the virus in "about 85% of patients with AIDS" as the only evidence for their hypothesis [1]. Although AIDS occurred despite antiviral antibodies, the researchers expressed "hope that a vaccine would be ... ready in about two years" [1]. In the scientific papers that followed the next month, HIV was said to cause AIDS by depleting T-cells [2, 3]. The hypothesis proposed that HIV would cause all of the 30 heterogenous AIDS diseases [4], including those that are not consequences of immunodeficiency, such as cancer, weight loss and dementia (Table 1) [5].

Infectious AIDS: From Hypothesis to Dogma

In 1986, the American Academy of Sciences and the Institute of Medicine assembled a blue ribbon committee of medical scientists to confront the growing AIDS epidemic. The committee, chaired by David Baltimore, concluded that the isolation of HIV by Montagnier et al. [6] and Gallo et al. [2] "led to its definitive identification as the cause of AIDS" [7]. Without mention of dissent [8, 9], a derivative committee declared in 1988: "The committee believes that the evidence that HIV causes AIDS is scientifically conclusive" [boldface in original] and proposed to rename AIDS "HIV disease" [10]. The committees had sealed the hypothesis into national dogma. However, the committee's conclusion was based only on circumstantial evidence including five questionable assumptions:

(1) The primary assumption was that, " ... close to 100 percent of the affected individuals can be found to harbor the virus" and "The probability that this distribution might have occurred by chance is less than one in a million" [10].

However, since no national HIV-AIDS statistics exist [11], the committee had to rely on selected individual studies and unpublished observations. For example, the committee selected a Science News & Comment article entitled "A rebel without a cause of AIDS" [9], an unpublished speech of the epidemiologist Winkelstein and the papers of Montagnier and Gallo as the source for the "close to 100%" correlation [10]. But the original paper by Montagnier et al. [6] only reported a single isolation of HIV from the lymph node of a person who did not have AIDS, and Gallo's isolate proved to be Montagnier's virus [12]. And the authenticity of the HIV-AIDS correlations from Gallo's group has since been questioned on several accounts [12].

(2) The committee also believed that "The virus is not found in persons who are not at risk for infection"-assuming that infection was restricted to AIDS risk groups, e.g. male homosexuals, intravenous drug users and recipients of transfusions [7]. However, HIV has since been found in 1 million healthy Americans, 0.5 million healthy Europeans, 1.5 million healthy South Americans, 1.5 million healthy Asians and 8 million healthy Africans [13].

(3) The committee further believed that " ... AIDS is unknown in populations that are free of HIV antibodies," i.e. that there is no HIV-free AIDS [10]. However, many HIV-free AIDS cases had already been reported by 1986 and 1988, when the committees confronted AIDS [11].

(4) The committee accepted without questioning the unique practice of the HIV researchers to present antibodies against HIV as pathogenic powers of HIV. Proponents of the HIV-AIDS hypothesis interpret these antibodies as indicators of current and future HIV disease. However, antibodies against all other microbes are signs of rejection of the microbe and protection against future disease.

(5) The committee accepted uncontrolled statistics as evidence for AIDS from transfusion of HIV [10]. For example, AIDS researchers blame HIV for pneumonia and other opportunistic infections that occur in about 2% of HIV-positive hemophiliacs per year [5, 10]. However, controlled studies have since shown that the incidence of immunodeficiency in matched groups of HIV-positive and negative hemophiliacs is the same [5].

Thus the committee had adopted the virus-AIDS hypothesis on the basis of questionable assumptions, primarily the assumption that all AIDS correlates with HIV.

How Good is the Correlation between HIV and AIDS?

The natural coincidence between HIV and AIDS can only be determined by first diagnosing AIDS clinically and then testing for HIV. However, since the HIV-AIDS hypothesis has been accepted in 1986, the definition of AIDS by clinical criteria alone has been abandoned in America and Europe in favor of an HIV-based definition [10]. Moreover all HIV-AIDS correlations are based on selected individual studies, because to date no national and international AIDS statistics reporting HIV tests exist [11]. As a result, proponents of the HIV-AIDS hypothesis bias HIV-AIDS correlations in several ways:

(1) They cite HIV-AIDS correlations from selected, individual studies which are frequently based on non-standardized and unconfirmed HIV antibody tests [11, 14].

(2) They present antibodies against HIV, instead of activities and titers of HIV, as a rational cause of AIDS.

(3) They exclude clinically diagnosed, HIV-free AIDS defining diseases from their statistics, e.g., the 4,621 cases cited below [11], because the HIV-AIDS hypothesis postulates that HIV causes AIDS. Therefore HIV-free AIDS cases are either diagnosed by their old names, e.g. Kaposi sarcoma, pneumonia, etc., or renamed "idiopathic CD4 lymphocytopenia," or ICL [15].

But the effort to set apart HIV-positive from HIV-negative AIDS cases is not based on any clinical or convincing epidemiological criteria [11, 16]. According to an editorial by Fauci: "Given the heterogeneity of the [ICL] syndrome, it is highly likely that there is no common cause" [15]. Yet at the same time the proponents of the HIV hypothesis, including Fauci, insist that HIV must be the common cause of the 30 heterogenous AIDS diseases.

The editorial also argues that the HIV-free AIDS or ICL cases are unlike the HIV-positive cases because "Approximately one third of the patients are women, as compared with 11% among those with HIV ..." (in America). But proponents of the HIV-AIDS hypothesis, including Fauci, insist that HIV also causes African AIDS, despite about 50% of the African patients being women [10].

Indeed, other retroviruses have been proposed as causes of HIV-free AIDS, particularly at the VIII International AIDS Conference in 1992 in Amsterdam [17, 18], because these cases were clinically indistinguishable from HIV-positive AIDS. Following the HIV precedent, these retroviruses were considered "new" AIDS causes simply because of their presence in these cases.

It follows that the primary argument for the HIV-AIDS hypothesis, the HIV-AIDS correlation, is a circular argument. It is in reality an artefact of the HIV-based AIDS definition, which is a restatement of the HIV hypothesis.

To date the virus-AIDS hypothesis has been a complete failure in terms of public health benefits: no vaccine has been developed, AIDS continues to spread despite efforts to stop the spread of HIV, and nobody has ever been cured from AIDS. However the acid test of a hypothesis is not to produce useful results, but to make accurate predictions.

Predictions of the HIV-AIDS Hypothesis

The HIV-AIDS hypothesis makes the following testable predictions, none of which proved to be correct [5, 19]:

The failure to make valid predictions is the hallmark of a flawed hypothesis. It raises two fundamental questions: (1) Is HIV a passenger virus rather than the cause of AIDS? (2) Is AIDS infectious?

Is HIV a Passenger Virus Rather than the Cause of AIDS?

The correlation argument assumes that the presence of a virus in a disease is sufficient proof of causation. But the presence of a virus in a disease is by no means proof of causation. Particularly since HIV does not cause AIDS if inoculated into chimpanzees or if iatrogenically introduced into hemophiliacs, it could be just a harmless passenger virus. Passenger viruses are "widely distributed ... in mammals, causing no obvious disease" [37]. In the absence of functional proof, the distinction between a causative and a passenger virus can be made by the temporal relations between infection and disease, by the consistency of its presence, and by the biochemical activity of the virus during the course of the disease as follows:

HIV meets all criteria of a harmless passenger virus in AIDS:

(1) HIV infection precedes AIDS by unpredictable intervals that average about 10 years. This time is referred to as latent period of HIV by proponents of the HIV-AIDS hypothesis, although HIV typically remains latent even when AIDS occurs [5]. Several groups report that HIV may reach high titers during the primary infection [40-42]. According to Piatak et al., these titers range from 10 to 104 infectious units per milliliter [42]. Despite these relatively high HIV titers in some people, and despite the absence of antiviral immunity in all, there is no AIDS during the primary infection [40-42]. In addition, the T-cell counts are normal [42, 43].

When the primary infection is terminated by antiviral immunity, no infectious HIV remains, the T-cell are normal and there is also no AIDS [42]. In the face of antiviral immunity, the virus persists as a latent provirus in healthy hosts (fig. 2).

(2) HIV also meets one of the most telling criteria of a passenger virus in relation to a disease: HIV-free AIDS (see above, fig. 2). At least 4,621 AIDS cases have been documented in the literature since 1984 in whom there is no HIV [11]. About a third of these, 1,691, were recorded in the US, 475 in Europe and 2,555 in Africa [11]. Since Africa uses the clinical, rather than the HIV-based AIDS definition, most of these cases were observed in Africa. The US and Europe bias AIDS statistics against HIV-free AIDS, because they use the HIV-based AIDS definition (see above).

(3) Several groups have documented that HIV may be either active or passive once immunodeficiency is acquired and AIDS appears [42, 44, 45]: Piatak et al. observe either no infectious HIV, e.g. 0 infectious units per milliliter plasma in 5 out of 27 HIV-antibody-positive AIDS cases, or fewer than 25 infectious HIVs per milliliter in 6 out of 27 cases, or 102-105 in 16 out of 27 otherwise identical AIDS cases [42, 43]. Others have reported similar noncorrelations between virus titers and AIDS [44-46].

Likewise, there is no correlation between AIDS and the number of HIV-infected cells. Simmonds et al. report that there are from 1 to 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 [47]. Bagasra et al. report that there are from 1 in 30 to 1 in 1,000 infected leukocytes in healthy carriers and from 1 in 10 to 1 in 1,000 in patients with fatal AIDS. [48] Thus there are healthy persons with 43 times (30,000:700) and 33 times (1,000:30) more HIV-infected cells than in AIDS patients.

It follows that there is neither a correlation between HIV titers, nor between the number of HIV-infected cells and AIDS-the hallmark of a passenger virus. (4) Even as an active passenger, HIV does not aggravate the course of AIDS by any HIV-specific symptom, as some other passenger viruses or microbes do. For example, cytomegalovirus, herpes virus, Pneumocystis carinii and Candida each cause corresponding opportunistic infections if they are activated by acquired immunodeficiency (table 1). By contrast, the AIDS cases with active or passive HIV appear to be identical, according to several groups of investigators [42, 44, 45, 48]. Indeed no HIV-specific AIDS symptom has ever been described, as all AIDS-defining diseases have been known previously [10, 49] and occur in HIV-free AIDS patients [11]. Thus HIV is not even a cofactor for AIDS.

It follows that HIV is a harmless passenger virus that does neither cause AIDS nor even contribute an HIV-specific symptom to AIDS. Since AIDS is not caused by HIV nor consistently associated with another active infectious agent [5], it may not be infectious.

AIDS Fails All Criteria of Infectious Disease

Proponents of the HIV-AIDS hypothesis acknowledge that "AIDS does not have the characteristics of an ordinary infectious disease. This view is incontrovertible" [50]. More specifically, the epidemiologists Eggers and Weyer [51] state that "the spread of AIDS does not behave like the spread of a disease that is caused by a single sexually transmitted agent." To reconcile AIDS with infectious disease they "simulated a cofactor [that] cannot be identified with any known infectious agent" [52]. The epidemiologists Anderson and May [53] had to invent "assortative scenarios" for different AIDS risk groups to match AIDS with infectious disease. Indeed, AIDS does not meet even one of the common criteria of all known infectious diseases:

Thus AIDS does not fit even one of the classical criteria of an infectious disease.

The Drug-AIDS Hypothesis

The paradoxa of the virus-AIDS hypothesis are all readily resolved by postulating noninfectious AIDS. In view of this I have proposed that AIDS in America and Europe is caused by the long-term consumption of recreational drugs and AZT [5, 59]. African AIDS has been proposed to be an unrelated epidemic caused by malnutrition, parasitic infections and poor sanitation [5].

Indeed, AIDS in America and Europe fits all classical criteria of a drug-induced disease syndrome. AIDS correlates epidemiologically and chronologically with the drug epidemics that started in America and Europe after the Vietnam war:

(1) About 30% of all American and European AIDS patients are intravenous drug users [4, 5]. This group includes nearly all heterosexuals with AIDS [4, 5]. It also includes 80% of all American and European babies with AIDS who were intrauterine drug users, because their mothers injected drugs during pregnancy [5].

It is known since 1982 that virtually 100% of homosexual males with AIDS or at risk for AIDS have been longterm users of oral, aphrodisiac drugs, particularly nitrite inhalants, that confer euphoria and facilitate anal intercourse [60-69]. Epidemiological studies from San Francisco and Vancouver have just confirmed, in 1993, that 100% of several hundred male homosexuals with AIDS had used multiple recreational drugs [70, 71, 81]. In addition some had also used the cytotoxic DNA chain terminator AZT as antiviral drug [72-75, 81]. The immunotoxicity of these recreational drugs has been documented in the literature since 1909 [5, 76].

About 200,000 HIV-positive healthy people and AIDS patients are currently treated four times daily with AZT and other DNA chain terminators as anti-HIV drugs. These drugs kill all growing cells, particularly those of the highly proliferative immune system [5]. Thus AZT is AIDS by prescription.

(2) In the US recreational drug use increased over the last years at about the same rate as AIDS [5]. For example, cocaine consumption increased 200-fold from 1980 to 1990 based on cocaine seizures that increased from 500 kg in 1980 to 100,000 kg in 1990 [5]. During the same time cocaine-related hospital emergencies increased 24-fold from 3,296 cases in 1981 to 80,355 cases in 1990 [5] (fig. 1b). Note the parallelisms between the spreads of AIDS (fig. 1a) and the spreads of cocaine and cocaine-related hospital emergencies since 1981, and the contrast with the non-spread of HIV since 1984 (fig. la).

(3) 90% of the American AIDS patients are male, because according to the US Bureau of Justice Statistics males consume about 75% of all illicit injected drugs, and because homosexual males are virtually the only consistent users of aphrodisiac drugs like alkyl nitrites [5, 59].

(4) AIDS occurs on average 10 years after initiation of risk behavior, because it takes years of recreational drug consumption to cause disease [5, 63, 77], e.g., 20 years of smoking to get lung cancer [78] or emphysema, or years of alcoholism to develop liver cirrhosis. The great variations in "latent periods" from HIV to AIDS that currently average 10 years [10] are euphemisms for the time required by individuals to accumulate sufficient drug toxicity to generate AIDS diseases [5].

(5) Different risk groups have risk-group-specific AIDS diseases, e.g., Kaposi sarcoma is observed almost exclusively in homosexuals [79], because homosexuals are the almost-exclusive users of aphrodisiac nitrite inhalants [5, 65]; tuberculosis and weight loss is observed in intravenous drug users, because intravenous drugs cause those symptoms [5]; anemia and lymphocytopenia is observed in recipients of AZT which kills proliferating bone marrow cells [5, 80]; and hemophiliacs get pneumonias and candidiases almost exclusively, because long-term transfusion of foreign proteins is immunosuppressive [5].

The drug-AIDS hypothesis is experimentally and epidemiologically testable and provides a rational basis for AIDS prevention and control. *

This article is the first of two in "Controversy: HIV and AIDS," sponsored by Georg Wick, editor-in-chief of International Archives of Allergy and Immunology.

Acknowledgements

I thank Jody Schwartz for a critical review and Bryan Ellison for discussions. Supported in part by the Council for Tobacco Research, USA, and private donations from Glenn Braswell (Los Angeles, Calif., USA), Dr. Richard Fischer (Annandale, Va., USA), Dr. Fabio Franchi (Trieste, Italy) and Dr. Friedrich Luft (Berlin, FRG).

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