Duesberg's theory

Duesberg's theory is: HIV is a harmless retrovirus that may serve as a marker for people in AIDS high-risk groups. AIDS is not a contagious syndrome caused by one conventional virus or microbe. AIDS is probably caused by conventional pathogenic factors: administration of blood transfusions or drugs, promiscuous male homosexual activity associated with drugs, acute parasitic infections, and malnutrition. Drugs such as AZT promote AIDS, rather than fight it.

His theory is explained in detail in "Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome: Correlation but not Causation", Proc. Natl. Acad. Sci. USA V86 pp.755-764, (Feb. 1989) and "AIDS acquired by drug consumption and other noncontagious risk factors", Pharmac. Ther.. .55 pp 201-27, 1992, as well as his book Inventing the AIDS virus.

The main objections to Duesberg's theory can be found elsewhere, such as the sci.med.aids FAQ (part 6) and Dr. Harris's paper in Skeptic.

A detailed evalution of Duesberg's claims can be found in Science, 266, December 9, 1994. To quote the conclusions of Science's investigation:

I recommend that anyone interested in Duesberg's claims should read this issue of Science.

Here, I will look at a few specific things in his Pharmac. Ther. paper to show that much of the reasoning in his paper just doesn't make sense. The following discussion won't shed light on the "big picture" of the validity of his theory. Instead, it looks at the "little picture" of specific things.

The quoted text in the following is all from this paper.

Dental statistics

Section 3.5.16:
"1100 further patients of the dentist came forward to be tested for HIV. 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. [...]

"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%, the incidence of HIV-positives among 1100 patients of the Florida dentist was 0.4% (4 to 5 out of 1100) [...]

Look closely at the above. The incidence of infection among the dentist's clients is 7 out of 1100, or 0.63%! The paper dropped the members in risk groups from the dental population but not the US population when computing the 0.4%! In my opinion, that is totally dishonest. Thus, according to an accurate computation with Duesberg's own figures, the incidence of HIV among the dentist's clients is 50% higher than in the US population.

Developments since Duesberg's article make this even more dramatic. Latest estimates of HIV in the US population are about 0.22%. Also, according to the New York Times (July 5, 1994), 10 of the tested clients tested positive, making the incidence 0.9%. Thus, rather than matching to the decimal point, the incidence of HIV infections among the dentist's clients is four times the incidence in the US population.

Kimberly Bergalis, a 22-year-old woman, developed candidiasis and a transient pneumonia 17 and 24 months, respectively, after the extraction of two molars. After her dentist had publicly disclosed that 'he had AIDS,' she was tested for HIV [...]

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, hair loss, uncontrollable candidiasis, anemia and muscle atophy (requiring a wheelchair) - the symptoms of chronic AZT toxicity. 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 and in some newspapers, but not in a single one of several scientific reports and not in The New York Times.

According to the February 9, 1991 New York Times, Acer performed a tooth extraction on Bergalis in 1987. In the spring of 1989, Bergalis suffered infections, sore throats, weakness, coughing, and thrush. In the summer of 1989, Bergalis suffered weight loss and hair loss, but doctors didn't make a diagnosis. In November 1989, Bergalis suffered P. Carinii pneumonia. Doctors then performed a HIV test, which was inconclusive. A second test in January 1990 confirmed HIV. In July 1990, the CDC released a report concluding that transmission had ocurred from Dr. Acer. In August 1990, Bergalis filed suit against Dr. Acer. After repeated pressure from the CDC, Dr. Acer then published a letter to his patients announcing that he had AIDS and that they should be tested, and died a couple days later on September 3, 1990. In February 1991, Dr. Acer's malpractice insurer paid Bergalis. She died December 8, 1991.

Thus, the description in Duesberg's article omits a few important facts. First, Bergalis didn't just have any pneumonia, but P. Carinii pneumonia, which is extremely rare in non-immunocompromised people. Second, Bergalis was tested almost a year before the dentist made his public disclosure. Finally, Bergalis had pneumonia when she was diagnosed with AIDS, so her AZT therapy started after the pneumonia. It is nonsensical to blame her problems on AZT, since she suffered the weight loss, hair loss, candidiasis, and P. Carinii pneumonia before AIDS was diagnosed and she started AZT.

Wives of hemophiliacs

"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 hemophiliacs die from sexual transmission of HIV is unfounded speculation.
If you examine the numbers very carefully, you will find that this paragraph makes no logical sense. Why on earth should there be 67 deaths among HIV-negative wives compared to 80 deaths for random women? Being a HIV-negative wife shouldn't dramatically decrease your death rate.

As another way of seeing the problem in this paragraph, suppose that instead of 13 deaths per year there were 90 deaths per year (i.e. 630 out of 5000). This is a perfectly reasonable assumption. However, if you apply the paper's logic, then you reach the conclusion that among HIV-negative wives, there should be 80-90 = -10 (!) deaths per year. Since this conclusion is nonsensical, the logic in the paper is clearly wrong.

1000 sexual contacts to spread

Section 3.5.2:
"'AIDS tests' from applicants to the U.S. Army and the U.S. Job Corps indicate that between 0.03% and 0.3% 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.

"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. 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.

There are so many bizarre things in the above two paragraphs that one hardly knows where to begin.

First, all positive teenagers would require an absurd 1000 contacts with a positive partner? The reasoning here is what is absurd. That's like saying that since the odds of dying on a plane flight are 1 in a million, then everyone who dies of a plane crash must have been on a million flights. Obviously, instead of every infected person having 1000 contacts, there could have been 20 people with 50 contacts, for instance.

The conclusion of 27,000 to 270,000 HIV carriers is very suspect. Note that it takes the infection rate of 17 to 19 year olds and multiplies by the number of 0 to 19 year olds. This is clearly wrong, since the infection rate varies greatly with age. The paper does a similar thing in section; it uses this same statistic on 17 to 19 year olds to compute the number of infected Americans of all ages.

Finally, the paper poses the false choice of sexual infection or perinatal infection. This neglects the very likely scenario that many of these teenagers were infected through IV drug usage.

Annual risk

Section 3.4.4:
"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 paper uses the concept of "annual risk" a great deal, where it divides the annual number of AIDS cases by the number of HIV-infected people to determine the "annual AIDS risk".

There are numerous problems with "AIDS risk". As a simple example of why it doesn't work, the US population is 246,329,000 and the number of deaths in the US is 2,171,000 (1988 figures), so the "annual risk" of death is 1/113. But the average person does not live to 113.

The biggest problem with annual risk is that it is meaningless if a disease is spreading and takes time to appear. For example, consider a hypothetical disease that shows up 5 years after infection. In country A, suppose there are 1000 people infected in 1990, and 10,000 people have become infected by 1995. Then 1000 cases show up in 1995 out of 10,000 infected, yielding an annual risk of 10%. In country B, suppose 1000 people are infected in 1990, but only 2000 people are infected by 1995. Then the annual risk in B is 1000/2000 = 50%. Exactly the same disease, but a totally different annual risk. Thus, the "annual risk" is a meaningless comparison for this sort of disease.

"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 (Ward et al., 1989).
Here we have an example of an AIDS risk computation that is simply bogus. As the paper mentions later, these 50% die of their original illness, not AIDS. Thus, claiming their AIDS risk is 50% is nonsensical.

HIV in the population for millions of years

Section 3.5.1:
"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%. [...] This is the predicted distribution of a long-established virus. 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 last 7 years is an infallible indication that the American 'HIV epidemic' is old. [...] HIV preceded AIDS by many, perhaps millions, of years.
Now this is quite the extrapolation from the given data. The CDC has been guessing at 1 million infected Americans (with huge error bars) since 1985, and the paper uses this data to conclude that HIV has been around for millions of years. Whether or not HIV has been around for a long time, attempting to prove this through the CDC's 1 million estimate is silly.

It should be obvious that HIV infection has not been constant. For example, study of homosexual men found that HIV infection increased steadily from 7% in 1979 to 44% in 1984. (Stevens et al, "Human T-cell lymphotropic virus type III infection in a cohort of homosexual men in New York City", JAMA 255(16), April 25, 1986.)

HIV has the same genes as any other retrovirus

Section 3.5.14:
Despite its presumed unique properties HIV has the same genetic complexity, i.e. 9000 nucleotides, and the same genetic structure as all other retroviruses. It shares with other retroviruses the three major genes gag-pol-env, which are linked in this order in all animal and human retroviruses. 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, 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. 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.


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.

The problem with this argument is that it basically boils down to "Retroviruses all have the same three genes. Well, HIV has novel genes. But some other viruses have novel genes. Therefore HIV and all other virus have the same genes." This is a silly argument, since these novel genes aren't the same and not all viruses have them.

Currently, researchers have found nine genes in HIV. Some of these genes do distinguish HIV from all other retroviruses. Click here for a detailed description of the genes.

The evidence shows that HIV has a different structure from other retroviruses:

First, there is not really a "profoundly conventional" retrovirus organization. There are features common to all retroviruses, such as the gag-pol-env organization. However, "considerable variation is apparent within a common framework. All viruses have the genes encoding virion proteins arranged in a common order, but each group has special features that distinguish it from the rest." (Fields, Virology, Chapter 51)

For instance, HTLV has genes beyond the basic gag-pol-env: the rex and tax genes. (Rosenblatt, "HTLV-II transactivation is regulated by the overlapping tax/rex nonstructural genes", Science, 240(4854), May 13, 1988, pp916-919.) But HIV doesn't have these genes, and HTLV doesn't have the novel genes that HIV does. So the discovery of novel genes in HTLV shows that the two viruses have a different structure; it hardly shows that HIV and HTLV have the same genetic structure as Duesberg's paper claims.

In particular, the lentivirus group of retroviruses (containing HIV) has a different genetic structure from other retroviruses. They contain the gag, pol, and env genes of all retroviruses. In addition, lentiviruses have unique small open reading frames (ORFs) located between pol and env and at the end called 3'. In HIV, visna, and EIAV these ORFs contain regulatory protein genes. These genes are through to result in the "slow virus" behavior of lentiviruses (Fields, Virology, Chapter 55). Note that visna causes slowly progressive disease in sheep with prolonged periods of subclinical infection and incubation periods of months to years. The behavior is similar to HIV, and not surprisingly both viruses have "novel" regulatory genes. (Click here for more information on visna.)

HIV and visna differ from oncoviruses (retroviruses such as HTLV) "in genomic structure, morphology, and replication. They share gag, pol, and env genes and LTRs with other retroviruses, but have a novel central region between pol and env." (Songio et al, "Nucleotide sequence of the visna lentivirus: relationship to the AIDS virus", Cell 42, pp 369-382, August 1985.)

Finally, HIV and SIV have genes that are not found in other viruses. There are genetic differences even among HIV-1, HIV-2, and SIV. The vpx gene is not found in HIV-1 or SIVmnd. The vpr gene is not found in some SIV. Neither vpr nor vpx has been found in nonprimate lentiviruses (i.e. viruses other than HIV or SIV). Myers et al, "The emergence of simian human immunodeficiency viruses, AIDS research and human retroviruses 8(3), 1992, pp 373.

In conclusion, the evidence shows that HIV has a genetic structure that is significantly different from other retroviruses.

The CDC definition

Section 2.2:
Because of this belief [HIV causes AIDS], 25 previously known, and in part entirely unrelated diseases have been redefined as AIDS, provided they occur in the presence of HIV.
Section 3.4.1:
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 towards a 100% correlation with HIV.
This is basically a restating of Duesberg's equations:
The claim that the CDC AIDS definition requires the presence of HIV is wrong. In fact, the CDC definition permits a diagnosis of AIDS even if HIV tests are negative! For example, P. Carinii pneumonia, no other cause of immunodeficiency, and a negative HIV test results in an AIDS cases under the CDC definition. Click here for the CDC definition of AIDS.

Acknowledgement: many of these problems were uncovered through discussion with David Canzi.

Ken Shirriff: shirriff@eng.sun.com
This page: http://www.righto.com/theories/duesberg.html Copyright 2000 Ken Shirriff.