Comments and an Analysis of Flegg's reference number 1 16 April 2003
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David Rasnick,
Chief Science Officer, Boveran, Inc.
San Ramon, CA 94583

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Re: Comments and an Analysis of Flegg's reference number 1

Peter Flegg continues to be frustratingly vague about his "facts". When I asked the simple question: where can one find the proof that HIV and AIDS are sexually transmitted?, he tries to skirt the awkward fact that the question remains unanswered by saying that, "[Rasnick] would only read into the data whatever he wishes to see. I [Flegg] have better things to do with my time than trot out a comprehensive list of references, only to see the material ignored, misquoted or misinterpreted".

Therefore, to save Flegg from trotting "out a comprehensive list of references" I once again ask only for the names of those people (even one name will do) who have proved that AIDS is contagious, sexually transmitted and caused by HIV. This does not seem to be an unreasonable request. As I recall, the Nobel committee can name no more than three people to share a single prize. So, Peter Flegg, what are the names of the people (up to three for each) who you would recommend to the Nobel committee for having shown that 1) HIV is sexually transmitted, 2) AIDS is sexually transmitted, 3) HIV causes AIDS? If it is impossible to come up with a list of these names, then can you give an estimate (an order of magnitude if necessary) of the minimum number of people that it took to prove each of the three mainstream assertions in question? After you have come up with this number (or even an estimate of its magnitude), would you kindly tell the observers of this debate exactly when and where the anonymous army of AIDS researchers marshaled the evidence, as you say, "to flog this particular horse [that] expired a very long time ago"? Who did the flogging, when and where did the execution take place? And, on what basis was the horse pronounced dead?

Second, Flegg accuses me of the sin he may himself be committing: "read[ing] into the data whatever he wishes to see". I am certainly guilty of ignoring some of the assertions and interpretations of individual papers--but not the data. Flegg accuses me of misquoting. I try very hard to quote people and texts accurately. Therefore, I ask Flegg to post the most egregious example(s) of where I misquoted him or others so that I can acknowledge the errors and correct them.

Third, the data are the data. It is largely a matter of judgment and taste as to whether data are being misinterpreted. Perhaps it is Flegg who is misinterpreting the data. Relying on their training, experience, and especially a critical eye, all scientists are not only free--but indeed obligated--to interpret the data as they see best. Multiple interpretations of the same phenomena are normal in science. In fact, there would be no science without different interpretations. When only one interpretation is allowed, science ends and dogma reigns.

Now let's examine reference number 1 that Flegg offered in response to my question: where is the evidence published in the scientific, medical literature that HIV is indeed sexually transmitted, whether early or late in infection?

Flegg says that Jacquez et al. [1] was "One [o]f the first papers to look at the contribution of early [sexual] transmission [and] concluded that chains of transmission grow rapidly, and this helps explain many observed population patterns for HIV infection (1)."

The first thing to note about the Jacquez et al. paper is that it was published in 1994, long after it had been pronounced that HIV was sexually transmitted and caused AIDS. Therefore, in order to get funded and published, Jacquez et al. were compelled to accept as axiomatic that HIV was sexually transmitted. They certainly did not attempt to test that belief. Within the constraints imposed by AIDS Inc., the authors were forced to come up with an explanation (no matter how ad hoc) for the very peculiar and truly unique Lazarus- like reemergence of HIV in AIDS patients a decade or more after they had developed immunity to the "deadly virus".

The very first paragraph of the Jacquez et al. paper sets the stage for their speculations: "Figure 1 shows scaled cumulative curves of the number of HIV seropositives obtained from the hepatitis B vaccine trial of the San Francisco City Clinic and from the Chicago MACS cohort. The epidemic curve for the San Francisco data was flattening by January 1983. The Chicago MACS cohort was at about the same point on its curve at the initial examination in September 1984...".

Thus, there was a rapid increase in the number of new HIV- positive (almost exclusively gay) men in San Francisco and Chicago beginning in the late 1970s that reached a plateau of short duration in the early 1980s followed by a steep decline to very low levels by the end of 1983. This scenario is not far removed from what one would expect for the spread of a new infectious agent in a closed population. It agrees with the so-called SIR dynamics, which stands for Susceptible, Infected, Recovered. In fact, the authors specifically state that, "the early spread of HIV may be viewed as the type commonly designated SIR or SEIR." The "E" stands for Exposed.

In order to explain the time course of HIV-antibody positives the authors speculated that: "High infectivity during the primary infection, followed by a long period of low infectivity, could give a rapid rising epidemic curve with sudden slowing of the process, i.e., an SIR dynamic. High activity groups are likely to have played an important role in the rapid rise. Other mechanisms that could have contributed to the sudden slowing are behavioral change to decrease risk and/or saturation of the high activity groups. Our goal is to examine the relative contributions of these mechanisms." But, since the HIV-antibody epidemic peaked before Robert Gallo had presented HTLV-III (alias HIV) to the world, the authors were forced to conclude that, "For the San Francisco epidemic and for the Chicago MACS cohort, behavioral change started too late to have much effect on the initial rapid rise."

Figure 1, as the authors state, was a cumulative curve. But, their Figure 3 shows the number of new HIV antibody positives for each year. The number of new cases rose from about 16 in mid 1978 to a plateau of around 400 from mid 1980 until the beginning of 1983 after which it dropped precipitously to 81 cases at the end of 1983. (In a previous letter I pointed out that there were fewer than 50 new AIDS cases--not HIV positives--in San Francisco in 2000 (the same level of AIDS cases seen in 1982) [2], and this was after three definition changes as to what constituted AIDS, each of which increased the number of new cases.) This peculiar situation led Peter Duesberg to quip that it was a good thing the Department of Health and Human Services had rushed to commit the US government into backing Robert Gallo's "deadly virus" as the cause of AIDS in April 1984 because if they had waited just a little longer there would have been no HIV epidemic to find.

Thus far in the Jacquez et al. analysis, HIV is behaving like a typical infectious agent. When it appears, it spreads rapidly and just as swiftly disappears as the infected individuals quickly develop immunity. If this scenario is correct, then why doesn't HIV cause AIDS during the period preceding the development of immunity? The authors find the answer to this important question in the AIDS catechism: "The difference with HIV is that the virus persists and gradually initiates a new process that leads eventually to immunosuppression with renewed infectiousness and ultimately death." The authors do not produce any evidence whatever to support their assertion, nor do they cite even a single reference to back it up. It is pure faith among the authors that this assertion, made by countless other AIDS researchers, must without question be true. Neither the authors nor Peter Flegg can tell us where we can find the proof for this central belief held by AIDS researchers, nor even give us the names of the people who may have produced that proof.

The rest of the lengthy paper by Jacquez et al. consists largely in arbitrarily adjusting a series of parameters so that their mathematical model could reproduce the broad features of the epidemiological data. As most everyone understands, a mathematical model is no better than the assumptions that go into it. As is typical of virtually all AIDS research, the authors neither included control experiments or studies. Absolutely crucial to the Jacquez et al. study would be a consideration of the accuracy of the HIV antibody testing that it relies on so heavily. However, the authors failed to take into account the well documented fact that vaccinations for hepatitis and other viruses [3-9], even hepatitis itself [10] among over 60 other diseases and conditions [11], will cause false positive antibodies to HIV. I have discussed in previous letters the serious problems with all surrogate testing for HIV and AIDS.

Analysis of the other references to follow.

David Rasnick

References

1. Jacquez, J. A., et al. (1994) Role of the primary infection in epidemics of HIV infection in gay cohorts, J Acquir Immune Defic Syndr 7, 1169-1184

2. Katz, M., et al. (2000)Quarterly AIDS Surveillance Report, San Francisco Department of Public Health, HIV Seroepidemiology and Surveillance Section, AIDS Surveillance Unit, www.dph.sf.ca.us/PHP/AIDSSurvUnit.htm

3. Lee, D. A., et al. (1992) HIV false positivity after hepatitis B vaccination, Lancet 339, 1060

4. Isaacman, S. H. (1989) Positive HIV antibody test results after treatment with hepatitis B immune globulin, Jama 262, 209

5. Pearlman, E. S., et al. (1994) False-positive human immunodeficiency virus screening test related to rabies vaccination, Arch Pathol Lab Med 118, 805-806

6. Proffitt, M. R., et al. (1993) Laboratory diagnosis of human immunodeficiency virus infection, Infect Dis Clin North Am 7, 203- 219

7. Challakere, K., et al. (1993) False-positive human immunodeficiency virus type I ELISA results in low-risk subjects, West J Med 159, 214-215

8. Mac Kenzie, W. R., et al. (1992) Multiple false-positive serologic tests for HIV, HTLV-1, and hepatitis C following influenza vaccination, 1991, Jama 268, 1015-1017

9. Hsia, J. (1993) False-positive ELISA for human immunodeficiency virus after influenza vaccination, J Infect Dis 167, 989-990

10. Sungur, C., et al. (1994) False-positive HIV antibody test following alpha-interferon therapy in a chronic hemodialysis patient, Nephron 67, 251

11. Johnson, C. (1996) Whose Antibodies Are They Anyway? Factors Known to Cause False Positive HIV Antibody Test Results, Continuum 4, 4-5

Competing interests:   None declared