The Rape of the Null Hypothesis 6 April 2004
Previous Rapid Response Next Rapid Response Top
Julian Turningheart,
teacher
Gainesville, Florida 32608

Send response to journal:
Re: The Rape of the Null Hypothesis

Dear Editor,

I can simply no longer resist the intellectual onslaught of the towering trifecta of reasoned suasion, Tony Floyd, Brian T. Foley and Christopher J. Noble (24-26 March, 2004). I now realize that, through lack of knowledge and training -or perhaps just naïve credulousness- I have been duped, hornswoggled, bamboozled, and otherwise misled by a devious coterie of HIV denialists. Tony Floyd’s post (24 March, 2004), in which he manfully tore himself away from his medical studies and Sesame Street watching (I assume, though without supporting evidence, that these are independent and distinguishable activities for him) long enough to cogently summarize all of the Rapid Responses relating to this debate, was the linchpin that led to my epiphany. I hereby wish publicly to renounce my membership in the Society of HIV Conspirators. I am turning in my decoder ring, and will no longer perform the secret conspiracy handshake. Furthermore, as atonement for my past indiscretions vis-à-vis proper HIV thought, I have composed a creed that I feel appropriately captures the essence of the HIV mainstream. I call it “The Rape of the Null Hypothesis”:

I believe that HIV is necessary and sufficient to cause the clinical syndrome called AIDS, and when confronted with inconvenient evidence to the contrary I will strive to emulate the skillful legerdemain of Christopher J. Noble, who brilliantly defends the HIV theory by demanding that the Perth Group “…provide some evidence for various claims that THEY have made.” 26 March, 2004).

I believe that the Perth Group’s insistence on electron micrograph evidence of HIV particle purification is a red herring that serves only as an attempt to bog-down HIV science in the atavistic techniques of a bygone era. I do not believe they were vindicated by the Bess, et al. (1), and Glushankof, et al. (2) papers of 1997. Furthermore, I applaud Brian T. Foley when he asks (Politics vs. Science, 5 September, 2003), “What part of ‘infectious molecular clone’ do you fail to understand? We have been over this a few times before, already. If you have a segment of DNA that produces infectious viral particles it is clear that this segment of DNA contains a viral genome.” I am neither aware of, nor interested in what evidence Dr. Foley has that any “infectious molecular clone” of HIV produces infectious viral particles. Neither do I understand how, in the absence of even a rudimentally pure isolation of such viral particles –demonstrated by electron microscopy- he is able to determine that the particles are infectious? Nevertheless, I believe.

I believe that the Perth Group is wrong to say that there is no evidence for the existence of gp120 spikes on the surfaces of mature HIV particles. This belief is strengthened by knowledge of a recent paper (3) that describes the use of atomic force microscopy to examine the surfaces of putative HIV particles obtained from chronically infected H9 cells, and concludes that, “The clusters of gp120 do not form spikes on the surface of HIV as is commonly described in the literature.” I believe that this finding, which may at first seem profoundly important in light of the tremendous effort to develop a vaccine based on models of gp120 kinetics, is really not very interesting, and deserves the collective yawn it has received from the HIV mainstream.

I do not find it humorous that the Fall 2003 Los Alamos National Laboratory Research Quarterly (available here: http://www.lanl.gov/quarterly/q_fall03/ ) has on its cover a cartoon of an HIV particle decorated with the very spikes that have not been proved to exist.

I believe that HIV is present in the blood of infected persons in stunningly high titer that, nevertheless, can only be detected by the use of exquisitely sensitive amplification techniques (4,5).

I am not troubled by the lack of persuasive evidence showing that full-length HIV provirus is present in any fresh cells or tissues of infected persons. Neither am I troubled by the fact that many important HIV studies were, and continue to be conducted with a cell line (HUT78/H9) that is infected with another retrovirus, HTLV (6).

I believe that HIV antibody tests are highly specific and reliable. No, seriously, I do.

I believe that mis-reading of Western blots due to cross-reactions and/or non-specific binding can be avoided by having the patient “help” the doctor interpret the test (Brian T. Foley, 27 June, 2003), and I find it head-slappingly obvious that the wild variation in positive Western blot criteria among continents (Perth Group, 20 June, 2003) is due not to confusion about what the test is actually measuring, but rather to the different –perhaps culturally informed- ways patients on these continents “help” interpret their tests.

I find it somewhat troubling that Bess, et al. (1) demonstrated qualitatively indistinguishable Western blot patterns when probing AIDS patient serum with proteins isolated from HIV- and mock-infected cells; however, in the absence of instruction from the arbiter elegantiarum of all things HIV, Tony Floyd, I think the tasteful thing to do is simply avert my gaze.

I do not believe that excluding clinically indistinguishable patients who are HIV antibody negative (i.e. idiopathic CD4+ lymphocytopenia) to maintain a perfect correlation between HIV and AIDS is an example of circular logic.

I believe that Koch’s Postulates are antiquated relics, and therefore am not troubled by the fact that they have not been fulfilled for the HIV- AIDS hypothesis.

I believe that HIV is sexually transmitted, even though there is no dispositive evidence of such transmission. More importantly, the HIV denialists have not succeeded in proving that sexual transmission doesn’t occur. So there.

I believe that there is female-to-male transmission of HIV, though this has never been adequately demonstrated. I believe also that, since receptive anal intercourse is the only sexual act that correlates with HIV acquisition in women (7), African heterosexuals must in engage in, shall we say, “indelicate” sexual congress with a level of enthusiasm seldom seen elsewhere. Furthermore, viewing Africans in such a way should not be viewed as racist condescension.

I believe it is wrong of the Perth Group to keep harping on the fact that estimates of HIV infection in Africa are extrapolations based on tests of pregnant women at antenatal clinics. And I do not believe they have been vindicated by recent reports showing that “The scope of Africa's AIDS epidemic may have been grossly overestimated…” (8).

I believe that maternal HIV antibodies are present in infants for at least twice as long as other maternal antibodies (9).

I am not troubled by the fact that the once signal AIDS-defining disease, Kaposi’s’ sarcoma (KS), has disappeared down the same memory hole that swallowed HL23(10). Furthermore, I do not think it reflects well on the Perth Group that they were questioning the HIV-KS link (11) at the same time Gallo was publishing a model for the pathogenesis of HIV- associated KS (see especially fig.7 in ref.12).

I believe that AZT is an effective antiretroviral, and should especially be prescribed to pregnant women and their babies to lower the risk of vertical HIV transmission. This belief is based on the excellent ACTG 076 study (13), which was wrongly criticized by the Perth Group (14) for failing to show a significant difference in vertical HIV transmission between AZT and control groups until several weeks after birth.

I believe that AZT is an effective in vivo DNA chain terminator, in spite of the fact that it’s level of in vivo triphosphorylation has yet to be demonstrated as high enough to have a significant inhibitory effect on HIV (15; and see appendix V in ref. 14 for a summary)

I do not find it oxymoronic to include, in clinical trials of antiretroviral drugs, HIV-infected persons in whom no virus can be detected (16).

My confidence is not shaken by the fact that “Hit hard, hit early” (17) has been replaced with “…um…er…let’s wait and see.”

Pace the Perth Group(18), I believe that HIV, which decays rapidly and is extremely fragile in cell-free form, could nevertheless survive Factor VIII preparation to productively infect hemophiliacs.

I believe that, by calling it “wretched”, Peter J. Flegg (2 March, 2004) has thoroughly, and with a degree of concision I previously thought unobtainable, rebutted all of the issues raised by the Perth Group in their 204 page monograph on mother-to-child transmission of HIV (14).

Finally, I do not believe that the sum of all of these errors and reversements –the ubiquity and transparency of which are exceeded in degree only by the arrogance of their perpetrators- could reasonably be construed as indicative of a fundamental flaw in the HIV theory of AIDS.

Wow. Who would’ve thunk knuckling under to peer pressure would be so liberating. Thanks, fellas!

References:

1) Bess, et al. (1997). Virology 230:134-144.

2) Gluschankof, et al. (1997). Virology 230:125-133.

3) Kuznetsov, et al., (2003). J. Virol. 77:11896-909.

4) Ho, et al. (1995) Nature. 373:123-6.

5) Wei, et al. (1995) Nature. 373:117-22. 6) Wong-Staal, et al. (1983). Nature 302(5909): 626-8.

7) The European Study Group (1989). BMJ 298:411-14.

8) Blomfield, A. & LaGuardia, A. National Post (Canada), 9 January, 2004.

9) The European Collaborative Study (1988) Lancet November 5: 1039- 42.

10) Gallagher & Gallo (1975). Science 187: 350-3.

11) Papadopulos-Eleopulos, et al, (1992). Medical Hypotheses 39:22- 29.

12) Ensoli, et al. (1991). In MZ Atassi (Ed.) Immunobiol. of Proteins and Peptides VI. pp. 27-38. Plenum Press, NY

13) Connor, et al. (1994) NEJM 331: 1173-80. 14) Papadopulos-Eleopulos, et al. (2001) Monograph on mother to child transmission of HIV and its prevention with AZT and nevirapine: a critical analysis of the evidence. ( http://theperthgroup.com/MONOGRAPH/MTCTJuly24.pdf).

15) Papadopulos-Eleopulos, et al. (1999). Curr. Med. Res. and Opin. 15(suppl.): S1-45.

16) Yarchoan, et al. (1986). Lancet, March 15 1(8481):575-580.

17) DD Ho (1995) NEJM 333(7):450-1.

18) Papadopulos-Eleopulos, et al. (1995). Genetica 95: 25-50.

Competing interests: None declared