Re: Re: Re: Re: Request for Peter Flegg and Outstanding 'Perth Group' Questions 1 December 2004
Previous Rapid Response Next Rapid Response Top
Christopher Tyler,
n/a
84043

Send response to journal:
Re: Re: Re: Re: Re: Request for Peter Flegg and Outstanding 'Perth Group' Questions

Peter Flegg wrote: "Firstly a general point about the diagnostic process. A positive result for any test seldom confirms -proof- of the disease..."

and;

"A single positive HIV antibody ELISA or similar screening test is proof of nothing except that the source has a reactive assay. The result is merely supportive of the clinical diagnosis of possible HIV infection."

We're not talking about a disease, we're talking about proof of infection of a putative virus. If 'a positive result' is not proof of infection, why are these tests advertised as being 99.9% accurate to the general public?

Again, www.thestophivsite.com says to the general public: "When both ELISA and the Western Blot are positive ("HIV-positive"), it is 99.9% certain there is HIV infection."
http://www.thestophivsite.com/abouthiv/?action=testing

And from thebody.com, "When the EIA or ELISA is used in conjunction with the Western Blot confirmation test, the results are more than 99.9% accurate." http://www.thebody.com/aawh/force/aawh09.html


Peter Flegg wrote: "The result need to be repeated, confirmed and placed into clinical context. Ultimately it is the clinician that makes the diagnosis, and not the laboratory."

If both 'HIV' tests are 'positive' and thus 'it is 99.9 certain there is HIV infection' why is the clinical context relevant for diagnosis? Why would my sexual orientation or history have any bearing on the results of my test result since, according to the orthodoxy, 'HIV' is transmitted through both heterosexual and homosexual sex, and the tests are almost entirely error free?

For instance in 1990, St. Louis et al., anonymously tested 89,547 blood specimens from 26 US hospital patients at no risk of AIDS, including those with even meager risks including 'gunshot and knife wounds'. Between 0.7% to 21.7% of men and 0-7.8% of women aged 25-44 years were found to be HIV WB positive. (1)

Since these individuals were tested because they were at no risk for AIDS, yet up to 21.7 of them had a 'confirmed' positive by Western Blot, one must conclude that if;

a) the tests 'are more than 99.9% accurate', then these individuals are de facto infected (If A is true, this leads to certain problems. At the five hospitals with the highest rates of HIV antibodies, one third of positive tests were in women. Yet men have greatly outnumbered women as AIDS patients/deaths in the West.)

or;

b) according to Dr. Flegg, 'A positive result for any test seldom confirms ?proof? of the disease', these people tested positive as a result of non- specific reactions. In other words, since these individuals' "clinical contexts" put them at no risk for AIDS, then their positive antibody tests must be the result of non-'HIV' cross-reacting antibodies. If B is correct, then the tests cannot have been '99.9%' accurate. If these individuals' antibody tests were the result of cross-reacting/non-specific antibodies, why then wouldn't gay men's tests be the same?

With regard to repeating a test to determine if it's 'accurate' or not, if your test is reactive 900 times in a row, this says nothing about the origin of the antibodies reacting to the test antigens. After all, all you see is a 'reactive assay'.


Peter Flegg wrote: "First generation ELISA assays, although quite specific, were prone to false positive antibody reactions in patients with HLA class II antigens and therefore later 3rd generation assays using only purified or recombinant antigens have been developed which have largely overcome this problem, so Tyler?s reference to the numerous causes of ?false positive? HIV tests is outdated."

'3rd generation assays' don't overcome the problem of the fact that antibodies are polyspecific. Antibodies cross react to even polished and scrubbed proteins (even assuming the origin of these proteins is known). The lack of a gold standard for the 'HIV' tests is critical. Antibodies directed against carbohydrate mannan structures (mycobacteria, fungi, semen [2,3,4]) are known to readily react to the 'HIV' tests as an example.


Peter Flegg wrote: "I would then request confirmation utilising assays that use different antigen targets. The scenario Tyler describes would not arise in practice."

Great. Therefore, do reactive bands of p24, p32, and p41 indicate infection by 'HIV'?


Dr. Flegg wrote: "In practice the issue is irrelevant, since with established HIV infection one usually sees more bands than you find at a LiveAid concert, and indeterminate reactions with only two or three bands are unusual. "

According to data presented in Lundberg et al.[5] when the US FDA criteria are used to interpret the HIV Western blot less than 50% of US AIDS patients are HIV positive, whereas 10% of persons not at risk of AIDS are also positive by the same criteria.

The crux of the orthodox argument for what constitutes a 'true' positive as opposed to a false one is the number of antibodies. Many must be 'real' infection, whereas only a few must be false. Yet the groups who are considered to be most at risk for AIDS are also groups of people known to have many antibodies to many things (both self and non-self antibodies), including concentrations of non-specific immunoglobulins. In other words, the groups of people with the greatest probability of having cross-reacting antibodies are the very groups in which these tests are advertised as rarely making a mistake.?


Peter Flegg wrote: "These may be a consequence of early HIV infection or represent a true false positive reaction. All indeterminate results will of course be repeated, and repeated again until it becomes clear what is going on."

How can repeating an antibody test tell you anything about the inducing origin of the antibody? After all, 'a positive result for any test seldom confirms ?proof? of the disease', so how can repeating it over and over again tell you what you don't already know? That is, that you have a reactive assay (whether ELISA or WB). The answer is that you can't, not without a gold standard which can be nothing other than 'HIV' itself. Using one antibody reaction as a gold standard for another is invalid since BOTH are antibody reactions.


Peter Flegg wrote: "The positive predictive value (and therefore the clinician?s interpretation) of an ?indeterminate? western blot or a weak positive ELISA is likely to be very different if the source comes from a high risk or low risk population."

No one doubts the significance of a reactive assay in the risk groups. But positive predictive value is different than saying a person is 'infected' with 'HIV'. PPV refers to the possibility of developing the syndrome. After all, these tests have not been validated against the actual finding of 'HIV' in those with a positive test, but against those with and without the clinical syndrome AIDS. Put differently, AIDS patients/healthy blood donors are the gold standard against which these tests are said to be made accurate, not 'HIV'. One package insert says, ?Random donors are assumed to have a zero prevalence of HIV antibody'. Notice the word assumed.


Dr. Flegg wrote: "I would also do an HIV-RNA level."

I certainly hope Dr. Flegg is not using PCR technologies for off-label uses for which they are specifically contraindicated.

1. St. Louis ME, Rauch KJ, Peterson LR, Anderson JE, Schable CA, Dondero TJ. (1990). Seroprevalence rates of human immunodeficiency virus infection at sentinel hospitals in the United States. NEJM 323:213-218.
2. Muller WEG, Schroder HC, Reuter P, Maidhof A, Uhlenbruck G, Winkler I. (1990). Polyclonal antibodies to mannan from yeast also recognize the carbohydrate structure of gp120 of the AIDS virus: an approach to raise neutralizing antibodies to HIV-1 infection in vitro. AIDS 4:159-162.
3. Muller WEG, Bachmann M, Weiler BE, et al. (1991). Antibodies against defined carbohydrate structures of Candida albicans protect H9 cells against infection with human immunodeficiency virus-1 in vitro. J. Acquir. Immun. Defic. Syndr. 4:694-703.
4. Kashala O, Marlink R, Ilunga M, et al. (1994). Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross- reactivity and antibodies to lipoarabinomannan. J. Infect. Dis. 169:296-304. 5. (JAMA 260:674-679)

Competing interests: None declared