Date: Mon, 5 Feb 1996 09:58:56 -0500
To: orgonomy@jefferson.village.virginia.edu
From: James DeMeo <demeo@mind.net>
Subject: Part 1: Turn your radio on...
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A two-part item of interest recently posted on the Rethink HIV newsgroup:

>    TEXT OF RADIO BROADCAST FOR THE AUSTRALIAN BROADCASTING
>                          COMMISSION
>
>
>Author: Dr. V. F. Turner
>
>Department of Emergency Medicine, Royal Perth Hospital, Perth,
>Western Australia
>
>Voice Int+ 619 2243221    Fax Int+ 619 2243511
>
>email <vturner@uniwa@uwa.edu.au>
>
>Please note: The original text has been amplified.
>
>          DO HIV ANTIBODY TESTS PROVE HIV INFECTION?
>
>What evidence authenticates a positive HIV antibody test as
>proof of HIV infection? This question has greatly interested
>me because those of us who work in Emergency Medicine spend a
>considerable part of our lives exposed to other people's blood
>and body fluids, a circumstance which, according to the
>experts, places us under constant threat of death from AIDS.
>Ironically, if the experts are right, the life we save may
>cost us our own and it's little wonder that some of us have
>pursued the question of proving HIV infection to the very
>limits. From the early days of AIDS I was fortunate to
>collaborate with Eleni Eleopulos, a Biophysicist at the Royal
>Perth Hospital, John Papadimitriou, Professor of Pathology at
>the University of Western Australia, and other colleagues, and
>in one of our papers, published in June 1993 in the journal
>Bio/Technology [1], we were compelled to confront many
>unsettling conclusions about the HIV antibody tests, none of
>which accord with current wisdom. Some of these I would like
>to share with you today.
>
>The HIV antibody tests do not detect a virus. They test for
>any antibodies that react with an assortment of proteins
>experts assure us are unique to HIV which, almost everyone
>agrees, is a retrovirus and the cause of AIDS [2]. What
>happens is this: A sample of blood serum is incubated with a
>mixture of these proteins in a test called an ELISA, an
>acronym for Enzyme Linked Immunosorbent Assay. The ELISA is
>positive if the solution changes colour thereby indicating a
>reaction between the proteins in the test kit and the
>patient's antibodies. However, according to many experts, the
>ELISA is not specific meaning it may react in the absence of
>HIV infection. In response to this, testing authorities have
>developed strategies such as repeat testing of all positive
>ELISAs and following up those twice positive with a third but
>different antibody test known as the Western blot. In the
>Western blot the "HIV" proteins, about ten of them, are
>located at discrete spots in a paper strip, rather like the
>one your doctor uses to perform multiple tests on your urine.
>Serum is added and wherever there is a reaction a colour
>change occurs which shows up as a dark band. The test is read
>by noting which bands show up, in other words, which proteins
>react. Certain combinations of bands are defined as a positive
>test. It is enigmatic that the location and number of bands
>required for a positive Western blot varies around the world.
>They may even vary between laboratories within the same city.
>In Australia four bands are required, in Canada and much of
>the United States, three bands suffice. And in Africa two will
>do. In the US Multicenter AIDS Cohort prospective study
>involving several thousand gay men, one "strong" band was
>deemed sufficient. If each of the above indicates HIV
>infection then HIV must cause different populations of
>antibodies to appear in different places. I don't know about
>you but to me that sounds very odd. But at least it gives some
>Africans a way out. All an African has to do is have a test in
>Australia because two bands would not be considered positive
>here. Nevertheless, in spite of lack of standardisation and
>other problems such as reproducibility, the Western blot is
>accepted to be in excess of 99.9% specific and if positive is
>regarded synonymous with HIV infection. In some countries
>similar claims are now made for the HIV ELISA without recourse
>to the Western blot.
>
>The rationale for the use of antibody tests is as follows: The
>immune system has the ability to detect foreign agents and to
>respond by producing antibodies which react with those agents.
>However, this does not work in reverse. By that I mean the
>observation of an antibody reaction with a particular agent is
>not automatic proof that the antibody was produced in response
>to that agent. The problem is that antibodies indulge in
>casual and indiscriminate relationships. They are in fact
>promiscuous. Antibodies meant for one agent may react with
>another agent, a perfect stranger. Or, if you want it put
>technically, there is ample evidence, some of the best in fact
>comes from the Pasteur Insititute, that antibody molecules,
>even the most pure, the monoclonal antibodies, are not
>monospecific and cross-react with other, non-immunising
>antigens. Here are some examples to illustrate this most
>crucial fact. Firstly, in a study of 1.2 million applicants
>for US military service [3], of the 1% or 12,000 who had first
>time positive HIV ELISAs, only 2000 were ultimately shown to
>be also WB positive and thus, according to the authors, HIV
>infected. That left 10,000 positive ELISAs which must have
>reacted for reasons other than "HIV antibodies", a fitting
>testimonial to the problem caused by cross-reacting
>antibodies. Secondly, there is the tantalising data reported
>in 1990 about dogs. Writing in the journal Cancer Research,
>Strandstrom and colleagues reported that 72/144 (50%) of dog
>blood samples "obtained from the Veterinary Medical Teaching
>Hospital, University of California, Davis" tested in
>commercial Western blot assays, "reacted with one or more HIV
>recombinant proteins [gp120--21.5%, gp41--23%, p31--22%, p24--
>43%]" [4]. Assuming Californian dogs are not infected with HIV
>(as did the authors) one must conclude these data are further
>proof of antibody cross reactivity to many of the "HIV"
>proteins. What all this means is that you're not necessarily
>infected with what your antibodies appear to tell you. This
>can be brought home by two further examples. Firstly, some
>AIDS patients have antibody reactions with laboratory
>chemicals but no one claims AIDS patients are infected with
>laboratory chemicals. Secondly, as an example removed from
>AIDS, the antibody test for glandular fever relies on the fact
>that patients with glandular fever make antibodies that react
>with the red blood cells of sheep and horses. But these
>patients are not infected with animal blood and animal blood
>does not cause glandular fever. Bearing all these examples in
>mind it is painfully obvious we cannot pronounce someone
>infected with what is regarded as a lethal human retrovirus
>merely because we observe an antibody reaction. Before we
>pronounce any such reactions indicative of HIV infection and
>long before we introduce the test into routine clinical
>practice, we must exact solid proof of precisely why these
>reactions take place. In doing we must not forget that biology
>is not mathematics and despite our clever technology, in
>biology still we must stoop to the relative ignominy of
>empirical proofs. Or, as Plato said, "experiential data must
>always be interpreted in the light of what Nature has
>revealed".
>
>In Science we must constantly resist the temptation to stray
>beyond our data and in that spirit I put it to you there are
>only two pieces of information which can be gleaned from an
>antibody test (for mathematical purists it's only one piece of
>information). Either you see a reaction or you don't. That's
>all. You don't see antibodies with labels attached saying what
>produced them. You cannot construe the genesis of antibodies
>by observing changing colours in a test-tube. The cardinal
>problem scientists face when ascribing meaning to a set of
>antibody reactions is how can they tell whether the reaction
>is caused by a real antibody or a ring in? One whose proper
>partner is something else but caught in a compromising act? In
>this context it is proper for a disinterested scientist to
>allow for the possibility that there are no real HIV
>antibodies whatsoever, that they're all pretenders. When the
>only information is a reaction, and that reaction has more
>than one possible cause, as is the case with an antibody test,
>you need extra information before you can ascribe a particular
>outcome. So, if you want to claim an antibody reaction signals
>a particular outcome, such as HIV infection, first you have to
>prove it. And just before we get to crunch time consider this
>little morsel. AIDS patients are exposed to many foreign
>agents are known to have antibodies reacting with dozens of
>different substances and it makes perfect sense that the more
>antibodies there are the more chance there will be some that
>will spoil the test. What this means is that in the very
>patients you suspect of harbouring a virus there exists the
>precise circumstances, lots of potentially cross reacting
>antibodies, which make it imperative to sort out what is
>really going on.
>
>What's the solution or, more to the point, what's the problem?
>The problem is how do you know, when you witness an antibody
>reaction, that is, a positive test, HIV is present too? After
>all, that's what you really want the test to tell you and the
>question on the patient's lips is bound to be "Is HIV
>infection the only cause of a positive test? If's there's
>something else I'd rather have that, thank you very much". In
>technical terms the patient's hopes are hanging on the
>specificity of the test. Let me first explain what is meant by
>100% specificity. One hundred per cent specificity means that
>positive tests only occur in HIV infected people. That's the
>same as saying positive tests never occur in uninfected
>people. And that's the same as saying all uninfected people
>have a negative test. This leads us to the formal,
>mathematical definition of specificity which is the number of
>negative tests in a large group of individuals who do not have
>HIV infection. If 100% of one thousand people who do not have
>HIV infection are seronegative the specificity is 100%. If one
>uninfected person is seropositive the specificity is reduced
>to 999/1000 or 99.9% by virtue of a lone false positive. Thus,
>to determine the specificity of an antibody test we need two
>pieces of data. The numbers of persons with negative tests and
>the numbers of persons with no HIV infection. By the way, and
>I'm sure it's obvious, the false-positive rate is (1-the
>specificity). An experiment to find the specificity also gives
>the false positive rate and vice versa. How should we design
>an experiment to discover this important data?
>
>Firstly, since the underlying problem is largely one of
>deciding between bona fide and cross-reacting antibodies we
>must include in our sample persons who are likely to have a
>large repertoire of antibodies to agents other than HIV. The
>more the merrier. Thus we must include persons who are sick
>and who have diseases similar to AIDS but not AIDS. Secondly,
>we need a way of determining the presence or absence of HIV
>infection. Obviously, this can't be the antibody test itself
>because that's what we're trying to validate. When we measure
>specificity we are trying to find out how often reactions
>occur in individuals who do NOT have HIV infection. Rather
>surprisingly, in the AIDS literature, the specificity of the
>HIV antibody tests has been evaluated by testing for reactions
>in healthy individuals such as blood donors. These persons are
>chosen as de factos for the absence of HIV infection. Under
>these circumstances few if any positive reactions are found
>but this is not necessarily, as the HIV/AIDS experts claim,
>because the tests are highly specific. In fact, this is the
>wrong experiment and wrong for two reasons. Firstly, healthy
>people do not have large number or variety of antibodies to
>react in the first place. That goes with being healthy. That's
>why we put them in the Army and let them donate blood. There
>are simply not enough antibodies available to measure the
>propensity for unwanted reactions. It's like going to a party
>where hardly anyone is hogging the Guinness because there's
>hardly any people. Secondly, good health cannot be used as a
>de facto for the absence of HIV infection any more than good
>health can be used as a de facto for the absence of gall
>stones, kidney stones, pregnancy, hydatid cysts, deep vein
>thrombosis, cerebral aneurysms, pathogenic bacteria or
>coronary artery disease. The practice, widely adopted by
>HIV/AIDS experts, of appraising HIV antibody tests by testing
>thousands of healthy blood donors, also creates an enormous
>dilemma. If healthy people are regarded as a de facto gold
>standard for the absence of HIV infection, counting the
>occasional one or two who do react as false-positives, by what
>criteria can similar or even the same individuals be regarded
>as infected at some future date? One week the same individual
>may be tested as member of a cohort of healthy blood donors
>and the following week when he or she requests an examination
>for Life Insurance or attends a doctor for a checkup. Is this
>person HIV infected or not? Does the outcome depend solely
>upon who you are and which door you knock on?
>
>Back to the problem of validation. We select our thousand
>people who are sick and let's make sure we include some who
>have diseases similar to AIDS and let's include a few healthy
>persons and some cases of AIDS as well. You never know, we
>might be in for a big surprise. We might find some AIDS
>patients too are antibody positive in the absence of HIV
>




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