The "HIV" tests may not detect HIV infection
Two main reasons for this:
The first is that from an antibody-antigen reaction can not be deduced, without further evidence, the antibody was originated by that antigen.
The second it that it is not proven the antigens (proteins) belong to a HIV virus, as the existence of that virus it is not proven either.
A "HIV positive" test result, within the so-called "risk groups", as the homosexuals, would mean a greater chance of developing diseases, including those belonging to AIDS, if measures are not taken to avoid it.
Problems with the interpretation of antigen/antibody reactivity
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Although antigen ‘X’ may be defined beforehand by other means and with the utmost precision, from an antibody test all a scientist may conclude is the presence or absence of a reaction. For several reasons, from this data alone it is incorrect to deduce that the antibody arises because of, or is directed against, antigen ‘X’. Additional steps must be undertaken before such a conclusion is vindicated. The explanation for this relates to three factors:
Cross-reactivity
According to Nossal antibodies “For each antigen there is a corresponding different antibody”. Yet also according to Nossal, “an antibody molecule made following the injection of one antigen frequently can combine also with a second antigen…in other words, the antibody cross-reacts with the second antigen…It is simply because the fit between antigen and antibody need not be 100 per cent perfect that the body can turn out antibodies to virtually everything…”.
Cross-reactivity is a property of all antibody molecules including monoclonal antibodies and there are instances where "cross-reactive antibodies may have higher affinity with antigens other than the inducing antigen”.All that one needs to be convinced that all "antibodies are polyspecific, that is, they are able to react with various dissimilar antigens such as: proteins, nucleic acids and haptens" and "they are able to react with more than to self or non-self antigens, often without any apparent antigenic similarities", is to read the scientific publications of the researchers, such as Stratis Avrameas, from the Pasteur Institute.
Failure to heed cross-reactivities is akin to pronouncing an unknown substance sodium chloride merely because its admixture in solution with silver nitrate results in a white precipitate. If this were the case analytical chemistry could be mastered in a matter of days. Few if any substances react monogamously and this property of matter pervades not only chemistry but also serology.
Non-specific induction
Antibody production may also be induced non-specifically, that is, antibodies directed against a defined antigen arise following exposure to an unrelated antigen. The classical example is that of Epstein-Barr virus infection which results in polyclonal B-cell stimulation and a large repertoire of antibodies including heterophile antibodies directed against sheep and horse erythrocytes.
A scientist may predict that an experiment where humans are injected with sheep or horse erythrocytes will result in the production of antibodies directed against these antigens. However, reactivity with these antigens, revealed for example in a patient by a MonospotTM test, is not interpreted as proof of infection with animal red blood cells, or that infectious mononucleosis is caused by these agents.
Identical antigens from dissimilar sources
Similar antibodies, even if specifically directed against a given antigen, may arise if the antigen is present in dissimilar sources.
For example, cardiolipin is a phospholipid found in cell nuclei, inner mitochondrial membranes and the plasma membranes of bacteria. Antibodies which react with this antigen appear following infection with T. pallidum and are demonstrated by the classical Wasserman, Kahn and VDRL reactions. However, similar reactivity occurs in numerous other conditions constituting the well known causes of false-positive syphilis serology.
No proof for the existence of HIV proteins
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The belief that certain proteins are those of a unique retrovirus HIV originate from data published in Science in 1983 by Montagnier and his colleagues from the Pasteur Institute and in 1984 by Gallo and his colleagues at the National Institutes for Health in the United States.
However, a thorough review of these papers fails to reveal any evidence that proteins attributed to a novel retrovirus HIV were obtained from purified retroviral-like particles proven infectious, that is, from a retrovirus.
It is important to stress that proof of infectivity, that is, the ability to replicate, is a sine qua non in proving retroviral isolation. This is because retrovirologists have cautioned "Release of virus-like particles morphologically and biochemically resembling type-C virus [retrovirus] but apparently lacking the ability to replicate have been frequently observed from leukaemic tissue". That is, the demonstration of retroviral-like particles with reverse transcriptase activity is not proof for the existence of such viruses.
The material which Montagnier and Gallo designated as “purified virus” was obtained from mitogenically stimulated cell cultures/co-cultures derived from AIDS patients. Aliquots of supernatants from these cultures were centrifuged through a sucrose density gradient and the material which banded at 1.16 gm/ml was claimed to be the “purified virus”.
A decade earlier, a group of several leading retrovirologists stressed that proof of retroviral isolation requires examination of banded material with the electron microscope in order to establish “virus count, morphology and purity”. Proof of purity requires that the 1.16 gm/ml band contains nothing else but retroviral-like particles with "No apparent differences in physical appearances", that is, all the particles must have the morphology of retroviral particles. However, neither Montagnier nor Gallo published electron micrographs (EM) of their “purified” material.
Thus, neither Montagnier nor Gallo in 1983/84, nor at any time since, demonstrated that the material they claimed to be “purified HIV” consists of any particles, be they retroviral, viral or of any other morphologies, pure or impure. Both groups did publish EM of their “unpurified” cell cultures which demonstrated a small number of particles claimed to be the novel retrovirus HIV but these particles were not purified and proven infectious. Indeed these particles were claimed to belong to a retroviral genus known as C-type Oncoviruses, a genus taxonomically distinct from Lentiviruses in which HIV is classified. Neither these EM nor any published since, confirm the existence of “HIV” particles bearing all the principal morphological characteristics of retroviruses.
Subsequent studies reveal that T‑cell and monocyte "HIV infected cultures" contain, in addition to particles with the morphologies attributed to HIV, many other "viral particles" unlike any of the "HIV particles". Most importantly, in the only EM study either in vivo or in vitro in which suitable controls were used and in which extensive blind examination of controls and test material was performed, particles indistinguishable from HIV were found in 18/20 (90%) of AIDS as well as in 13/15 (88%) of non-AIDS related lymph lymphadenopathies.
The existence of HIV proteins is not predicated on an origin from retrovirus particles or even material known to contain retrovirus-like particles. Instead it is predicated on reactions between a few of the many proteins present in the material banding at 1.16 gm/ml band, regarded as the “purified virus”, and antibodies present in the sera of AIDS patients. However, as argued above, from an antibody/antigen reaction it is impossible to define the origin of a protein or conclude that reacting antibodies arise as a result of specific exposure to that protein.
Subsequently, the proteins attributed to “HIV” have been found in non-HIV-infected tissues and tissues of healthy individuals at no risk of AIDS. These include the p18, p24, p32, p41, and p120/160 proteins.
It is impossible to determine the test accuracy
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What is fundamental to an antibody test is not the origin and nature of the antigens employed but the specificity of the antibody reactivity induced by whatever agent the clinician is endeavouring to demonstrate.
By definition, specificity is the proportion of HIV free individuals having a negative antibody test. In a hundred percent specific test every non-HIV-infected individual tests negative denoting a false-positive rate of zero.
Obviously the means to achieve this distinction cannot be the antigen/antibody reaction as this would amount to an antibody test acting as its own gold standard.
A gold standard must be independent of whatever is being appraised and, in the case of HIV infection, can only be HIV itself, that is, HIV isolation/purification performed on the same individuals at the same time as the antibody tests. However, such a gold standard has never been applied. This is because to date there is no proof that any scientist, laboratory or institution has achieved HIV isolation/purification.
Thus at present it remains impossible to define the specificity of the HIV antibody tests, a fact affirmed by the disclaimer repeatedly present in the Abbott Laboratories packet insert, “At present, there is no recognized standard for establishing the presence or absence of antibodies to HIV-1 and HIV-2 in human blood”
Despite lack of scientific evidence, the CDC and WHO simply assert that the HIV antibody tests are “extraordinarily accurate” in terms of sensitivity and specificity. Examination of the data published by HIV experts, institutions and biotechnology companies reveal methodologies which ignore validation against an independent gold standard. All methodologies amount to using the clinical syndrome or antibody reactivity acting as its own gold standard.
What a positive “HIV” antibody test means
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By “refining” the test antigens, by altering the criteria for a positive test as well as the definition of AIDS, and by restricting testing largely to the risk groups, HIV experts have sought and obtained a high degree of correlation between the presence or absence of “HIV” antibodies and the presence or absence of the clinical syndrome.
Notwithstanding such partiality, (and also ignoring confounders such as psychological, behavioural and treatment factors which may prove injurious to health), there is no doubt, at least in the risk groups, that a positive antibody test does predict an increased likelihood of developing diseases including both AIDS indictor and non-AIDS diseases, and dying prematurely.
Since there is no proof that a positive “HIV” antibody test is caused by a novel retroviral infection, the underlying reason for the correlation must be sought elsewhere. The explanation which accords with both non-specificity and clinical relevance is that the antibody tests are similar to measurements of the erythrocyte sedimentation rate (ESR).
An elevated ESR "is a measure of the presence and intensity of morbid processes within the body" and, like a positive "HIV" antibody test, also has the capacity to predict "a likelihood of death within the next several years far above" a normal ESR.
As far back as 1988 researchers from the Institut National de Transfusion Sanguine, Paris, France, found that "An increased ESR in HIV-seropositive subjects seems to constitute a predictive marker of progression towards AIDS before the decrease of the CD4 count".
In other words the ESR is a better predictive marker for AIDS than decrease in the CD4 cell count although the latter is said to be the cause of the syndrome.
