We have repeatedly criticised the “Trojan Horse” strategy of Profs. Bauer and Ruggiero for being ultimately self-contradictory, thereby running an unnecessary risk of being ultimately self-defeating. The last time we did so was in The End of Dissent. However, we recently came across another kind of Trojan horse presented by a team of researchers from Tanzania last year (2010):
Kabati, C. I. A., 1* Chande H., 2 Maurice, H. B.3 and Fatima G.1
1 Department of Pharmaceutics. Muhimbili University of Health and Allied Sciences. 2 Department of Histopathology and Morbid Anatomy, Muhimbili University of Health and Allied Sciences. 3 Department of Medicinal and Pharmaceutical Chemistry, School of Pharmacy, St John’s University of Tanzania.
In a simple, direct, unequivocal experiment Kabati et al. highlight the core problem of the HIV tests and put it in the proper context. Below we cite all but the most technical parts of the Kabati et al paper:
Theiller albino mice were used to carry out various experiments in order to check for the presence or absence of HIV specific proteins in Western-Blot negative blood donors and recipient mice.The results of this study have shown one or more HIV specific bands and some indeterminate bands for positive but not complete absence of bands. The most likely explanation is that the mice had antibodies that cross-reacted with one or more of the proteins of HIV.
We know that AIDS exist and there is a correlation between AIDS and the antibody tests. And that sex plays a role in the development of a positive antibody test and AIDS. We do, however, have misgivings that the HIV antibody proteins in the Western Blot are not specific. There is no proof that all of the supposed HIV proteins actually come from HIV. The reason is that many attempts at virus isolation have presented numerous insurmountable difficulties. Thus one cannot say for sure that any of the HIV antibody proteins actually come from HIV. It follows therefore that if you cannot know for sure that the proteins in the antibody test come from HIV, then you cannot know for sure whether these proteins are anti-HIV antibodies.
In the Western Blot (WB), the presumed HIV proteins are present separately instead of in a mixture and, after being allowed to react with a blood sample, each protein is capable of giving a visible signal if it has bound an antibody. These tests which are thought to be highly specific are generally used to confirm them. In fact so much weight is put on these Western Blots that a positive result is almost always taken to equal an active HIV infection1. In order to realize that this problem exists, for analogy purposes, diagnosing infections using antibodies is serological diagnosis, and is like trying to identify objects from the shadow they cast on the ground. There is a connection but clouds, buildings, trees and so forth may produce shadows that may look the same or similar. The best way therefore is to prove the existence of HIV in every patient by means that are unambiguous for a unique retrovirus. Although many claims are made that the HIV antibody tests have a high specificity, some schools of thought think that this is not the case1, 7 A test that is not specific will give a positive reading in the presence of other (proteins) than those it is supposed to detect. Clearly, if an HIV antibody test is not specific, a positive result is at best ambiguous2, 3.
Some groups of people generally make a lot of antibodies because they are exposed to a much greater than the normal amount of diseases and unhealthy conditions. This includes poverty-stricken Africans and intravenous drug users. Reactivity in both Elisa and Western Blot analysis may be nonspecific in Africans.4, 6
A study by Kion and Hoffman using alloimmune mice (mice that have been exposed to cells from another murine strain), the mice were shown to make antibodies against gp120 and p24 of human immunodeficiency virus (HIV), and mice of the autoimmune strains MRL-1pr/1pr and MRL-(+)/+ made antibodies against gp120. This was surprising because the mice were not exposed to HIV. Furthermore, anti-anti-MHC antibodies (molecules that have shapes similar to those of major histocompartibility complex molecules) were detected in both alloimmune sera and MRL mice5 .
After blood grouping and cross-match, the HIV negative blood from donor to recipient mice showed bands corresponding to gp120 and gp160 were observed in nine mice. Two mice had both gp120 and gp160 bands and one unidentified peak, two showed only one band gp160 and five had weak gp160 bands the so called indeterminate bands for positive but not complete absence of bands.
The western blot (WB) is a general laboratory technique for visualizing individual protein/antibody reactions (bands). One would think that if there really were HIV proteins, and that the HIV antibodies were truly specific, then just having one band light up would be proof that HIV is present. But according to experts, that is not the case, you need more than one (band)3. The intriguing thing is, even if one or two bands are not sufficient to diagnose HIV infection, there must still be a reason why they are there. In fact cross-reaction is the explanation given by all HIV experts for “noninfected” Western Blots3. But if one or two bands in the WB can be caused by non-HIV, cross reacting antibodies why cant three or four or five or all of the ten bands be caused by cross reacting non-HIV antibodies.
Around the world different combinations of two or three or four bands of the possible ten bands are deemed proof of infection. In Africa you need only two, envelope proteins without gag or pol to prove HIV infection, (WHO Criteria). FDA and Red Cross rules you need three bands. We conclude therefore that the HIV antibody proteins in the Western Blot antibody test are not specific. These findings are similar to those obtained by Kion and Hoffman.
Simple, direct, unequivocal, this paper deals a blow to the HIV antigen-antibody mythology without denying the correlation between a positive test or sex and disease/AIDS. Kabati et al. make no secret of the fact that their paper is based on the Perth Group’s 1993 paper Is a positive Western Blot Proof of HIV Infection, and their insight that antibodies are inherently promiscuous and therefore cannot be relied on to identify “HIV”. Neither do they seek to “improve on” the Perth Group’s original critique or be “all-inclusive” or “up-to-date” by quoting derivative sources, such as de Harven, Johnson, Bauer, or rely on clever re-interpetations of the mainstream’s epidemiological guesswork, accepting epidemiology known to be based on flawed premises, as is Duesberg’s wont. The Kabati paper’s strength, its single sharp point stabbing right at the heart of the matter and warranting its publication as a piece of independent research, is the simple, indisputable test they present of the supposed specificity of the HIV antigen-antibody reaction coupled with their bold, crisp discussion of the implications.
Kabati’s et al second inspiration, the Kion and Hoffman paper referenced, appeared in the prestigious journal Science in 1991. The abstract states:
Alloimmune mice (mice that have been exposed to cells from another murine strain) were shown to make antibodies against gp120 and p24 of human immunodeficiency virus (HIV), and mice of the autoimmune strains MRL-lpr/lpr and MRL-(+)/+ made antibodies against gp120. This is surprising because the mice were not exposed to HIV. Furthermore, anti-anti-MHC antibodies (molecules that have shapes similar to those of major histocompatibility complex molecules) were detected in both alloimmune sera and MRL mice. These results are discussed in the context of a possible role for allogeneic stimuli in the pathogenesis of acquired immunodeficiency syndrome, as suggested by an idiotypic network model.
Kion and Hoffman’s “surprising” result not only corroborates the Tanzanian study, but also includes p24 among cross-reacting “HIV” antigens.