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Trojan Horse from Tanzania

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):

Testing for HIV Specific Proteins in Otherwise Western Blot  Negative Theiller Albino Mice

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.


One Response to “Trojan Horse from Tanzania”

  1. Gene Semon says:


    Congratulations are in order to the authors for demonstrating to Professor Bauer what should have been reference 1 for HIS paper, “HIV” tests are not HIV tests”.

    They have also made a great contribution to the “core problem” of HIV tests as originally stated by PG. And I agree that provided evidence came without self contradictory statements, advancing the ball forward.

    We have an issue, clearly, of whether or not a secure biological phenotype HIV-1 exists, as our previous comments on the “new views” of Gelderblom and Montagnier demonstrate.

    Here’s how the phenotype exogenous HIV-1 was originally defined (A, B and C). Take note of the phrase “compelling biological and structural similarities” in A-iii:

    A. “We are writing to propose that the AIDS retroviruses be officially designated as the human immunodeficiency viruses, to be known in abbreviated form as HIV.

    “We have considered several issues* that bear upon this proposal.

    (i) the name conforms to common nomenclature for retroviruses, beginning with the host species (“human”), ending with “virus”, and containing a word that denotes a major (though not the only) pathogenic property of the prototypic members of the group (“immunodeficiency”). (“Feline leukemia virus” and “mouse mammary tumor virus” are two well-known examples of such names for retrovirus species.)

    (ii) The name is sufficiently distinct from the names of other retroviruses to imply an independent virus species, a group of isolates that can presumably exchange genetic information readily with each other but not with members of other known retrovirus species.

    (iii) Any future isolates of human retroviruses with clear but limited relationship to isolates of HIV (for example, more than 20% but less than 50% nucleic-acid sequence identity) should not be called HIV unless there are compelling biological and structural similarities to existing members of the group.” (1)

    B. “We propose a revised standardized nomenclature for the proteins common to all retroviruses on the basis of biological function, enzymatic activity, and/or virion location data. (We do not discuss proteins specific for subfamilies or only some retroviruses.)

    (Edited from table for clarity) “HIV Type 1: p17= matrix protein (MA), p25= capsid protein (CA), p7= nucleo-capsid protein (NC), p12 = protease enzyme (PR), p66 = RT enzyme, p32= integrase (IN), gp120= envelope surface glycoprotein (SU), gp41= envelope transmembrane glycoprotein (TU).” (2)

    C. Complete dimeric RNA genome and “accessory proteins” (1990).

    So it was early on that some HIV experts caught on IMO. Although Kion and Hoffman (1991) never explicitly said so, the “existence” of HIV-1 as “secure biological material” and completely exogenous, was in question. At least there was compelling evidence from these two Trojan Horses that it was at least partially endogenous.

    Later, more Trojan horses, based on astonishing** discoveries (partial list below), starting around the same time the HIV-1 “accessory genes” were being mapped, confirmed the nonexistence of such a phenotype as HIV-1 as defined by A, B and C.

    Nor did I have to dig too far into my stack to obtain evidence that “HIV” is a surrogate for TH2 shift and “auto-immune microvesicles”, (sometimes labeled “autovirions” because they can cause inflammatory reactions in vivo).

    I think these references are self explanatory and deserve more scrutiny:

    Polyanskaya et al; Infection of macaques with simian immunodeficiency virus induces a species-specific antibody response to major histocompatibility complex class I and class II molecules. Journal of General Virology (2003), 84, 1671–1676

    “Envelopes of immunodeficiency lentiviruses including human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) contain, in addition to virus-encoded glycoproteins, host cell membrane proteins, particularly molecules encoded by the major histocompatibility complex (MHC) (reviewed in Tremblay et al., 1998). MHC molecules are present in virions at levels exceeding gp120/gp41 (Henderson et al., 1987; Arthur et al., 1992) and are incorporated non-randomly” (Hoxie et al., 1987; Poon et al., 2000; Nguyen & Hildreth, 2000). Furthermore, it has been shown that incorporation of HLA-DR by clinical isolates of HIV-1 expanded in primary human cells depends on the producing cell and the donor source (Cantin et al., 2001).

    Arthur, L. O., Bess, J. W., Jr, Sowder, R. C., II, Benveniste, R. E., Mann, D. L., Chermann, J. C. & Henderson, L. E. (1992). Cellular proteins bound to immunodeficiency viruses: implications for pathogenesis and vaccines. Science 258, 1935–1938.

    Cantin, R., Martin, G. & Tremblay, M. J. (2001). A novel virus capture assay reveals a differential acquisition of host HLA-DR by clinical isolates of human immunodeficiency virus type 1 expanded in primary human cells depending on the nature of producing cells and the donor source. J Gen Virol 82, 2979–2987.

    Henderson, L. E., Sowder, R., Copeland, T. D., Oroszlan, S., Arthur, L. O., Robey, W. G. & Fischinger, P. J. (1987). Direct identification of class II histo-compatibility Dr proteins in preparations of human T-cell lymphotropic virus type III. J Virol 61, 629–632.

    Hoxie, J. A., Fitzharris, T. P., Youngbar, P. R., Mathews, S. D. M., Rackowski, J. L. & Radka, S. F. (1987). Non-random association of cellular antigens with HTLV-III virions. Hum Immunol 18, 39–52.

    Nguyen, D. H. & Hildreth, J. E. (2000). Evidence for budding of human immuno-deficiency virus type 1 selectively from glycolipid enriched membrane lipid rafts. J Virol 74, 3264–3272.

    Poon, D. T., Coren, L. V. & Ott, D. E. (2000). Efficient incorporation of HLA class II onto human immunodeficiency virus type 1 requires envelope glycoprotein packaging. J Virol 74, 3918–3923.

    Tremblay, M. J., Fortin, J.-F. & Cantin, R. (1998). The acquisition of host-encoded proteins by nascent HIV-1. Immunol Today 19, 346–351.

    *Note: there are 7 “issues” in original Letter to Science.

    **At least they should have startled the HIV experts, e.g. reappraising the “accessory genes”.

    1. John Coffin, Ashley Haase, Jay Levy, Luc Montagnier, Steven Oroszlan, Natalie Teich, Howard Temin, Kumao Toyoshima, Harold Varmus*, Peter Vogt, Robin Weiss; Human Immunodeficiency Viruses. Science. V232, pg 697 (May 9, 1986)

    *Chairman, Human Retrovirus Subcommittee

    2. Leis et al; Standardized and Simplified Nomenclature for Proteins Common to All Retroviruses. JOURNAL OF VIROLOGY, May 1988, p. 1808-1809

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