July 22, 2002

AIDS DEBATE

COMMENTARY BY ELENI PAPADOPULOS-ELEOPOLOS AND THE PERTH GROUP

Dear Dr Urnovitz:

We read with great interest your "The HIV Myth. Itching for a Debate". Our aim is not so much as to debate with you but to clear up various aspects of your view. There seems to be some contradictions between the views expressed in your scientific writings and those in the popular media. We would be thankful if you clarified some of the difficulties that we now outline.

1. In your 1996 review paper "Human Endogenous Retroviruses : Nature, Occurrence and Clinical Implication in Human Disease" you consider HTLV-1 and HIV-1 as typical exogenous retroviruses. That is, unlike the human endogenous retroviruses (HERVS) which are integrated in the germ cells and are transmitted by Mendelian mechanism, HIV is not integrated in the germ cells but it is horizontally transmitted. In your 1996 paper "Urine-based diagnostic technologies" you wrote: "In addition, studies must address the contribution of specific immune responses to HERV gene products on the immune responses to exogenous retrovirus infection such as HIV-1". In your 1999 paper "Antibody to Human Endogenous Retrovirus Peptide in Urine of Human Immunodeficiency Virus Type-1 Positive Patients" you wrote: "A recent evaluation of the results of a large clinical study showed that there was a compartmentalized response to the exogenous retrovirus HIV-1". In the review describing the infectivity and replication of HIV you wrote: "The envelope spikes of HIV-1 are made up principally of glycoproteins gp120 and gp41. For T cells, particularly those that have been activated, gp120 binds to the T-cell CD4⁺ receptor prior to internalization of the viral core". In regard to the HIV-genome you wrote: "As a group, the lentiviruses are complex. They have at least eight genes that encode regulatory proteins in addition to the gag-pol-env genes of the simple retroviruses…The HIV-1 genome (Fig. 4) is ca. 9.5 kb and is made up of two broad categories of genes, gag, pol and env code for viral constituents or enzymes. The remaining genes are regulatory. These in turn make up two categories, i.e. either essential or accessory. Tat and rev serve as master switches that dictate the kinds and amount of RNA (spliced or unspliced) transcribed from the DNA of integrated provirus during the early and late phases of replication. Both are required for replication. The accessory genes seem to function as fine-tuning agents of the replication process".

In your statement for the Durban AIDS conference you always refer to HIV as "HIV", but do not mention the reason(s) for the inverted commas. In "The HIV myth" you wrote: "For the record, I consider HIV to be associated with AIDS. I base this opinion on the clinical data I have collected over the years. But unlike Fauci, I view HIV as only a "marker" (or a set of cellular signals) that can be detected when AIDS develops".

Is HIV an exogenous retrovirus, that is, a microscopic particle with unique morphological characteristics and mode of replication (infectivity) having as its genome a unique molecular entity with well-defined genes? Or is it "a set of cellular signals"?

If the latter, what made you change your mind?

2. In "Increased sensitivity of HIV-1 antibody detection" (1997) you wrote:

"Like most other chronic diseases, AIDS is a complicated multifactorial, multistep process, with HIV-1 infection being a principal component. Accurate diagnosis of HIV-1 infection is important in determining an individual's risk of developing AIDS".

In "Antibody to Human Endogenous Retrovirus Peptide in Urine of Human Immunodeficiency Virus Type 1-positive Patients", (1999) we read: "….antibodies to HERV-related peptide 4.1 were found more frequently in patients with advanced stages (category B and C) of HIV-1 disease than in those patients with an earlier stage (category A) of HIV disease…This suggests that progression to symptomatic stages in HIV disease correlates with the presence of antibodies to HERV gene products in urine". Similarly, in "AIDS epidemic at the beginning of the third millennium: time for a new AIDS vaccine strategy (2001): "At the beginning of the third millennium, HIV has infected 50 million people, and so far killed 16 million. The epidemic is still spreading worldwide with, according to WHO estimations, 16,000 new cases of HIV infection daily and projections of 100 million infected individuals by the end of the next decade. The expedient introduction of HIV antibody tests in the early phase of the epidemic saved the lives of many by preventing the transmission of disease through blood transfusions".

In "Itching for a Debate" you wrote: "These are truly dark times for science and medicine. Fauci is one of the US Government's major architects of the myth that HIV has been proven to be the cause of AIDS and that stopping HIV will save lives…a myth that has become so entrenched in medicine's conventional wisdom that to question it is tantamount of treason".

In "Autism Research Takes Wrong Turn" you wrote: "In AIDS research, the NIH and CDC lead the way in making sure the public doesn’t figure out that researchers don’t have a clue what causes AIDS."

Is or is not AIDS an "HIV disease"? If not, what made you to change your mind?

3. In "HIV-1 antibody serum negativity with urine positivity" (1993), you, Montagnier et al wrote: "We have described the use of urine HIV-1 antibody test to indicate vertically transmitted HIV-1 infection in children of HIV-1 infected women…Our data highlight the need to study HIV-1 infection in populations other than those identified as HIV-1 positive on serum EIA. Screening of seronegative high-risk populations with urine EIA with testing for cell-mediated immune response to HIV-1 peptides may add significantly to the understanding of the pathophysiology of HIV-1 infection".

In "Urine based diagnostic technologies" (1996): "In studies carried out since 1990 on more than 11,000 paired urine and serum specimens, we have documented that urine-based tests have essentially the same sensitivity and specificity as conventional serological assays; such results have been verified independently. A modified western blot was used to confirm repeatedly reactive enzyme-linked immunosorbent assay (ELISA)-positive serum specimens. The band found most consistently in the urine of patients exposed to HIV-1 is that for the antibody to gp160. Table 1 shows that the one-band criterion for antibody to gp160 in the urine corresponds with the two-band criteria used for serum antibody tests [which are claimed to be 100% specific for proving HIV infection].

Therefore, we counted the occurrence of an antibody band to gp160 in the urine as the interpretative criterion for a positive antibody response to HIV-1 exposure…Further tests confirmed that HIV-1 urine antibodies were found in two patients with AIDS defining illnesses, low CD4 T-cell counts and serum indeterminate results; virus isolated from one subject was typed as HIV-1 group "O". These findings documented that HIV-1 seronegative subjects had specific antibody to HIV-1 in their urine…Such results suggest that urine assays might be useful for determining the clinical stage of AIDS, or for monitoring the response to therapeutic modalities".

In your 1996 review on Human Endogenous retroviruses you wrote: "Barbacid et al and Snyder and Fleissner discussed, respectively, how antibodies to modified cellular glycoproteins or to carbohydrate structures of the Forsmann type can be mistaken as antiretroviral antibodies".

In "AIDS epidemic at the beginning of the third millennium : time for a new AIDS vaccine strategy" (2001) we read: "…the anti-V3 loop [of gp120] and anti-1g antibodies of healthy individuals have complementary structures and that V3-reactive antibodies are present in HIV-negative sera…An interesting approach is that of peptide mimicry of carbohydrates expressed on the gp160 as a substitute for envelope glycoproteins. Agad Jaman et al have demonstrated that mice being infected with peptides that are mimicking these mucin-type carbohydrates, are developing antibodies capable of neutralising HIV-111B and…-MN…Betaieb and co-workers also demonstrated that the immune platelet destruction observed in AIDS-free HIV-infected patients was associated with the presence of a cross-reactive antibody, recognising both HIV-1 gp120 and platelet gpIIIa (CD61)…Recently, it has also been reported that human autoantibody which binds gp160 and which reacts with both HIV-1 infected cells and uninfected lymphoid cells, does enhance HIV-1 infectivity in a complement-dependent manner…It has been reported that some cancer antigens are cross-reactive with peptides derived from the HIV-1 env protein and that neutralising anti-HIV-1 antibodies elicited by the gp120 promote cancer growth…Based on this compilation of published results, it is evident that HIV-1 gp120 vaccines are unlikely to be effective in the prevention of HIV-1 infection and furthermore that they reported a real and present danger for recipients".

In statement for the Durban AIDS Conference," you state: "In 1999, at the Oak Ridge Conference (1), my colleagues and I cited the case of a French farm woman who died of AIDS-like illness but whose "HIV" blood antibody status was inconclusive. Analysis of an "HIV"-like virus (called HIV Group O) isolated from her suggested that she created the viral envelope by reshuffling her own genetic material. Therefore, it is likely that CD4 binding ligand [gp120] can occur as a byproduct of poikilogenic events".

In "The HIV Myth" you wrote: "I also endorse the use of easy-to-administer urine and saliva tests to help us to detect this "marker" [set of cellular signals] and to thereby understand the breadth of the AIDS problem; these "marker" tests are better epidemiological tools than mathematical guesses".

Does your licensed "HIV-1 urine antibody" test detect:

 

 

• "Specific antibodies to HIV-1", and a unique exogenous retrovirus, HIV-1, with a specificity of 100%;
• Antibodies to modified cellular glycoproteins or carbohydrates;
• Cross-reactive antibodies to platelets, lymphocytes or cancer antigens;
• Antibodies to "envelope" proteins which occur as by-product of poikilogenic events;
• A "marker"?

We are very interested to hear of any debate that you may have with the HIV experts and the additional arguments that you can present against HIV being a exogenous retrovirus and a cause of AIDS which have not been already expounded by us, Peter Duesberg and the other dissidents.

Good luck.