AIDS: Court Case Exposes Scientific Contradictions
A legal case in South Australia has brought the scientific contradictions of the pharmaceutical AIDS paradigm into the spotlight. The defendant, Andre Chad Parenzee is appealing against his conviction on three counts of endangering life.
The case challenges the validity of the theory that a virus called HIV does indeed cause a large number of disrelated illnesses that, individually, have been known before AIDS became a household word.
Helen Lobato, in an article that first appeared on Melbourne Indymedia, put it this way:"An appeal case has HIV-AIDS specialists on tenter hooks awaiting the outcome which they say could set a dangerous precedent for public health campaigns and the criminal law. He is in custody awaiting sentencing and could face up to 15 years in prison. He was found guilty in February 2006 of endangering the lives of three women because he had unprotected sex with them without telling them he had HIV."
The court has heard witnesses for the defense for a week and is now listening to what the prosecution's experts have to say. What is being discussed amid heated arguments against "aids deniers" are the scientific merits of the isolation of the virus that is said to cause AIDS, and thus of the tests that determine whether a person is infected or not. Next step: Does the virus actually cause all the illnesses that are ascribed to it or is it an innocent passenger that all of us carry while other 'risk factors', such as intravenous drug use, do the major damage.
Beldeu Singh's recent article GALLO vs MONTAGNIER gives us a good look into the inconsistencies that exist, even in the words of the proponents of the "HIV-causes-AIDS" theory. Those are serious doubts which plague the debate the Australian judge will have to resolve. Typically, we don't find the "HIV-Aids experts" willing to discuss the merits of their views when challenged, but in this case, they have no choice. Here the article by Beldeu Singh:
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GALLO vs MONTAGNIER
The two persons who claimed to have discovered a new virus, they called it the HIV, are Robert Gallo and Luc Montagnier. Dr. Gallo claimed in his seminal paper that HIV is the probable cause of AIDS. It was supposed to be a virulent pathogen that targeted the cells of the immune system, including T4 cells that eventually weakened or destroyed the immune system and opened it for opportunistic infections.
A close study of AIDS shows that there are people who test seropositive and show no symptoms of the disease and there are those who have AIDS but do not test positive. Of course, all the test kits carry a disclaimer, saying that you must do another test for an affirmative diagnosis. In other words, these tests are not specific as one would expect them to be in diagnosing viral infections, but that is quite another matter.
The establishment does not like anyone questioning the official “HIV causes AIDS” dogma. One wonders why, for that is not scientific temper. Montagnier has actually stated that “it would be a tribute to their (dissidents like us) courage and honour to abandon the HIV cause of AIDS in the face of overwhelming evidence (Virus, New York, WW Norton & Company Inc, 1999). Ok fine. Lets abandon the questioning of that dogma but lets look at their science. At least that should be allowed. It is still science, isn’t it?
In that book, Montagnier states that in AIDS patients, oxidative stress is massive and it occurs at an early stage. The cause of the oxidative stress is HIV!. In an interview in 1995, Montagnier said that for the progression of AIDS, oxidative stress is a key factor. The contradiction here is that we should expect massive oxidative stress only at a later stage, after a large number of HIV replications have occurred, certainly not in the initial stages.
Montagnier gave a talk to the European Union Parliament on 8th December 2004. He told the EU Parliament that "the clinical phase of opportunistic infections and cancers which result in death of the patient is principally due to a decline in T4 cells and the decline in T4 cells is due to their propensity to die from apoptosis."
Apoptosis or programmed cell death (PCD) is a highly regulated process. In contrast to necrosis, which is a form of cell death that results from acute cellular injury, apoptosis is carried out in an orderly process that generally confers advantages during an organism's life cycle, as for example in the process of differentiation in the embryo. The way the apoptotic process is executed facilitates the safe disposal of dead cells and fragments. Apoptosis can occur if a cell is damaged beyond repair or if it is infected with a virus. If a cell's capability of apoptosis is impaired by mutation or if the initiation of apoptosis is blocked by a virus, that cell can continue dividing without restrictions, developing into cancer. So, HIV does not block apoptosis.
Chronic infections by viruses have been strongly linked to the development of disease conditions including carcinomas. Viruses are also known to induce oxidative stress as seen from elevated levels of reactive oxygen species (ROS). Usually when a clear link with any particular viral gene product is elusive, the elevated levels of ROS are thought to cause death of cells that harbour these viruses.
The genetic material of HIV is RNA. Hence, it is called a retrovirus.“HIV depends on the cells it infects to make new copies of itself. One of the main targets of HIV is a white blood cell called a CD4. HIV infects a CD4 cell by attaching itself to the surface of the cell and injecting its genetic material (RNA) into the host cell. Since RNA can not direct the reproduction of new viruses, HIV must first turn its RNA into DNA. HIV turns its viral RNA into a viral DNA copy through the use of an enzyme called reverse transcriptase. This process is know as "reverse transcription". Once the conversion process is done, the viral DNA may become part of the host cell’s DNA. This process is known as "integration". At this point infection is complete. Once the viral DNA copy is successfully made part of the infected cell’s DNA, the infected cell goes on to produce new HIV every day. As many as 10,000 new HIV copies can be produced before the infected CD4 cell is destroyed. The new copies of HIV then go on to infect other cells. In this way, HIV spreads throughout the body. This allows for billions of new viruses to be produced every day. Forced to manufacture new HIV (viral replicas), the host cell neglects its own life processes. Gradually, like a machine wearing out, the CD4 cell starts to fail and dies” (Ch. 2: HIV: Biology and Safe Sex; UCSD, Official Web Page of the Univ. of California, San Diego, undated).
That mechanism was the classic explanation of how HIV causes AIDS.
In the Journal Of Infectious Diseases (1997; 176;655-64), Montagnier wrote that "in AIDS pathogenesis oxidative stress is proposed as a metabolic alteration that favours disease progression by inducing both viral replication and apoptotic (cell) death." He claims to have "evidence that oxidative stress indeed induces, while antioxidants inhibit, HIV replication and apoptosis" and suggests the use of these molecules as an antiretroviral therapy to reduce cell death in AIDs patients. Firstly, note that here we have Montagnier suggesting the use of antioxidants in AIDS patients to reduce apoptosis of T4 cells and as an antiretroviral therapy. Secondly, the “oxidative stress induces HIV replication” assertion by Montagnier creates another paradox.
Earlier on it was claimed that HIV attacked T4 cells. Then, it is claimed that HIV causes oxidative stress and that oxidative stress induces viral replication. In medical science pathogens are killed by oxidative stress that causes oxidative injury but it is just the other way around with the HIV. The key factor that is lethal at the molecular and submolecular level is now claimed to induce HIV replication, making HIV the first pathogen whose replication is free radical induced! Oxidative stress in cells impairs protein synthesis. That ought to slow down and prevent the replication of the virus. Oxidative stress also damages enzymes that are required in converting HIV RNA into HIV DNA and other enzymes involved in the processes that result in viral replication.
Montagnier fails to explain why the “massive oxidative stress that occurs at the early stage” does not kill the T4 cell. Originally, it was claimed that the HIV attacked T4 cells and how such an oxidative stress could be managed by the virus in such a way that it does not kill the “infected” T4 cells but it remains under its control for the purpose of inducing its replication. Dr. William Haseltine at the Harvard University School of Medicine, says T4 cells are primed to die once they are infected. The reason, he said, is that the virus ends up destroying the cell membrane of any T4 cell that it infects.
Next, there is a need to explain how such a small virus, with so little genetic information, can utilize oxidatively damaged molecules in T4 cells for its replication when the cells themselves do not have such machinery. An elevated level of ROS causes oxidative stress and it is toxic for living cells by reason of oxidative injury to membranes and oxidative damage of cellular structures and free radical reactions with proteins, lipids, nucleic acids etc. Reactive oxygen and nitrogen intermediates are important antimicrobial defense mechanisms of macrophages and other phagocytic cells. What protects the HIV protein and its genetic material from oxidative injury? Yet, the free-radicals-generating drugs, like AZT are supposed to be anti-HIV.
All the drugs used in AIDS patients are toxic and induce free radical damage. AZT is probably the most toxic of them. They generate oxidative stress as well as create oxidative damage to a large number of molecules and going by what Montagnier wrote in the Journal Of Infectious Diseases, that oxidative stress induces HIV replication, it would mean that these drugs are inducing HIV replication in “HIV-infected” patients. That is simply astounding indeed, but medical authorities take no cognizance of it for therapy.
The observation that “virtually all T4 cells eventually die in people with AIDS” may in fact be due to the susceptibility of T4 cells to oxidative stress rather than the fact that they are infected with a virus.
Oxidative stress is the key to the progression of AIDS, for there are people with AIDS who are not HIV positive and many respond to antioxidant interventions while AZT, a highly toxic chemical that generates free radicals in the body that can destroy cell membranes as well as a large number of molecules, can produce the very symptoms of AIDS. AZT, benzene and many compounds made from benzene can deplete glutathione which is very essential to the functioning and which determines the life span of T4 cells.
In a 1998 study, researchers from Canada reported that supplementation of vitamin E and C reduces oxidative stress in “HIV” positives. "This study is the first randomised controlled trial to demonstrate that, in an HIV-positive population, daily supplementation of 800 IU vitamin E and 1000 mg vitamin C significantly decreases oxidative stress and produces a trend towards a reduction in HIV viral load suggesting that there may be some clinical benefit worthy of larger clinical trials…consideration of the potential for this antioxidant therapy remains important for the developing world” (Allard et al. 1998, Effects of vitamin E and C supplementation onoxidative stress and viral load in HIV infected subjects. AIDS, 12:1653). Antioxidant activity clearly reversed whatever was triggered by oxidative stress.
On one hand we understand that viral toxins can create oxidative stress and that appears to be the cause of secondary diseases eg carcinomas or leukemia, especially in cases of chronic infections but the Montagnier-HIV (M-HIV) is actually induced by oxidative stress and its replication is inhibited by antioxidants. This sounds more like a latency disease wherein a certain length of a viral genome forms a conjugate with a protein molecule produced by the T4 cell or cells of the immune system and can enter the cells without inhibition, only to be reactivated later on by oxidative stress that breaks the conjugate. Oxidative stress could break the viral genome-protein conjugate, releasing the viral genome to produce a latency disease. Naturally, antioxidants would prevent such breakage and help prevent the latency disease (see: THE EPSTEIN-BARR VIRUS IN AIDS). If so, HIV cannot be a new virus, but one that is already a harmless passenger in many people. And if oxidative stress is a factor in the reactivation, it is nothing more than a problem of nutrition and antioxidant intake as a measure of curbing the AIDS problem and by direct implication, toxic medication and drugs and chemical stressors work towards initiating the disease and aid its progression. It appears, quite clearly that Gallo and Montagnier proved this point.
Interestingly, in 1983 Luc Montagnier and in 1984 Robert Gallo stimulated cell cultures from tissues of AIDS patients with numerous oxidising agents (Sekkat et al, 1988, Oxidative phenomena are implicated in human T-cell stimulation. Immunology, 63:431-437) and mitogenic chemical agents. These are toxic chemicals that generate free radicals that cause oxidative stress. By 1986 Montagnier and Gallo acknowledged that the "HIV" phenomenon cannot be detected unless the cells are “stimulated”.
Montagnier and his associate David Klatzmann were the first to draw attention to the fact that LAV infection of T4 cells in vitro does not lead to HIV expression unless the cells are stimulated. "Infection of resting T4 cells does not lead to viral replication or to expression of viral antigens on the cell surface, while stimulation by lectins or antigens of the same cells results in production of viral particles, antigenic expression and the cytopathic effect" (Klatzmann and Montagnier, 1986, Approaches to AIDS therapy. Nature 319:10-1).
Gallo also expressed the view that without "activation" the T4 cells do not express the virus (Zagury et al (1986) Long term cultures of HTLV-III-infected T cells: A model of cytopathology of T-cell depletion in AIDS. Science, 231:850-853). In other words, here is a virus that infects T4 cells but cannot replicate in them. So, there is no HIV-AIDS without oxidative stress and this turns out to be starkly at variance from the classic explaination on how HIV infection kills T4 cells. What eluded those scientists was the fact that oxidative stress, in some manner, had triggered the reactivation of a viral genome that is already present in many of us. It is certainly not a case of a “stimulated” cell that causes the virus to replicate.
The point to note is that T4 cell exposure to oxidizing agents produces both cytopathic effect and results in the production of viral particles. Glutathione deficiency in CD4 T cells from AIDS patients is associated with markedly decreased survival time and glutathione deficiency is a key determinant of survival rates in AIDS patients. Several studies, quite expectedly show positive response by selenium supplementation.
T4 cell susceptibility to oxidative stress arising from toxic chemicals that deplete glutathione is the key in understanding AIDS and the progression of the disease. Quite possibly, mature T4 cells and mature macrophages may not be able to produce glutathione or selenoproteins from selenium. This may also explain why narcotics and recreational drugs like ecstasy and most of the drugs used as medications reduce T4 cell counts and white blood cell counts.
The role of oxidative stress as the causative mechanism of AIDS was already proposed by the Perth Group as long ago as 1983 and E Papadopulos-E has argued in favour of oxidation as being a critical factor in the pathogenesis of AIDS (Res. Immunol. 1992, 143, 145-148 . Oxidative Stress, HIV and AIDS. E. Papadopulos-Eleopulos (1) V.F. Turner (2) and J.M. Papadimitriou (3). (1) Department of Medical Physics, (2) Emergency Department and (3) Department of Pathology, (University of Western Australia), Royal Perth Hospital, Wellington St., Perth 6001 (Western Australia)) and elaborated in other articles by other researchers. Oxidative stress is a factor in the progression of every disease and disease condition. A wide range of diseases are associated with altered levels of antioxidant enzymes, especially glutathione and coenzyme Q10. Selenium deficiency, low levels of antioxidant enzymes in the blood and low antioxidant activity in the body are independent predictors of cell death, mortality and progression of diseases.
Selenium deficiency was found to produce an elevated risk in AIDS patients (High Risk of HIV-Related Mortality Is Associated With Selenium Deficiency. Marianna et al, 1997, JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY, 15:370-374). And there are many studies that show that “nutritional problems have been a part of the clinical aspects of AIDS from its earliest recognition as a new disease. In fact, in many AIDS patients, death seems to be determined more by the individual’s nutritional status than by any particular opportunistic infection. This is, when wasting of lean body mass approaches 55% of what is normal for age, sex, and height, death is imminent regardless of the forces resulting is such profound malnutrition. Furthermore, the severity of the clinical manifestations of AIDS is proportional to the degree of the nutritional deficiencies" (cf: John Kirkham and James Whitehead, Some immune stimulating treatments and the scientific bases for them, undated). Natural vitamin C can recharge glutathione directly or indirectly through alpha-lipoic acid while natural vitamin E can recharge it through alpha lipoic acid and that explains why supplementation helps reduce viral loads or produces clinical benefits.
Montagnier had been obviously ignored by the pharmaceutical industry and the medical authorities and the EU governments as far as his assertion on the use of antioxidants to prevent replication of HIV is concerned. What comes out loud and clear is that while Gallo and Montagnier propounded the HIV-causes-AIDS hypothesis, they told people that after HIV infects cells in the immune system, it replicates in them and it leads to the ultimate devastation of the immune system, while on the other the standard prescription is primarily large doses of immunotoxic and immunosuppressive “medicine”!
Montagnier stated that for the progression of AIDS, oxidative stress is a key factor. Drugs that create oxidative stress, in that light, are in fact aiding the progression of AIDS in patients. Why is that assertion by Montagnier largely ignored by medical science? It would mean throwing out all of the toxic medications.
But there is a bigger contradiction between these discoverers of the HIV. In 1984 Dr. Gallo registered a patent which shows that he has been mass producing his HIV in an immortal line of T4 cells, which means the T4 cells are alive and intact after 21 years. This Gallo-HIV (G-HIV) does not produce oxidative stress in T4 cells and does not cause apoptosis either. And that means we have a very strange situation that can be rolled up into a question as follows:“If HIV is claimed to cause AIDS by killing T-cells, how is the mass production of HIV in immortal T-cell lines possible, as shown in the 1984 patent for a source of HIV proteins for “AIDS tests” by Gallo/NIH, Weiss/Burroughs Wellcome (UK), and Montagnier/Pasteur?.”
If HIV actually attacks these infected cell lines, how come they are still producing HIV 21 years later! The proponents of the Gallo-HIV (G-HIV) theory have exactly the opposite view - the G-HIV does not kill cells, unlike the HIV that was made out to be the cause of AIDS. So, even in the T4 cells that are “stimulated” by oxidizing agents in his culture in which they are growing, the HIV does not attack and kill the T4 cells. Which ever way you look at it, this boils down to the fact that their experiments prove that the so called HIV does not kill T4 cells and does not deplete them by replicating in them. Something else is independently at work, either as direct damage from oxidative stress or as an oxidative stress that triggers a latency disease.
Gallo and Montagnier need to reconcile the difference between G-HIV and M-HIV, but that does not seem to bother those who hold the HIV dogma sacred, nor has it stirred a controversy on how AIDS patients ought to be treated – drug or antioxidant therapy. The bottom line is not the science and the ethics of science but the money from drugs. Science is secondary to the treatment already decided. There is more money in drugs than antioxidants, but science will kill the AIDS industry. Much of the controversy rests in the fact that HIV has never been isolated and that there is no antibody test that is specific to such an isolated virus. There also is no explaination as to why the antibodies that are used to test for HIV are not able to stop the infection just like in all other viral infections. These antibodies must work if they are specific to the viral coat proteins etc.
The dissidents have challenged the HIV-causes-AIDS dogma. They have said their piece. They are correct in pointing out all the inconsistencies, but I am not saying, listen to the dissidents. I am saying, listen to the the two persons who claim to have discovered the virus and it was Dr. Gallo who said HIV is the “probable cause of AIDS.” Listen to their inherent contradictions.
REFLECTING ON GALLO’S TESTIMONY AT THE TRIAL OF ANDRE PARENZEE
by Beldeu Singh
HIV ON TRIAL IN AUSTRALIA OR IS IT LOYALTY THAT IS ON TRIAL?
by Beldeu Singh
Prof Robert C. Gallo says history is in the past
Mr. Gallo said that Ms Papadopolous-Eleopolos and Dr. Turner's assertions are "nonsense" because the research on which it is based is outdated. If that is the case, could he also mean his own research and "discovery" of HIV is also outdated? Gallo squirmed on the camera on Monday to a line of questioning about his wrongdoings and ethical breaches in 1984.
Beyond the 'HIV-Causes-AIDS' Model
AIDS disease is generally characterised by a decline in CD4+ T lymphocytes circulating in the blood, which are responsible for cell-mediated immunity. As a result, the patient becomes susceptible to opportunistic infections (those affecting weakened immune systems) such as tuberculosis, pneumonia, meningitis, and other diseases caused by parasites, bacteria and viruses that can enter and multiply in the cells of the body.
But models that assume the human immunodeficiency virus (HIV) plays a central role in disease progression run into considerable difficulties. If the decline in CD4+ cells is due to HIV killing the cells, then there should be a correlation between the ‘viral load’, which estimates the amount of virus in the body, and the CD4+ cell count. But that is not the case. CD4+ cell count is not a reliable indicator of disease progression at all, nor for that matter is viral load (Chapter 2, Unraveling AIDS, ISIS Report), and they bear little relationship to each another. This has been confirmed in a recent study on untreated HIV+ individuals.
posted by Sepp Hasslberger on Wednesday February 7 2007
updated on Wednesday April 4 2007
URL of this article:
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