AIDS: Court Case Exposes Scientific Contradictions

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Epidemics

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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
Beldeu Singh

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