Don’t Question the Gallo–HIV AIDS Dogma

According to the HIV theory of AIDS, the virus is sexually transmitted and that should produce an HIV-AIDS explosion in the heterosexual population within 25 years. But it did not happen.

This point is well put forth by Dr. Robert Root-Bernstein. Female prostitutes often have 200-300 sexual partners per year and are therefore assumed to have much higher rates of exposure to HIV and AIDS than the vast majority of heterosexuals. Many AIDS researchers assumed that female prostitutes would be the vectors (or means of transmission) of HIV and AIDS to the heterosexual community based on the fact that a single HIV-infected intravenous drug user or bisexual man could infect one female prostitute, who in turn could infect dozens or perhaps even hundreds of non-drug using heterosexual men. These men could, in turn, infect their other sexual partners, and an explosion of HIV and AIDS could occur among people without any obvious risk for AIDS. Paradoxically, no heterosexual epidemic has occurred and no evidence of female prostitutes transmitting HIV or AIDS into the heterosexual community exists for any Western nation. Transmission almost always seems to be drug related. In fact, sexual acquisition of HIV and AIDS among female prostitutes themselves is almost unknown in the absence of concomitant intravenous drug use. Cell-free viral particles have never been found directly in semen. In 'American Journal of Epidemiology' (Vol. 146, No.4), Nancy S. Padian et al reported: “We estimate that HIV infectivity for male-to-female transmission is low, approximately 0.0009 per contact, and that infectivity for female-to-male transmission is even lower.”

In New York City, for example, 40 to 50 percent of streetwalkers (a very low caste of prostitute) who have used IV drugs over the past decade are HIV seropositive. Among call girls in New York City (a higher caste of prostitute), no seropositivity was found among those who were drug free. These figures were constant between 1984 and 1989. These statistics have significant implications on the causative factor or factors of AIDS.

The biggest problem in the gallo-HIV theory which says that a pathogenic virus attackes the T4 cells of the immune system is this:

“If HIV is claimed to cause AIDS by killing T-cells, how is it possible for the mass production of HIV in immortal T-cell lines as shown in the patent in 1984 as source of HIV proteins for “AIDS tests” by Gallo/NIH, Weiss/Burroughs Wellcome (UK), and Montagnier/Pasteur?”

If the gallo-HIV actually attacks these infected cell lines, how come they are still producing HIV 21 years later!? The proponents of the gallo-HIV theory have shown exactrly the opposite – that HIV does not kill cells, just like all other retroviruses. But that does not seem to bother those who hold the gallo-HIV dogma sacred, nor has it stirred a controversy or outcry in the mainstream media!

HIV does not behave like a typical sexually transmitted disease. There is only one possible conclusion: as Japanese physician Y. Shiokawa has suggested, it is probable that drug use, multiple concurrent diseases, malnutrition, and other immunosuppressive factors are required to increase susceptibility. In fact, it better fits a model based on oxidative stress in cases of malnutrition and selenium deficiency and on oxidative damage and oxidative injury to cells of the immune system and cells in organs targeted by recreational drugs or immunotoxic medication.

The most difficult aspect of the HIV postulate is to have first decided that their HIV virus is an aggressive pathogen which they claim to target the immune system itself, as HIV was said to infect the key CD4+ T cells that regulate the immune response, modifying or destroying their ability to function and to reconcile this 'science' with scientific data and evidence that some people “appear better able than others to resist progression of HIV infection or developing AIDS,” resulting in “long-term survivors” who can be divided into three groups:

1. Long-term nonprogressors who maintain healthy or steady levels of CD4+ T cells despite many years of infection
2. Those tested HIV-positive individuals who lose a significant proportion of CD4+ T cells but remain healthy, and
3. The people who remain uninfected despite repeated “exposure to HIV”.

So, to save the HIV postulate for AIDS they also claim that, once the virus infects CD4+ T cells, the virus' genetic material is permanently integrated into the cell's chromosomes, establishing permanent latency within infected cells. After infection, the HIV incorporates its genetic material into the host cell DNA. If a cell reproduces itself, each new cell also contains the integrated HIV genes. The virus can hide its genetic material for prolonged periods until the cell is activated and makes new viruses. So, its not an aggressive pathogen.

They also claim that other cells act as HIV reservoirs, harboring intact viruses that may remain undetected by the immune system while it “targets” the cells of the immune system.

There is also no explaination on how an infected cell remains normal and remains undetected as an abnormal cell by NK cells or activated macrophages after the HIV incorporates its genetic material into the chromosomes of the cell. Such a virus, with such a capability, having a sophisticated enzyme system to incorporate its genetic material into the cells' chromosomes and activate it later on into replicating itself cannot be so small and illusive that it avoids isolation and replication by other virologists. It must have a large amount of genetic material to be do all of those things but retroviruses as the fictitious gallo-HIV is “gifted” with too little genetic material.

The causal relationship between HIV and any disease is not settled. “HIV is an ordinary retrovirus. There is nothing about this virus that is unique. Everything that is discovered about HIV has an analogue in other retroviruses that don't cause AIDS. HIV only contains a very small piece of genetic information. There's no way it can do all these elaborate things they say it does,” according to Dr. Harvey Bialy (Molecular Biologist and former editor of Bio/Technology and Nature Biotechnology as reported in Spin June 1992). Dr. Gordon Stewart (Emeritus Professor of Public Health, University of Glasgow) agrees that “AIDS is a behavioral disease. It is multifactorial, brought on by several simultaneous strains on the immune system - drugs, pharmaceutical and recreational, sexually transmitted diseases, multiple viral infections,” (Spin June 1992). Dr. Alfred Hässig, (1921-1999) was professor emeritus in immunology at the University of Bern, Director of the Swiss Red Cross Transfusion Service, and President of the Board of Trustees of the International Society of Blood Transfusion. His Swiss research group doesn't believe that HIV causes AIDS either.

So, how did the world get duped into believing that HIV causes AIDS? Very simply but on a very serious note, one of the reasons is aptly stated by Dr. Richard Strohman (Emeritus Professor of Cell Biology at the University of California at Berkeley) when he said, “In the old days it was required that a scientist address the possibilities of proving his hypothesis wrong as well as right. Now there's none of that in standard HIV-AIDS program with all its billions of dollars,” (Penthouse April 1994).

Work by scientists, shoddy clinical trials and highly improper statistics concerning HIV and AIDS have been passed off as science. Unsuspectingly, non-governmental organizations, medical practitioners and the top members of scientific establishment have carelessly supported or joined the media in spreading misinformation about the nature of AIDS and HIV as the pathogenic factor in AIDS although there are hundreds of thousands of healthy people who tested HIV-positive and live as long as HIV-negative people and there are many people with non-HIV AIDS who respond to proper nutrition.

And the 'establishment' has created bigger problems. There is no Universal Gold Standard 'HIV' test to prove 'HIV' positivity. The 'HIV' antibody test does not detect a 'virus' but an assortment of proteins that are non-specific to the hypothetical 'HIV'. The proteins that are used in the 'HIV' test are merely the biological outcome of stressed white blood cells used in the lab. There can be no Gold Standard 'HIV' test because there is no Gold Standard 'HIV' isolate. Methods of classical virology require that all evidence of 'HIV' positivity must be confirmed by pure culturing of a patient's lymphocytes and detection of whole, cell-free viral particles; so far this has never been achieved. The proteins that are used in the 'HIV' test are merely the biological outcome of stressed white blood cells used in the lab and in 'Bio/Technology', June 1993, 'Aids' analyst, Dr Eleni Eleopulos exposed the non-specificity and unreliability of the 'HIV' 'antibody test'.

'HIV' is an artefact of cell-culture invented by Dr Robert Gallo. The phenomena collectively known as 'HIV' are non-specific: reverse transcriptase is non-specific; PCR is non-specific; Viral Load is non-specific. Each property relating to 'HIV' can be shown to pertain to the cells used in co- cultivation experiments. No particle of 'HIV' has ever been obtained pure, free of contaminants; nor has a complete piece of 'HIV' RNA (or the transcribed DNA) ever been proved to exist. Moreover, Dr David Ho admits that 99.8 per cent of putative 'HIV particles' are non-infectious; the remaining 0.2 per cent of 'viral particles', being defective, are not capable of replication. As a transmittable entity, 'HIV' could not survive in nature. This indicates that what we are calling 'HIV' is a misinterpreted, non-transmissible, endogenous epiphenomenon that should never have been classed as a virus.

Dr John Papadimitriou states that the proper controls have never been done: “They have not proven that they actually have detected a unique, exogenous retrovirus. The critical data to support that idea have not been presented. You have to be absolutely certain that what you have detected is unique and exogenous, and a single molecular species…('Aids: The failure of contemporary science', Neville Hodgkinson, Fourth Estate, 1996, page 375). Since 1989, detection of a 24,000 molecular weight protein (p24) in cell cultures, (T cells from persons presumed to be infected), or co- cultures, (of T cells from persons presumed to be infected, with T cells from normal individuals), has been used to quantify HIV in cells, “cellular viremia” (Masquelier et al., 1992). Detection of p24 in cultures of T cells from normal individuals with plasma from those presumed to be infected has been used to quantify HIV in plasma, “plasma viremia” (Coombs et al., 1989; Ho et al., 1989; Clark et al., 1991). There are many reasons why p24 cannot be used to quantitate or even detect the presence of “HIV infectious particles”. There is ample evidence that the p24 protein is not HIV specific (Papadopulos-Eleopulos et al., 1993a).

Look at some of the key points:

1. HIV does not behave like a typical sexually transmitted disease.
2. Other immunosuppressive factors are required to increase susceptibility.
3. “AIDS is a behavioral disease. It is multifactorial, brought on by several simultaneous strains on the immune system - drugs, pharmaceutical and recreational, sexually transmitted diseases, multiple viral infections.”
4. There is nothing about this virus that is unique. Everything that is discovered about HIV has an analogue in other retroviruses that don't cause AIDS. HIV only contains a very small piece of genetic information.
5. Like in all other viral infections, eg smallpox,. you have to be absolutely certain that what you have detected is unique and exogenous, and a single molecular species, not particles.
6. The 'HIV' antibody test does not detect a 'virus' but an assortment of proteins that are non-specific to the hypothetical 'HIV'. The proteins that are used in the 'HIV' test are merely the biological outcome of stressed white blood cells used in the lab.
7. “99.8 per cent of putative 'HIV particles' are non-infectious; the remaining 0.2 per cent of 'viral particles', being defective, are not capable of replication. As a transmittable entity, 'HIV' could not survive in nature”.
8. “It is multifactorial, brought on by several simultaneous strains on the immune system - drugs, pharmaceutical and recreational, sexually transmitted diseases, multiple viral infections.”
9. Gallo claimed that the interaction of gp41 with antibodies found in AIDS patient sera is proof that gp41 is coded by the “HIV genome”, and that both gp41 and the antibodies are specific to a retrovirus.
10. The Epstein-Barr virus (EBV) resides as a persistent infection in human leukocyte antigen (HLA) class II+ B lymphocytes and is associated with a number of malignancies. The EBV lytic-phase protein gp42 serves at least two functions: gp42 acts as the coreceptor for viral entry into B cells and hampers T-cell recognition via HLA class II molecules through steric hindrance of T-cell receptor-class II-peptide interactions (Maaike E. Ressing et al, Epstein-Barr Virus gp42 Is Posttranslationally Modified To Produce Soluble gp42 That Mediates HLA Class II Immune Evasion, Journal of Virology, January 2005, p. 841-852, Vol. 79, No. 2).
11. In 1980, two research groups, one from the Laboratory of Cellular and Molecular Biology, National Cancer Institute and the other from the Laboratory of Viral Oncology, Memorial Sloan-Kettering Cancer Center, using the “viral glycoproteins”, found that the antibodies present in human sera which reacted with these proteins were “directed against carbohydrate structures” and concluded that “The results are consistent with the idea that the antibodies in question are elicited as a result of exposure to many natural substances possessing widely cross-reacting antigens and are not a result of widespread infection of man with replication competent oncoviruses”.
12. Exposure of RAW 264.7 macrophages to JP, a cell permeant analog of phalloidin that increases and stabilizes polymerized actin in living cells, reduced the ability of RAW 264.7 macrophages to phagocytose fluorescent Klebsiella by 50%. This indicates that increased actin polymerization is a potential mechanism explaining impairment of phagocytosis by oxidative stress and since AIDS is a condition caused by excess free radicals (in malnourished people) (see Philip J et al, Hyperoxia Impairs Antibacterial Function of Macrophages Through Effects on Actin, American Journal of Respiratory Cell and Molecular Biology. Vol. 28, pp. 443-450, 2003), quite clearly proves that oxidative stress on macrophages leads to increased actin polymerisation and formation of prominent stress fibers and actin aggregates which could occur in people recovering from malaria, influenza or in people sufferring from chronic fatigue due to mitochodrial oxidative stress or ethanol toxicity or drug induced oxidative stress.
13. The serological diagnosis of HIV infection is usually made on the basis of the detection of circulating antibodies specific for viral antigens gp41, gp120 and gp160 and possibly gp42. Studies show them to be non-viral glycoproteins or polymer actins that have suffered cleavage at different points. Quite possibly hydrogen peroxide that accumulates in people who are low in glutathione or the seleno-antioxidant enzyme that converts it into water and oxygen, can cause cleavage in polymer actins produced by cells of the immune system under oxidative stress. With relatively lower oxygen generated by the enzymatic conversion of hydrogen peroxide, people with chronic malnutrition and low selenium intake could create a cellular environment of hyperoxia thereby initiating marked changes, including an increase in the degree of actin polymerization, loss of cortical actin, and the formation of prominent stress fibers and actin aggregates.

What appears to be consistent is the observation supported by scientific tests the viral antigens in the Gallo isolate are actin polymers produced by cells or white blood cells in oxidative stress and consistent with the free radical theory of AIDS that oxidative stress produces a broad range of symptoms and illnesses and that includes suppression of the immune system or immunodeficiency. One certainty that emerges is that it diametrically opposes the claim of a specific disease caused by a specific virus that has antigenic specificity like other viruses.

But could the body be producing antibodies to these polymer actins produced under oxidative stress and hence being recognized as non-self or could some of these actins especially gp41 and gp42 act as conjugating glycoproteins that bind with EBV viral genomes that can hide in cells of the immune system and that conjugate is later broken by excess hydrogen peroxide during chronic oxidative stress or severe oxidative stress caused by chemicals and drugs? Quite possibly both, which means that AIDS is more likely to be ab EBV latency disease trigerred by oxidative stress, whether by chronic malnutrition or drugs. That does explain the different rates of “progression” of AIDS and opportunistic infections in the very poor societies and in the developed world (see:THE EPSTEIN-BARR VIRUS IN AIDS, newmediaexplorer.org/sepp ).

On one hand their HIV-cause-AIDS hypothesis tells people that after the 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 prescription is primarily large doses of immunotoxic and immunosuppresive “medicine”!

WHY is this enigma approved by the medical authorities?. Other drugs such as, sulfnamides and trimethoprim are also used in the treatment of PCP, which cause severe hematological complications, including agranulocytosis, hemolytic and megaloblastic anemia and thrombocytopenia. The results of clinical trials on AZT and protease inhibitors have revealed that these agents are poisons and not cures. AZT is a very toxic poison that promotes cancer formation in the human body. “Granulocytopenia”, is a deficiency of the most numerous cells of our immune system, which in turn leads to opportunistic infections. Prolonged use of AZT attacks the immune system through free radical toxicity.

And now, the situation as described by Dr. Roger Cunningham (Immunologist, Microbiologist and Director of the Centre for Immunology at the State University of New York at Buffalo) has become rather grave because “Unfortunately, an AIDS 'establishment' seems to have formed that intends to discourage challenges to the dogma on one side and often insists on following discredited ideas on the other,” (Sunday Times (London) 3 April 1994).

The greates intrigue remains locked in the question - “How is it possible for the mass production of HIV in immortal T-cell lines, if Gallo claims that they attack these cells as pathogens?” Them comes the riddle - “How does a small retrovirus, with so little genetic material, is able to infect and incorporate itself into the cell DNA and later become virulent, killing it?”

The gallo-HIV enters the Guiness Book Of Records as the tiniest fictitious artefact that created a multi-billion dollar industry.

Ooops, I forgot, we are not supposed to question the gallo-HIV dogma. Science is meant to be applied elsewhere, not within the haloed confines of the gallo-HIV disease and the AIDS industry it spurned.