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Given knowledge of the information available on this website it can only be through a strenuous effort of faith that the perception of HIV as a deadly virus can be maintained. I never cease to be amazed by how strong this faith is, immune to all rational objections. Never before has a proposed scientific model presented more scope for criticism.

The information on this site invites the open minded, logical thinking reader to recognise how redundant and inadequate the HIV model is as an explanation for AIDS and its effective treatment. The aim of this piece is to set the scene for the rest of the information on this site.

As critics of the AIDS model, it is not up to us to prove that HIV does not cause AIDS rather it is up to those making the positive claim that it does to prove their case beyond reasonable doubt, especially as those making and supporting this claim have enormous power and use the claim as justification for their exercise of that power.

I do feel, however, that those who mount challenges to ruling hypotheses (dogma) are obliged to provide alternative hypotheses to account for what is seen. The oxidative stress theory of AIDS does this. It has been established beyond doubt that oxidative stress plays a key role in "progression" to AIDS and that treatment based upon oxidative stress theory is effective as well as being non-toxic. For a sampling of the scientific evidence for this you are referred to:

http://www.altheal.org/treatments/oxidative.htm

In the world of HIV, the established scientific practice of testing hypotheses by making direct observations from nature has been abandoned. Instead technological markers developed by humans substitute for observing nature directly. On a basic level this can be seen in the example of looking at the viral load of a patient and then giving them toxic combo on that basis, ignoring the fact that they presented as healthy and well. On this site the extent to which the technological marker called “viral load” is a distorted measure of nature is revealed, see in particular the piece on fundamental flaws in HIV/AIDS. It is this blindness to natural significance that makes HIV/AIDS a technological construct rather than a scientifically derived theory. HIV/AIDS is founded upon the indirect approach of genetic technology (detecting genetic fragments and simply calling them HIV), and the abuse of that technology, rather than the detection of actual physical virus. We will see shortly the problems inherent in equating a genetic sequence with an actual physical virus.

As referenced on this site, it has been admitted that the phenomena attributed to HIV only arise when the “infected” cells are stimulated by oxidising agents. There is clear evidence presented on this site showing how an oxidising environment inside cells can increase antibody production which can give rise to a positive result in the non-specific HIV test which is an antibody test. It is postulated that these oxidising conditions can also cause genetic rearrangements which give rise to genetic sequences picked up by the PCR “viral load” test.

To quote the Perth group from the BMJ debate:

http://bmj.bmjjournals.com/cgi/eletters/326/7387/495#44053

“1) The oxidising agents to which the AIDS patients and those at risk are exposed would cause the appearances of AIDS [1], that is, infectious and non-infectious diseases and thus high levels of antibodies including MCA, that is hypergammaglobulinemia and thus a positive "HIV" antibody test;

(2) The oxidising agents, to paraphrase Barbara McClintock [2] cause a "….."shock" that forces the genome to restructure itself in order to overcome a threat to its survival", thus leading to the appearance of novel non-viral RNAs, which may be detected with PCR. (Let us not forget that to date nobody, not even Gallo [the supposed discoverer of HIV], has proven the existence of the "whole HIV genome" in the fresh lymphocytes in even one AIDS patient).

Since oxidising agents induce both hypergammaglobulinemia and novel RNAs an apparent correlation between antibody and PCR HIV tests may be detected in the total absence of “HIV”.

References

1. Papadopulos-Eleopulos E. Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Med Hypotheses 1988;25:151- 162. www.virusmyth.net/aids/data/

2. McClintock B. The significance of responses of the genome to challenge. Science 1984;226:792-801.”

Many retroviral genetic sequences are known to occur naturally in the human genome. The main problem with defining HIV purely on the basis of genetic sequence is that this says nothing about the origin of the genetic sequence. Although this lack of scientific rigor is bad enough, the lack of definition of HIV is further apparent in the unprecedented genetic variability of HIV such that it cannot be defined in molecular terms. HIV has shown variations of over 40% in a small, essential internal protein within a single subgroup within the same living population in a single country. This exceptional variability is just one more reason why the application of PCR to HIV detection is inappropriate. To quote the Perth group again from the BMJ debate:

http://bmj.bmjjournals.com/cgi/eletters/326/7387/495#51351

“It is true that we have drawn Christopher Noble's attention to the genetic diversity of "HIV-1". It was Christopher Noble who, all along in this debate, tried to convince us that a virus can vary by more than 50% at the nucleic acid level and by more than 81% at the amino acid level and:

1. it would still be possible to define "HIV-1" infection in molecular terms.
2. "HIV-1" infection could be diagnosed using the same antibody test. (Although he claimed that different tests are used to prove infection with "HIV-1" group 0 he could not provide such evidence).
3. the proteins would still perform the same function.
4. it would still be possible to develop a vaccine.

Our view was, and still is, the opposite.

In particular we have claimed that, given the genetic diversity of "HIV-1", it would not be possible to define "HIV" infection in molecular terms, that is by hybridisation and PCR. The Damond et al findings support our claim. Although they used a small number of patients (42) and 5 primers, they could not detect the "HIV-2" env gene in all the 42 "HIV-2" positive individuals. To detect the env gene in all "HIV-2" positive individuals many more primers would be necessary. If similar numbers of primers are necessary for the detection of all the other genes the detection of the whole "HIV-2" genome would require the use of a very large number of primers.

Given that the "HIV-1" genome is more diverse than that of "HIV-2" and that many more people are infected with "HIV-1" the number of primers needed to detect the whole "HIV-1" genome in all "infected" individuals, that is, to define "HIV-1” infection in molecular terms in these individuals, would be prohibitory.

The Perth group also explain why there is no real basis for the distinction between HIV-1 and HIV-2

One major class of "anti-HIV" drugs are known as nucleoside analogs. They are supposed to act by interferring with a process called reverse transcription. For "HIV" the genetic material is RNA and reverse transcription involves the synthesis of DNA using this RNA as a template so that "HIV" genetic code can then integrate into human genetic material as DNA. DNA and RNA are made up of building blocks called nucleotides. Nucleotides are phosphorylated nucleosides. There are 4 different natural nucleosides that make up DNA and 4 that make up RNA, the order in which these are combined to make up a particular DNA or RNA strand constitutes the genetic code. One nucleoside analog is AZT which acts by mimicing thymidine, a naturally occuring nucleoside. The idea is that nucleoside analogs become incorported into a growing DNA chain but once they are incorporated chain growth stops because the nucleoside analogs lack the reactive chemical group that is needed to attach another phosphorylated nucleoside. AZT is therefore supposed to act by stopping the generation of "HIV DNA" from "HIV RNA" by stopping the "HIV DNA" chain growth. Note that AZT was never designed as an anti-HIV drug. Nucleosides cannot be incorporated into a growing DNA chain unless they are first triphosphorylated (three phosphate groups added) and all studies have shown that AZT is not triphosphorylated by the body at a level anywhere near the level required to exert the "anti-HIV" action that it is intended to have, see Current Medical Research and Opinion 1999, Vol. 15, supplement 1. Ever willing to use the surrogate technological marker "viral load" as an absolute gold standard, the AIDS industry say that AZT must have an anti-HIV effect because it makes "viral load" go down but we already know that it is impossible for this reduction to be caused by AZT acting in the expected HIV specific manner proclaimed by the AIDS industry. Whilst it is true that the nucleoside analog drugs make “viral load” go down (even though they are oxidizing agents) this lowering effect is generally only present within the first two years of HAART. There is evidence that such drugs can act to disturb the balance of triphosphorylated nucleoside pools in cells (Proc. Natl. Acad. Sci. USA 1986, Vol. 83:8333-8337) and we can reasonably hypothesise that different combinations of such drugs will disturb this balance in different ways. The disturbance in the balance of these nucleosides will cause a general interference with RNA synthesis sufficient to manifest as a reduction in the number of "HIV RNA" genetic sequences picked up by the "viral load" test and therefore a reduction in "viral load". It is clear that this GENERAL, NON-SPECIFIC effect is what must be happening with AZT. After the first two years, HAART causes significant deletions in mitochondrial DNA, in addition we can hypothesise that during this time cells adapt their nucleoside balance to compensate for drug disturbance and that this effect is interpreted as HIV becoming resistant. The damage to mitochondria caused by the combo interferes with ATP (the chemical fuel of the cell) production, this causes a large free radical increase and therefore greatly increased oxidative stress which produces increased cell debris, this is why all nucleoside analog drugs are not just directly oxidising (with the exception of 3TC) but all (including 3TC) have a major indirect oxidising effect. Some of the cell debris is picked up by the PCR “viral load” test, we can speculate that another class of anti-HIV drugs, the protease inhibitors, have a non specific effect that reduces cell debris although this effect is gradually overwhelmed as a result of excessive oxidative stress. See also the piece "The True Nature of AIDS Drugs" We can hypothesise that such increased oxidative stress also increases the expression of genetic sequences attributed to HIV and may even induce genetic rearrangements that create such sequences. The AIDS industry is obviously not interested in any non-HIV based hypotheses so alternative possibilities/explanations will never be scientifically investigated/considered.

HIV/AIDS is spearheading the way towards a world where scientific evidence is constituted by a collective “because we say so” from powerful establishment interests. The Durban Declaration (Nature 2000 vol. 406, 15-16) epitomises this collective mentality.