What if HIV was simply a natural signal of cellular death (apoptosis)?

After having considered the last major mainstream publications on HIV and AIDS in 2006, I have concluded that the orthodoxy mistook the part for the whole.

The work of Benigno Rodriguez et al., published last September, shows that the viral load explains only about 5% of the decline of the CD4+ immune cells.

Another interesting study, that of the Huber et al, published in December, reminds me that the apoptotic immune cells themselves are the source of ‘infectious’ particles, independently of any infection. This is true for macrophages, but it is quite likely also true for lymphocytes.

Finally, I wonder if HIV is not simply a natural signal of cellular death, but so weak that it passes unnoticed in a healthy person.

In fact, while the mechanism of apoptosis has been well understood only within the last ten years, especially its biochemistry, which involves nitrogen oxides, peroxynitrites (Zhao et al), and proteins which control them (as well as the associated reducers – thiols), the research in the 1980s focused on something (HIV) which is associated with the fall of lymphocytes, but which is not the root cause.

The endogenous nature of the hiv can be verified by some facts:

• Nobody, except a person consuming HAART (Highly Active Anti-Retroviral Therapy) has a zero viral load.
  
  An example: The Frankfurt doctor Juliane Sacher performed a fascinating experiment: “I removed my own blood and put it in two tubes. One was sent under my name to the laboratory for an antibody test but the other was sent with the name of one of my HIV-positive patients to measure the viral load in the same laboratory”. She received the results some days later: “the blood tested under my own name was negative, but my blood which was sent under the name of my patient, had a viral load of 1800.”
  
  Note that Frau Sacher was not HIV-positive. Why is this important? Well because seropositivity implies the detection of a quantity of antibodies above a limit (cut off). A normal person also presents these antibodies, but only in small quantities. It is normal if small quantities of these vesicles (called HIV) are present, as they are necessary to allow apoptosis.
• There are many publications by Kion et al, Faulk, Labarrère et al and Panem et al.

But these microvesicles are not nevertheless HERVs (Human Endogenous Retro-Viruses). Where do they come from?

The mechanisms of the cellular apoptosis and thus that of the lymphocytes have been thoroughly studied, showing that the process involves a very large number of proteins or other molecules. It seems more and more certain that the essential factor is the normally endogenous forming of peroxynitrites (Zhao et al). Luc Montagnier insists that oxidative stress was responsible for this apoptosis. We can go further and realize that it is due to the action of peroxynitrites.

This natural process would thus be amplified in the AIDS. Why? Let us not forget that we still have to explain 95 % of the death of lymphocytes.

I think that the real causes of the AIDS, such as described by Professors Duesberg and Bialy, are practices such as drug abuse that unfortunately interfere with this natural process, because they are the source of massive quantities of peroxynitrites. These are formed by a very fast reaction of the nitrogen monoxide with a normal product of cellular respiration, the ion superoxide.

A lot of compounds consumed from the years 1960–1980 are donors of nitrogen monoxide. This includes recreational drugs: nitrites (known as poppers), tertiary amines such as cocaine and secondary amines such as crystal meth. Everybody knows that the pharmaceutical pill Viagra allows its users to maintain the quantity of nitrogen monoxide at a high level.

Finally and especially, we find donors of nitrogen monoxide in all the medicines which contain a bond between a nitrogen and an atom (Chlorine, Nitrogen, Oxygen) whose electronegativity is superior to that of carbon. Examples are: bactrim (isoxazole ring); chloramphenicol (now mostly used in developing countries), metronidazole, nitrofurantoin (nitrocompounds); isoniazide against tuberculosis (mainly in Africa) (a hydrazide) and AZT (azide : alkyl azides act as ionic azides).

But these donors of nitrogen monoxide have an anti-apoptotic action as long as the quantity of glutathione (and of glutathione peroxidase) is normal (glutathione transports NO in excess). Otherwise they have an apoptotic effect.

Luc Montagnier and others have noted that AIDS patients have an enormous deficit in glutathione. This is due to the donors of nitrogen monoxide described above, that are also oxidizers capable of slowly destroying the glutathione (thiols) to give compounds which cannot be metabolized (sulfates). A good example is the first approved AIDS drug: AZT.

The door is then opened to the massive synthesis of peroxynitrites which provoke the massive apoptosis of lymphocytes. During this apoptosis these lymphocytes release the famous microvesicles, which we call HIV, in large quantity (from which comes an increase in both the viral load and antibodies)

How to explain the initial beneficial action of AZT, measured during the first weeks of the trial of Fischl et al?

This is because AZT reacts easily with peroxynitrites to produce NO and an anti-apoptotic effect. But this effect does not last, and bit by bit the NO formed regains its apoptotic properties due to the depletion of glutathione.

The sulphurated ring of 3TC (aka Lamivudine), another nucleoside analog used to treat AIDS, is easily oxidized by peroxynitrites, (see Carey and Sundberg and the reactivity of sulphurated acetals with the nitrosyle ion NO+), and thus resulted in an important decrease in the apoptosis of CD4+ cells in medicated AIDS patients from 1996.

This hypothesis explains why the orthodoxy stuck with the model of the infectious virus, taking the part for the whole, why Peter Duesberg always defended the existence of the virus, but realizing that it did not explain AIDS.

This explanation would also allow one to understand the position of the Perth Group and of Etienne de Harven (oxidative stress).

References

1. Predictive value of plasma HIV RNA level on rate of CD4 T-cell decline in untreated HIV infection. Rodriguez B et al. JAMA. 2006 Sep 27;296(12):1498-506. ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17003398&query_hl=1&itool=pubmed_docsum
2. The role of membrane lipids in the induction of macrophage apoptosis by microparticles. Huber LC et al. Apoptosis 2007 Feb;12(2):363-74. ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17191114&query_hl=2&itool=pubmed_docsum
3. Functional studies of an HIV-1 encoded glutathione peroxidase. Zhao L et al. Biofactors. 2006;27(1-4):93-107. ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17012767&query_hl=5&itool=pubmed_docsum
4. Saar Echo AIDS- Forschung - das große Roulette saar-echo.de/de/art.php?a=32564
5. Roberto Giraldo : EUROPEAN PARLIAMENT CONFERENCE ON AIDS IN AFRICA Brussels, December 8, 2003 robertogiraldo.com/brussels/montagnier.doc
6. Cocaine increases inducible nitric oxide synthase expression in rats: effects of acute and binge administration. Elliott JC et al. Int Immunopharmacol. 2003 Jul;3(7):1011-8. ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12810358&query_hl=5&itool=pubmed_docsum
7. Methamphetamine-induced selective dopaminergic neurotoxicity is accompanied by an increase in striatal nitrate in the mouse. Anderson KL et al. ; Ann N Y Acad Sci. 2006 Aug;1074:225-33 ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17105919&query_hl=9&itool=pubmed_docsum
8. Increased nitric oxide production by neutrophils from patients with chronic granulomatous disease on trimethoprim-sulfamethoxazole. Tsuji S et al. Nitric Oxide. 2002 Dec;7(4):283-8 ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12446177&query_hl=19&itool=pubmed_docsum
9. Nitric oxide generated from isoniazid activation by KatG: source of nitric oxide and activity against Mycobacterium tuberculosis. Timmins GS et al. Antimicrob Agents Chemother. 2004 Aug;48(8):3006-9 aac.asm.org/cgi/reprint/48/8/3006.pdf
10. Nitric oxide as a bifunctional regulator of apoptosis. Young-Myeong K. et al. Circ. Res. 1999; 84; 243-256 http://circres.ahajournals.org/cgi/reprint/84/3/253.pdf
11. Sodium azide as indirect nitric oxide donor: researches on the rat aorta isolated segments. Iakovenko IN; Ukr Biokhim Zh. 2005 Jul-Aug;77(4):120-3 ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16568613&query_hl=10&itool=pubmed_docsum

© Copyright 2007 – Jean Umber and the Alberta Reappraising AIDS Society