AIDS defining illnesses, their causes and treatment


Treatment recommendations after the book „The silent Revolution in Cancer- and AIDS-Therapy“* by MD. Heinrich Kremer, (Barcelona), and works of Prof. Alfred Hässig (Berne), Dr. Stefan Lanka (Stuttgart), Eleni Papadopulos-Eleopulos (Royal Hospital, Perth), Etienne de Harven (France), MD Roberto Giraldo (USA) and Kary B. Mullis (USA) available at www.virusmyth.com and the works of L.A. Herzenberg, J.D. Peterson et S.C. De Rosa, W. Droege, J.K. Shabert, G. Ohlenschlaeger, C. Richter, V.Hack, H. Rode, E.A. Newsholme, C. De Simone, S.J. Ferrando, C. de Back, M. Clerici, G.M. Shearer, M.C. Dalakas, G.Tomelleri, E. Benbrik, G.A. Cannon, B D. Cheson, R.F. Fuchgott and C.J. Ignarro and L. Chaitow available at www.ncbi.nlm.nih.gov


The many and varied diseases that can define the AIDS syndrome: fungal infections of the lung, of the mucous membranes, the brain, and the gut, and the degenerative changes in the endothelial cells of blood vessels and lymphatic vessels (Kaposi Sarcoma), occur because of an ongoing change in the production of gaseous nitric oxide and oxygen radicals in immune cells and other cells.

If these changes continue, CD4 helper cells mature predominantly to cells with the Th2 cytokine profile, which migrate to the bone marrow where they stimulate B cells to produce antibodies against external pathogens (bacteria and toxins) but only a few mature into Th1 cells which activate the detection and destruction of fungus and virus infected cells and of altered cells. If this situation persists, the release of gaseous nitric oxide (NO) gets entirely inhibited so that the destruction of cells carrying viruses, fungi and mycobacteria by killer cells is blocked. Then, as an effect of heightened cell decay, a higher quantity of proteins of the cyto-skeleton and of mitochondria is released. Against these proteins a higher rate of antibodies are formed. These antibodies and antibodies against a big variety of antigens and against products of toxic pollution are detected by the HIV-tests. Once an arbitrarily set level is reached, the patient is declared "HIV positive".

An ongoing Th1-Th2 switch in the cytokine profile of CD-4 helper cells comes about as a result of:

The effects of the "anti-retroviral" treatment

Chemo antibiotics inhibit the synthesis of folic acid, of purine and of the enzyme dihydrofolatereductase (DHFR). They also damage the mitochdonrial DNA, which is inherited from the mother to the child and inhibit the formation of the glutathione molecules in the liver, used for the reduction and transportation of oxygen to the cells. They also inhibit the formation of gaseous nitric oxide (NO), used for the destruction of cells containing viruses, fungi and mycobacteria. By doing this they block continuously the entire cellular immune reactions and cause a lasting Th1-Th2 switch in the cytokine profile of CD-4 helper cells, which induces an ongoing functional immune deficiency. By suffocation of the cellular respi-ration they induce chronic fungal infestation (e.g. PCP, Candida Albicans)in mucous membranes, in the intestine (causing chronic di-arrhoea) and on the skin. Due to the damage on mitochondrial DNA they cause lasting energy decline and severe damage to the brain, internal organs and to muscles, causing heart attacks and paralysis. They also inhibit the release of tetrahydrofolate, which is used for the synthesis of uracil. Uracil deficiency results in the inhibition of production of the growth factor Interleukin 2. By inhibition of production of the biologically active form of folic acid they also inhibit the transformation of the rna-base uracil into the dna-base thymine and thereby the repair of DNA by means of reverse transcription.

Nucleoside analog drugs (e.g. Ziduvine, Retrovir, Nevirapine) inhibit after a short time of administration the ripening of immune cells in the mucous membrane (B-cells, T-cells, macrophages and dendrite cells). The damage to the ripening of B-cells causes a decrease of their number and activity and thereby the weakening of the antibacterial defence by antibodies, which leads to persisting bacterial infections. If TH2-T-cells then circulate they only meet a reduced number of B-cells, that they can activate. Without the contact to B-cells most of them circulate for 24 hours through the blood circulation system and the lymphatic tissue, unable to activate the detection and elimination of cells that contain viruses, fungi and mycobacteria. Then a higher rate of T-4 cells is countable in the plasma. This measurement of T-4 cells does not give any valid information on the defence capability in the person tested.

Nucleoside analogy drugs and protease inhibitors cause disorder to the biological synthesis of proteins and enzymatic proteins and damage the synthesis of nucleic acids that are needed for the for-mation of new cells in all organs. They also change the codification patterns in the cell nucleus and in the mitochondria DNA. Thereby they damage the DNA in the cell nucleus and in mitochondria and the repair of DNA by means of reverse transcription (transmission of the messenger substance RNA into DNA). The rate of RNA measurable in the plasma then increases (increase of the so called „viral load“, „resistant HIV viruses“). For the repair of the growing number of DNA damages occurring after HAART treatment the consumption of RNA increases, so that the rate of the so called „HIV-virus-particles“ measured as „viral load“ by means of the PCR-test, decreases. On prolonged impairment of mitochondria, the mitochondria dissolve their symbiosis with the host ("Warburg Phenomenon"). The cells then increasingly switch over to producing energy by anaerobic fermentation, which results in excess lactic acid production, the growth of fungi and opportunists, and ultimately the formation of cancerous cells and wasting, at which point cells obtain essential nutrients directly from mycoprotein.

Nucleoside analog drugs (e.g. AZT, DDC, DDI, 3TC), that block for a limited time the formation of DNA in bacteria and fungi, are prac-tically not incorporated into the cell nucleus, where they should work as DNA terminators against HIV. As has been demonstrated by various animal trials since 1990 they cause irreversible damage to the mitochondrial DNA and thereby damage to the brain, the bone marrow, the muscles and internal organs and also a lasting decrease to CD-4 and CD-8 cells, that induces opportunistic infections (cy-tomegalo virus, herpes simplex, PCP and toxoplasmosis), which can define the AIDS-syndrome.

Synthetic protease inhibitors, which are supposed to inhibit the formation of essential "viral particles", hinder the formation of nucleotides needed for the formation of new cells in all organs and thereby cause malaise, diabetes, kidney stones and liver failure in patients given them. Administrated together with nucleoside analog drugs in the HAART treatment they cause syndromes like those occur-ring in children with inherited defects in the mitochondrial DNA (Kees Brinkmans in The Lancet, 25th September 1999)

Means of treatment to reconstitute cell-symbiosis and flexible de-fence capacity.

...a flexible resistance in people with AIDS defining illnesses can be restored.

If limited administration of antibiotics is necessary, this basic therapy has to be continued. The treatment has to be adapted to the individual illnesses occurring. Progress achieved by these measures to bolster the immune system can be monitored by measuring stress hormone profiles, the T4/T8 cell ratio, macrophage activation (neopterine test) and cutaneous anergy (DTH test: skin reaction on antigens), and the glutathione level in plasma and in CD-4 helper-cells.

Study Group AIDS Therapy
c/o Felix A. de Fries
Eglistr. 7 CH-8004 Zürich
E-mail : felix.defries@bluewin.ch; Tel./FAX: 0041 1 401 34 24

*The book by MD Heinrich Kremer is not available in English. A translation of the therapy chapter from it will be available in summer 2004

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