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Therapeutic Recommendations for HIV Positive and AIDS Patients.

By Felix de Fries (last updated Jan 2008)

(Therapeutic recommendations from the studies of Dr. Heinrich Kremer (Barcelona), Prof. Alfred Hässig (Bern), and Dr. Eleni Papadopulos (Perth), Dr. Stefan Lanka (Stuttgart), Etienne de Harven (France), MD Roberto Giraldo (USA) and Gerry B. Mullis (USA) available under: www.ummafrapp.de and www.virusmyth.com and the studies of L.A. Herzenberg, J.D. Peterson and 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, and L. Chaitow under: www.ncbi.nlm.nih.gov.

The diverse diseases which define the AIDS syndrome: fungal infections of lungs, the mucous membranes, the brain and inner organs, degenerative transformations of the endothelial cells of the blood-vascular system and lymphatic pathways (Kaposi's sarcoma) are the consequences of a persistent autoimmune reaction in which antibodies are formed and dock onto the body's own cells (amongst others T4 helper cells) and forming with them so-called immune complexes. The causes of these persistent autoimmune reactions are contamination by heavy metals and other environmental toxins, which by obstructing the ion channels in mitochondria compromise energy production (ATP production) and just like repeated infections, lead to a depletion of glutathione molecules (the body's own antioxidants) which causes a reduction in the production of gaseous nitric oxide (NO) in immune cells and other cells. If this takes place then T4 helper cells are produced predominantly with a Th2 cytokine profile, which on contact with B cells instigate defence against bacteria and toxins via antibodies but still only to a minor degree as T4 helper cells with a Th1 cytokine profile that activate killer cells to attack cells carrying fungi, viruses and mycobacteria with NO gas and also trigger macrophages to break down immune complexes. If this Th1-Th2 switch takes a long time then the NO gas production becomes completely disrupted leading to degenerative processes, to an amplified reverse transcription and through an increase in cell death to an increased release of those cell skeleton and mitochondrial proteins that have been named as HIV particles. In the process increased amounts of antibodies are produced against the body's own cell envelope and cell skeleton proteins and against a multitude of diverse antigens which on reaching a certain level in the HIV antibody tests lead to the 'laboratory result' of HIV positive.

A permanent Th1-Th2 cytokine switch of T4 helper cells results from:

The Consequences of Antiretroviral and Antibiotic Treatment.

The so-called HIV retroviruses, which today have been made responsible for more than 30 AIDS defined diseases, have yet to be isolated as transmittable, propagable viruses, photographed and biochemically characterized according to Koch's postulates. In AIDS only known viruses, bacteria and fungi as well as autoantibodies and immune complexes are transmitted via blood and semen. This can lead to a Th1 - Th2 switch in immune deficient recipients and in cases of chronic stress to advanced autoimmune reactions (and to a positive HIV antibody test result).

For Gallo and Montagnier's postulation of 'HIV retroviruses' in 1984, lymph cells were cultivated with leukemic, white blood cells and embryonic cells of AIDS patients, which exhibited a heavily increased activity in reverse transcription that was further activated by doses of hydrocortisone. The increase in the incidence of reverse transcription in these cell cultures was then interpreted as proof of the existence of a new, infectious, transmittable virus. The later developed HIV tests correspondingly identify an increased titer of antibodies against leukemic cells, which appear in various immune reactions, as HIV positive.

Nucleoside analog substances (Acyclovir, Nevirapine, DDI etc.), even after a short time of administration, have a sustained effect on the maturation of all immune cells in the bone marrow: the B-cells, the T-cells that are later developed in the thymus, and the antigen-presenting dendritic cells and the macrophages. The damage to the new growth of B-lymph cells means that their activities and numbers are severely compromised and defense by antibodies against bacteria is weakened so that they can disperse in cells without hindrance. When T-4 helper cells then circulate they find only reduced amounts of B-cells in the lymphatic tissues that they can activate. As T-4 helper cells with a Th-2 cytokine profile they then circulate in the plasma and lymphatic tissues for 24 hours without a function. This results in a higher measurable number of T-4 helper cells in the plasma.

Nucleoside analog substances, protease inhibitors and fusion inhibitors severely reduce the levels of thiol and thereby further aggravate the already present glutathione deficits in HIV positives. Glutathione deficiency in antigen-presenting cells leads to the formation of T-4 helper cells principally with a Th-2 cytokine profile, which trigger an increased production of antibodies and only a small number of the Th-1 cells that activate defense against fungi, viruses and mycobacteria via macrophages. Protease inhibitors impair the development of proteins for nucleotides needed for the structuring of new cells in all organs. Treatment results in diabetes, the shift of fatty acids to the extremities, retinitis, the formation of kidney stones and to liver failure.

Chemoantibiotics (Bactrim, Septrin, TMPSMX etc.) that block the formation of folic acid, purines and DHFR enzymes, damage glutathione production in the liver, NO production and oxygen transport in the cells, in the process continuously blocking the whole cell-mediated defense resulting, via a permanent Th1-Th2 switch, in ongoing functional immune deficiency. By choking cell respiration they promote fungal infestations (PCP, candidas albicans etc.) in the mucosa, intestines (chronic diarrhea) and skin. Long-term dispensing of chemoantibiotics also leads to an inhibition of tetrahydrofolate necessary for uracil production and thus results in an inhibition of the T-cell growth factor, interleukin-2. By inhibiting the biologically active folic acid, chemoantibiotics also impair the transformation of the RNA base, uracil, to the DNA base thymine and thus hinder DNA repair via reverse transcription. Additionally, by altering the genetic structure in bacteria, which exchange plasmids with each other, they increasingly cause antibiotic resistance.

Nucleoside analog substances (like AZT, DDI, DDC etc.) reduce by blocking the development of DNA for a limited time bacterial infections, fungal infestations and the production of the non-characteristic particles with mediators (RNA) that are termed HIV particles, as well as immune complexes of antibodies and the body's own cell proteins. This process further promotes autoimmune reactions. However, nucleoside analogs are only 1% phosphorylated and practically not integrated at all in the nucleus where they are supposed to inhibit the 'HI' viruses as DNA terminators. Nucleoside analogs and protease inhibitors, furthermore, cause disturbances to the biosynthesis of proteins and enzyme proteins and by impairing the production of nucleic acids lead to damage both in the nuclear and mitochondrial DNA. Sooner or later this leads to sever damage to the brain, muscle cells (heart attacks and paralyses) and in the internal organs as well as to the formation of cancer cells.

Under the above-mentioned conditions the cells increasingly switch to an oxygen-free fermentation metabolism, burdening the organism with lactic acid or causing wasting, in which the cells draw essential substances, as an alternative, directly from muscle proteins. With continuing damage to mitochondria through the blockage of their membranes, glutathione deficiency and DNA damage the symbiosis between mitochondria and the nucleus breaks down (Warburg Phenomenon) with the consequence that nuclear sections with agents that had been previously successfully isolated, are activated and the survival of nuclear DNA is increasingly assured by reverse transcription. In the process the numbers of measurable RNA in the plasma increases (increase in the so-called HI viral load).

The consumption of RNA markedly increases for repairing the increasingly recurring DNA damage caused by combination therapy (HAART), so that the numbers of cell particles decline. This is measured by means of the polymer chain reaction test (PCR) as the viral load. Through disruption to the synthesis of nucleic acid the coding patterns of nuclear and mitochondrial DNA are altered by combination therapy and the DNA repair, via reverse transcription, is further impaired. Depletion of the repair enzymes eventually leads to the products of reverse transcription no longer being able to be adopted by DNA (renewed rise in the 'viral load' and irrevocable resistance to combination therapy).

Elements of a Compensatory Therapy Supporting the Immune System.