Why Retroviruses Appear in AIDS, Cancer and Autoimmune Diseases

Readers' Comments

Cal Crilly's observed "connecting links" as posted by him as a comment to Glutathione Peroxidase - Selenium, Aminoacids Overcome AIDS and in the article "Why Retroviruses Appear in AIDS, Cancer and Autoimmune Diseases" are interesting and they point to the Oxidative Theory as the primary cause of AIDS.

Intracellular levels of glutathione are depleted in patients with acquired immunodeficiency syndrome in whom the risk of tuberculosis, particularly disseminated disease is many times that of healthy individuals. No direct viral cause is the primary cause of AIDS but viral toxins can exert oxidative stress on white blood cells.

In AIDS patients, chronic inflammation and elevated levels of cytokines seem to be associated with lower levels of GSH: Chronic inflammation becomes a site for free radical generation and as lipid peroxidation increases, blood MDA levels also rise. GSH levels decrease rapidly upon ROS-NO oxidative stress in cells and that causes the depletion of selenium and the selenoproteins which means that the function of the electron transport system in the affected cells declines and the production of natural biomolecules, repair proteins and antibodies declines. That, in turn explains how the immune system is compromised and why opportunistic infections establish in AIDS patients with severe oxidative stress. As lipid peroxidation of mitochondrial membranes progresses, The ROS and ROS-NO induced oxidative stress depletes mDNA and many patients experience fatigue or chronic fatigue and muscular pains.

Under oxidative stress whether arising from malnutrition or from disease and malnutrition or from chronic poisoning from chemicals such as benzene, there is a biochemical problem due to depletion of natural antioxidants in the body and white blood cells, because of excess free radicals or toxins that generate oxidative damage to molecules and cell membranes. There is depletion of not only GSH but also natural vitamin C in white blood cells and when the natural antioxidant levels in such cells drop drastically, their function is impaired. At a certain level, perhaps at 60%, these cells may produce polymer proteins that are recognized as non-self by the body as they are not produced in the healthy state and the polymer actins and their broken parts elicit an autoimmune response. Tests might be showing this condition rather than the presence of a specific virus that is said "may be the primary cause of AIDS". Further drop in the antioxidant level in the white blood cells, by more than 80% causes cell death and explains the low white blood cell count in AIDS patients.

If the Oxidative Stress Theory as the primary cause of AIDS is correct, it would explain:

1. Why the HIV (virus) Theory as the primary cause of AIDS does not conform to the mathematical models of its spread,

2. Why people who are recovering from malaria or flu or a host of other conditions accompanied by oxidative stress or in which oxidative stress occurs due to drugs or toxins or chemicals also test positive for HIV,

3. Why there is a wide range of symptoms in AIDS patients from muscular pains to chronic fatigue to accelerated aging accompanied by low blood cell counts and severe and prolonged oxidative stress results in opportunistic infections,

4. Why there are AIDS patients who do not have the so called HIV,

5. Why many of those who test positive do not get AIDS,

6. Why a toxic chemical like AZT, can precipitate AIDS-like conditions (through generating fres radicals in the body), and

7. Why symptoms in AIDS patients dissappear by selenium and antioxidant therapy or why they respond to such supplementation.

It is trite to note that in poorer societies in which more people have chronic malnutrition, AIDS is more common but in poor societies that consume relatively more coconut oil AIDS is unknown. We do not consume enough medium chain fatty acids as found in natural antioxidant oils such as coconut oil that help to maintain integrity of the cell wall and membranes.

When there is oxidative damage to cell walls and membranes, the integrity of membranes suffers and normal function of cells is affected leading to disease states. Any harmless viruses in the vicinity of cells with damaged cell walls enter them with relative ease and replicate in them but this is not a biological state of affairs in which one can claim that the virus is the primary cause of the disease. It is incidental to oxidative damage.

The oxidative damage may be sufficient to establish inflammatory biochemical pathways or it may create cell walls with a positive charge that is capable of converting the oxygen molecule as it passes through it into ROS or cause the secretion of excess NO and/or establish ROS-NO induced non-enzymatic reactions or deplete mDNA through disruption of the methylation-demethylation cycles.

One of the ways cells control which genetic information is to be used (for a celluar function or process) is to chemically modify the DNA. It is basically a lock and open biochemical system that uses methyl groups. By adding methyl groups to some of the DNA inactivates that part of the chromosome and the information cannot be accessed and hence cannot be used.

An enzyme is required to cause methylation and possibly another is required to remove the methyl group so as to make the information in that part of the chromosome available for use in a cellular process. Oxidative damage to the enzymes would disrupt this process and disrupt the information flow and the sequence of information or slow the process or shut it down altogether. Equally, if the methyl groups suffer oxidative damage, they cannot participate in the cellular processes such as producing repair proteins or GSH or other antioxidant enzymes or antibodies or hormones such as insulin in Type I diabetes wherein the pancreas cannot produce insulin.

The biological methylation and demethylation process is effectively controlled in the presence of the natural antioxidant enzyme network for which selenium is essential. The information flow from the genome through the methylation-demythylation process is also used in the electron transport system for producing natural biomolecules. Excess free radicals demethylate the genome and that clearly explains why cancers are more common in older persons (as their blood antioxidant levels decline with age) and in persons with relatively higher population of free radicals as in diabetics and obese people or people exposed to toxic drugs and chemicals.

Demethylation of the genome, as a study suggests, results in activation of previously silent retroviruses but this may be more likely due to information that cannot be shut down by methylation, requiring the production of certain retroviruses used in normal biological function, including in the skin or some regulatory function, but which are then produced in excess. That may explain the occurrences of skin lesions in AIDS patients and in people exposed to toxic chemicals.

So, excess free radicals as in people taking narcotics or certain drugs or in patients with certain diseases or the abuse of condoms that use talc and silicon as lubricants are triggers to the production of excess retroviruses in the body and that is nothing more than a measure of oxidative damage to cellular biochemistry that may later on produce other diseases. It does not prove the HIV Theory of AIDS but rather kills it. On the other hand, such a sound postulate built on recent scientific works provides a broader support for the Oxidative Theory of Disease, including AIDS.

Macrophages suffer not only on account of chronic malnutrition and oxidative stress but possibly also on account of the fact that they become reservoirs of viruses as well as reservoirs of excess retroviruses produced endogenously by free radical stress that demythylates the genome. As reservoirs of viruses and retroviruses due to their phagocytic role, they represent the most focal point in the central nervous system (CNS) but they are not the targets of a virus as made out to be in AIDS. White blood cells may be involved in the phagcytosis of cells that are producing excess endogenous retroviruses (such cells being regarded as abnormal) and after that they, too die off. That may offer another explanation of low white blood cell count in people with excess endogenously produced retroviruses due to demethylation of certain parts of the genome.

Cal Crilly became "incredibly ill" from Phenol (Benzene) exposure at work and that's because benzene is still the most obvious culprit involved in the T-cell depletion that causes AIDS. I had fingered benzene (in AIDS, NON-HIV AIDS AND PRESCRIPTION AIDS)
and its presence as an ubiquitous pollutant after it was used as an additive in automobile fuel and its use in allophatic pharmacopia as an immunosupressant as one of the factors in the rise of AIDS and skin conditions. Its widespread use is an important factor in the rise of modern illnesses, including cancers as it is a known carcinogen.

"By carefully measuring individual laborers' exposure to benzene and other chemicals, the researchers showed that the 109 workers exposed below the 1 ppm level still had white blood cell counts almost 15 percent lower than similar workers who were not exposed. The reduction was larger for individuals subjected to more than 10 ppm of benzene." This reported finding in the article confirms the dose-related damage of benzene which is what you would expect for most toxic chemicals.

AS science accumulates more information, the picture will certainly become clearer and more definite and AIDS and other disease conditions will be better understood. Antioxidants will play a far greater role in the treatment and management of diseases and disease states.

BELDEU SINGH

Posted by: BELDEU SINGH on June 1, 2006 11:02 AM

 

Beautiful research and writing Cal. My goodness! You've given me some twenty new papers to read.

Outstanding. I'll be posting on it.

Posted by: Liam Scheff on June 2, 2006 08:20 PM

 

FINGERING BENZENE AND ITS DERIVATIVES MAY HAVE BEEN CORRECT

There are studies that looked at such contaminants as benzene, formaldehyde, acetaldehyde, and butadiene, coming from sources ranging from cars to forests fires to industrial polluters. Such pollutants that are part of haze can increase health risk by 100 times.

Benzene is a known carcinogen just like formaldehyde. Benzene is now a component of petrol.

In many areas, the atmospheric concentrations of several toxic chemicals exceed state ambient health standards, many of which were established in the 1980s to protect public health from the adverse impacts of toxic chemicals in the air we breathe. One contaminant of particular concern is a known human carcinogen: benzene.

Benzene is a volatile organic compound emitted from both natural and human-created sources. The internal combustion engine can contribute upto 48% of atmospheric benzene in some places. Indoor air can also contain high concentrations of benzene from common household cleaning products, glues, paints, and cigarette smoke. Natural sources include forest fires.

Both controlled and wild fires are the biggest benzene producers. The emissions from all these industrial facilities may be a small proportion of the total benzene emissions in areas prone to bushfires. Bushfires are huge contributors to benzene emission.

Benzene can be found in the air, water, or soil, although it evaporates quickly from the soil and water surfaces. Once in the air, the pollutant reacts with other atmospheric chemicals and breaks down within a few days. Benzene in the air may be returned to the ground by rain.

The minimum detection limit during the six-year period for benzene was 0.38 µg/m3, a value 3.2 times higher than the standard itself. As the minimum detection limit is above the standard, it is possible that non-detect levels of benzene still exceed the health standard. Of the 619 samples collected at the four monitoring sites during the period, only 5 percent were below the minimum detection limit (0.38 µg/m3), and 80 percent of the non-detects occurred at Underhill, the rural site. The maximum concentration measured in Vermont (15.4 µg/m3), on the other hand, occurred in Rutland on February 19, 1994. This concentration exceeded the air standards by 128 times.

Fuel with lead or benzene as an additive, allophatic medication with benzene derivatives and other products where benzene is used in some part of the manufacturing process and biomass burning are modern problems that coincide with the rise of disease conditions over the last 30 years. Biomass burning is a problem because the impact on air pollution is huge and produces long term health problems. Burning a kilogram (2.2lbs.) of wood in a new wood stove will produce about 130 grams of carbon monoxide, 51 grams of hydrocarbons (including up to 10 grams of carcinogenic benzene), 21 grams of fine particulates, and about 0.3 grams of the highly carcinogenic poly cyclic organic hydrocarbons (EPA, 1984, Larson, 1993). Wood burning also produces from 10 to 167 milligrams of highly carcinogenic dioxins per kilogram of fuel burning (Abelson).

In a haze created by forest fires or by forest fires and automobile exhaust fumes there is the added problem of very fine particles that can damage cell walls in the lungs and heart causing sudden heart failure in many cases. Benzene initiates free radical chain reactions and can cause oxidative stress, especially in malnourished societies and in urban communities with low antioxidant intake.

Exposure to low levels of benzene may be harmful to blood cells found in the marrow, according to a new study published in the journal "SCIENCE". The study found that white blood cells and platelet counts were lower even with benzene exposure levels below one part per million (ppm), the current level deemed safe by the US Occupational Health and Safety Administration. It also found that benzene exposure lowered the number of progenitor cells, which include stem cells in the blood. These stem cells and progenitor cells are precursors to all blood cells.

And it strengthens the link between benzene exposure and blood cancers and cancers in general. It also strenghtens the role of benzene in promoting free radical activity and oxidative stress associated with many chronic conditions, inlcuding AIDS, especially oxidative stress on white blood cells, cell membranes and within the mitochodria that leads to the depletion of MDNA.

It is logical to conclude that benzene derivatives will also lower white blood cell and platelet count as is noted with the long term use of certain drugs.

The increase of pollutants and the widespread use of chemicals, whether in household products, in industry and in the treatment of diseases coupled with decreasing antioxidant levels in fruits and vegetables due to leaching soils etc or otherwise low antioxidant intake is a recipe for chronic illnesses and health problems (see The Rise In Modern Illnesses).

The more you read the growing literature and scietific papers on free radicals and study how natural antioxidants scavenge free radicals, the more you will be convinced about natural antioxidant medication and therapies that can also help eliminate free radical-induced nonenzymatic reactions and pathways that produce disease states.

BELDEU SINGH

Posted by: Beldeu Singh on June 6, 2006 08:46 AM

 

There was an interesting comment on an article on Indimedia Ireland Why Bono And HIV/AIDS Inc. Will Be Stopped by Cal but it appears to have been "lost", i.e. someone (accidentally?) deleted it.

If Indy is getting into censorship, that would indeed be grave. So I repost it and also put it on my own site... appending it to a number of articles on AIDS. Anyone interested can search the site for aids related articles (top center of page is the search window)...

Sepp

Here is what Cal said:

"OK ... I'm precisely going through the flaws in the HIV tests.

REVERSE TRANSCRIPTASE
The first is the Reverse Transcriptase test or viral load test.

"Reverse Transcriptase from HIV-1 is of tremendous medical interest as it is the target enzyme for the best known of anti-AIDS drugs, AZT, which acts by causing chain termination of the polymerase reaction."
HIV-1 Reverse Transcriptase
http://www.biochem.ucl.ac.uk/bsm/xtal/teach/repl/rt.html

The problem is that our genome contains 8 retrovirus in our DNA and these endogenous retroviruses also use Reverse Transcriptase, so how do we tell if it's our own HERVs or HIV. It all depends on the HIV antibody test to confirm if it is HIV Reverse Transcriptase.

Identification of an Active Reverse Transcriptase Enzyme Encoded by a Human Endogenous HERV-K Retrovirus
http://jvi.asm.org/cgi/content/abstract/73/3/2365

"Phylogenetic analyses of retroviral elements, including endogenous retroviruses, have relied essentially on the retroviral pol gene expressing the highly conserved reverse transcriptase. This enzyme is essential for the life cycle of all retroid elements, but other genes are also endowed with conserved essential functions. Among them, the transmembrane (TM) subunit of the envelope gene is involved in virus entry through membrane fusion."

Identification, Phylogeny, and Evolution of Retroviral Elements Based on Their Envelope Genes
http://jvi.asm.org/cgi/content/full/75/23/11709?view=long&pmid=11689652

P24
The next flaw is the p24 antigen of HIV which is claimed to be specific to HIV...

"A major core protein of the human immunodeficiency virus encoded by the HIV gag gene. HIV-seropositive individuals mount a significant immune response to p24 and thus detection of antibodies to p24 is one basis for determining HIV infection by ELISA and Western blot assays."

HIV Core Protein
http://medical.webends.com/kw/HIV20Core20Protein20p24

But everyone who consumes milk products or eats cattle will be exposed to the p24 of the Bovine Leukemia Virus and also can test positive to the test.

"Using immunoblotting to test the sera of 257 humans for antibodies of four isotypes (IgG1, IgM, IgA, and IgG4) to the BLV capsid antigen (p24), we detected at least one antibody isotype reactive with BLV in 74 of the human sera tested."

Humans Have Antibodies Reactive with Bovine Leukemia Virus 2003
http://www.liebertonline.com/doi/abs/10.1089/088922203771881202

And anyone with lupus or hyperthyroid autoimmune diseases can also test positive to p24.
These diseases also have the similar symptoms to so called HIV infection.

"We have previously demonstrated that about one-third of patients with either Sjögren's syndrome (SS) or systemic lupus erythematosus (SLE) react to human immunodeficiency virus (HIV) p24 core protein antigen without any evidence of exposure to, or infection with, HIV itself."

Reactivity of Sera from Systemic Lupus Erythematosus and Sjögren's Syndrome Patients with Peptides Derived from Human Immunodeficiency Virus p24 Capsid Antigen
http://cvi.asm.org/cgi/content/abstract/5/2/181

This is where it gets terrifying, I have in the last month swapped emails with a pregnant lady diagnosed with HIV, she was given all sorts of medication and also put under great pressure to take abortion pills which she did. She then re-tested and came up negative.
The reason for the positive cross-reaction with the test is due to the endogenous retrovirus HERV-W which is involved in attaching the fetus to the placenta, within the HERV-W is a gp24 transmembrane subunit. GP stands for glycoprotein and is shortened to protein when called P24, they are the same and react to an antigen test.

"Syncytin is a fusogenic protein involved in the formation of the placental syncytiotrophoblast layer. This protein is encoded by the envelope gene of the ERVWE1 proviral locus belonging to the human endogenous retrovirus W (HERV-W) family. The HERV-W infectious ancestor entered the primate lineage 25 to 40 million years ago. Although the syncytin fusion property has been clearly demonstrated, little is known about this cellular protein maturation process with respect to classical infectious retrovirus envelope proteins. Here we show that the cellular syncytin protein is synthesized as a glycosylated gPr73 precursor cleaved into two mature proteins, a gp50 surface subunit (SU) and a gp24 transmembrane subunit (TM)."

Synthesis, Assembly, and Processing of the Env ERVWE1/Syncytin Human Endogenous Retroviral Envelope
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1082723

At the beginning of pregnancy a wave of de-methylation occurs and this is a normal part of pregnancy, this is also why the retroviruses come out of the genome and get active.
They are not a disease though, they have function.
Of course a drug like AZT which they give to pregnant women worldwide completely wrecks this process.

T-CELL TESTS
Hypomethylation affects T-cells as well as makes retroviruses come out of our DNA.
The T-cell test is really picking up changes in T-cell counts attributed to other real infections and problems with Methylation due to a lack of nutrients needed to Methylate.
It is not HIV causing the lowered count.

"Procainamide and hydralazine inhibit T cell DNA methylation and induce autoreactivity in cloned CD4+ T cells. These drugs also induce an autoimmune syndrome, suggesting a possible relationship between DNA hypomethylation, T cell autoreactivity, and certain autoimmune diseases. To test this relationship, DNA methylation was studied in T cells from patients with rheumatoid arthritis and patients with systemic lupus erythematosus, and was found to be impaired. These results support a relationship between DNA hypomethylation and some forms of autoimmune disease."

Evidence for impaired T cell DNA methylation in systemic lupus erythematosus and rheumatoid arthritis.

"DNA methylation plays an essential role in maintaining T-cell function. A growing body of literature indicates that failure to maintain DNA methylation levels and patterns in mature T cells can result in T-cell autoreactivity in vitro and autoimmunity in vivo. Defective maintenance of DNA methylation may be caused by drugs such as procainamide or hydralazine, or failure to activate the genes encoding maintenance DNA methyltransferases during mitosis, resulting in the development of a lupus-like disease or perhaps other autoimmune disorders. This paper reviews the evidence supporting a role for abnormal T-cell DNA methylation in causing autoimmunity in an animal model of drug-induced lupus, and discusses some of the mechanisms involved. T cells from patients with active lupus have evidence for most if not all of the same methylation abnormalities, suggesting that abnormal DNA methylation plays a role in idiopathic human lupus as well."

DNA methylation and autoimmune disease.

"Thus, the HIV LTR appears to be susceptible to transcriptional inactivation by methylation, a process that is proposed to play a modulatory role in viral latency."

Methylation as a modulator of expression of human immunodeficiency virus.

And researchers are looking at drug therapies to Methylate HIV and stop it.

Methylation Therapy

The main nutrient needed for Methylation is Selenium and this is probably why low Glutathione (a Selenium compound) is an indicator of AIDS progression.

Harold Foster is using it in Selenium trials in Africa
http://www.hdfoster.com/

And Tine Van Der Maas is teaching Africans to treat themselves by using Lemons and Garlic (a food containing Selenium)
http://www.health-e.org.za/news/article.php?uid=20031252

Nothing changed in the early 80s, the tests picked up retroviruses that came out when gays using Amyl Nitrate had depleted their bodies of Methylation Nutrients.
The HIV tests themselves have been the source of the epidemic.

It's up to the scientists now to go back to the drawing board and find a way out of this without massive litigation crippling the biomedical industry.

More if curious ... I‚ve written about it in detail.

Why Retroviruses Appear in AIDS, Cancer and Autoimmune Diseases

Have a good day all."

Posted by: Sepp on November 10, 2006 06:46 AM

 

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