Health Supreme by Sepp Hasslberger

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May 18, 2006

AIDS - Retrovirus Expression Regulated by Methylation?

AIDS may not be what we are told it is - a retrovirus-mediated disease.

VirusAids.jpg

Illustration of what HIV is thought to look like. Image source

Rebecca Culshaw, a statistical mathematician and biologist came to the conclusion that the official explanation of how AIDS is caused does not make sense, when analyzing the statistical data with a view to finding ways to overcome the syndrome. Culshaw quit her AIDS related work and she explains why in her recent article.

Looking for the real cause of AIDS, geo-epidemiologist Dr Harold Foster discovered that selenium, as well as three aminoacids are generally found to be low in AIDS victims and are also low in the food supply where AIDS is found in higher concentrations. In a recent newsletter, the Orthomolecular Medicine News Service makes reference to Harold Foster's discovery saying that high doses of the trace element selenium, and of the amino acids cysteine, tryptophan, and glutamine can together rapidly reverse the symptoms of AIDS.

Chinese researchers have found selenium to be an important mineral nutrient to prevent both AIDS and Avian Flu. The article of Qu Yuan, Qu Lai and Qu Shaozhong Avian influenza’s “internal factor" of selenium deficiency and an epidemic prevention strategy of "treating the cause” makes interesting reading.

Beldeu Singh from Malaysia says that AIDS and CFS are Caused By Oxidative Damage.

Now to tie this together even more, Cal Crilly, an artist from Brisbane Australia and long time AIDS activist, adds an important piece to the puzzle. He explains that retrovirus expression is suppressed by proper methylation of our DNA, which in turn depends on a selenium compund, S-adenosyl-methionine.

Here is Cal's contribution to the discussion. Perhaps one day - hopefully soon - we will see this accumulating knowledge on the real etiology of AIDS translated into actual solutions for those who are suffering... CDC take note.

- - -

Cal Crilly found these connecting links and posted them as a comment to
Glutathione Peroxidase - Selenium, Aminoacids Overcome AIDS

I have to point out what everyone may be missing

Our genome is made up of about 40% transposable elements in the DNA.

Transposable elements means they can move around.

These are kept in check by a thing called DNA methylation, if your DNA isn’t properly methylated with the right nutrients then the transposons can move around.

The transposons include 8% retroviruses and one of them is called HERV-K and cross reacts with the HIV antibody test.

The main nutrient for methylation is a selenium compund called S-adenosyl-methionine.

Folic acid and Choline as well.

When you look at studies on HIV and our own retroviruses (my opinion is that HIV is normally in everyone’s body) you find over and over again that Hypomethylation (lack of methylation) makes the retroviruses come out.

Or if you hypermethylate (over-methylate) they get suppressed.

“These results suggest that DNA hypermethylation of the HIV LTR may change the binding characteristics between LTR sequences and cellular proteins, thereby suppressing HIV LTR transcription and modulating viral expression.”
Inactivation of the HIV LTR by DNA CpG methylation: evidence for a role in latency
http://embojournal.npgjournals.com/cgi/content/abstract/9/4/1157

These studies show this phenomenon.

“Several cytidine analogs with known mutagenic capability were tested for their effects on DNA methylation and on induction of endogenous murine retrovirus. For each of the compounds tested it was found that DNA methylation was inhibited at the same concentrations that were required to induce virus expression. With each compound it was observed that increased dose levels produced an increase in the ability to inhibit methylation and an increase in the ability to induce virus.”

Effects of cytidine analogs on methylation of DNA and retrovirus induction.

CpG Methylation Directly Regulates Transcriptional Activity of the Human Endogenous Retrovirus Family HERV-K(HML-2)

The problem is that all illness including cancer, AIDS and the autoimmune diseases have an increase in retroviral expression so how can we tell if HIV is a transmitted retrovirus when all our own retroviruses come out when we are ill?

HERV-W, another of our retroviruses is also involved in pregnancy and this is why pregnant women in Africa are at risk from the HIV test.

Here it turns up in cancer but only because our DNA is hypomethylating.

L1 and HERV-W retrotransposons are hypomethylated in human ovarian carcinomas

This is one of the reasons why Glutathione a Selenium compound helps with HIV and cancer.

It is also cell protective.

“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. In this study, we examined the role of glutathione in immunity against tuberculosis infection in samples derived from healthy and human immunodeficiency virus infected subjects. Our studies confirm that glutathione levels are reduced in peripheral blood mononuclear cells and in red blood cells isolated from human immunodeficiency virus-infected subjects (CD4>400/cumm). Furthermore, treatment of blood cultures from human immunodeficiency virus infected subjects with N-acetyl cysteine, a glutathione precursor, caused improved control of intracellular M. tuberculosis infection.”

Glutathione and growth inhibition of Mycobacterium tuberculosis in healthy and HIV infected subjects.

“In AIDS patients, chronic inflammation and elevated levels of cytokines seem to be associated with lower levels of GSH: GSH levels decrease rapidly upon infection with HIV and continue to decline as the disease progresses. Investigators have shown that agents that increase intracellular levels of GSH inhibit HIV replication.”

Potential role of reduced glutathione as an antiviral agent

Now they knew as far back as 1991 that Glutathione stopped HIV but in this study they also mentioned AZT causes Glutathione depletion, this means AZT causes HIV expression and AIDS in the long run.

AZT only seems to work in the short term because it hypermethylates DNA.

“Azidothymidine causes functional and structural destruction of mitochondria, glutathione deficiency”

Suppression of Human Immunodeficiency Virus Expression in Chronically Infected Monocytic Cells by Glutathione, Glutathione Ester, and N-Acetylcysteine 1991

Cal Crilly

- - -

A more recent (March 2007) addition of links and information by Cal Crilly:

Hello to you all,

This may be of interest and is a very cheap and non toxic way to address AIDS.

I believe the Selenium effects HIV via two mechanisms. Higher Selenium levels will create Glutathione, this is cell protective and simply reduces T-cell turn over by protecting cells from antioxidant damage.

The other is because of Methylation. HIV and all our own retroviruses are suppressed by Methylation and this is done with a Selenium compound called S-Adenosylmethionine or SAMe.

If Selenium levels drop both Glutathione and SAMe are reduced causing cell damage and hypomethylation of the genome. This causes HIV levels to rise. AIDS drugs such as AZT cause hypermethylation of the genome and inhibit HIV but are toxic. SAMe is cheaper, more effective and non toxic in the doses required. Links to relevant articles are below.

Selenium may help lower HIV levels

“NEW YORK (Reuters Health) - Selenium supplements can slow the rise in virus levels in HIV-positive patients, which allows the number of beneficial CD4 immune cell to increase, according to results of a clinical trial supported by grants from the National Institutes of Health.

Low blood levels of selenium have been linked to high HIV virulence and more opportunistic infections, Dr. Barry E. Hurwitz and associates at the University of Miami in Florida report in the Archives of Internal Medicine. In lab experiments, the element suppresses HIV-1 replication.”

SOURCE: Archives of Internal Medicine, January 22, 2007.
Selenium may help lower HIV levels


Cerebrospinal fluid S-adenosylmethionine (SAMe) and glutathione concentrations in HIV infection: effect of parenteral treatment with SAMe.

“The methylation and transsulfuration pathways are intimately linked and have been implicated in the progression of neurologic damage and immune cell depletion caused by human immunodeficiency virus (HIV) infection. We studied the following metabolites related to these pathways: S-adenosylmethionine (SAMe), homocysteine, cysteine, cysteinyl-glycine, and glutathione (GSH) in blood and CSF of 16 HIV-infected patients with neurologic complications and 20 HIV-negative control patients undergoing lumbar punctures for other medical reasons. We confirmed recent studies of decreased CSF SAMe concentrations in HIV infection and demonstrated that diastereomers of SAMe are present in CSF but not in plasma or erythrocytes from both HIV-infected and HIV-negative patients. In HIV-infected patients, CSF GSH and cysteinyl-glycine, but not homocysteine or cysteine, were significantly reduced. This is the first report of decreased CSF GSH induced by HIV infection. GSH has a regulatory effect on the synthesis of SAMe in hepatic tissue, and the same mechanism may also apply in the CNS. Administration of SAMe-butanedisulphonate, 800 mg/d intravenously for 14 days, was associated with significant increases in CSF SAMe and GSH. These findings have potentially important therapeutic implications for the use of SAMe in protecting against SAMe and GSH deficiency in the CNS of HIV-infected patients.”

- - -

Harold Foster is doing trials in Africa with Selenium and it would be good to observe his work.

- - -

Glutathione and growth inhibition of Mycobacterium tuberculosis in healthy and HIV infected subjects

"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. In this study, we examined the role of glutathione in immunity against tuberculosis infection in samples derived from healthy and human immunodeficiency virus infected subjects. Our studies confirm that glutathione levels are reduced in peripheral blood mononuclear cells and in red blood cells isolated from human immunodeficiency virus-infected subjects (CD4>400/cumm). Furthermore, treatment of blood cultures from human immunodeficiency virus infected subjects with N-acetyl cysteine, a glutathione precursor, caused improved control of intracellular M. tuberculosis infection."

Yours Sincerely
Cal Crilly


This is my innovation patent that is at the Brisbane patent office.

I’ve let it expire because I needed the cash to see my folks in the UK and I really haven’t the slightest interest in making money from it.

I do dispatch, I’m sure it’s of absolutely no use to me in this shed and it’s a useful research tool for a bunch of experiments that haven’t been done yet.

So I hope someone uses the idea one day, I really just registered it so people would know it was my thought bubble.

http://www.physforum.com/index.php?showtopic=25048

- - -

See also:

Why Retroviruses Appear in AIDS, Cancer and Autoimmune Diseases
Cal Crilly wrote a more extensive discussion of what he said here. It is published on Fintan Dunne's MyLongLife.com
Fintan's comment:
Cal Crilly's devastating analysis of AIDS, below, highlights the outdated science behind current treatments and shows the true causes and cure. He takes us on a densely referenced tour through the largely unknown mechanisms underlying viruses, reterovirus, cancer and autoimmune diseases. So this has implications far beyond AIDS. Cal's treatise is based on existing mainstream scientific and medical research. The kind of research the vendors of medicine's magic pills simply ignore in hope it will just go away. Crilly makes it impossible to ignore. An eye opener!

There is a substance called S-adenosylmethionine or SAM-e, which aids in methylation. It is effective for depression, but not only. The article linked here is a chapter of the book Stop Depression Now: SAM-e: The Breakthrough Supplement that Works as Well as Prescription Drugs, by Richard Brown, M.D., Teodoro Bottiglieri, Ph.D. The SAM-e Story: Stop Depression Now
There is nothing more fundamental to human life than DNA. It’s the genetic "software" which runs the cells and contains the genetic code for every living thing. When SAM-e reacts with DNA by donating a methyl group, it allows our genes to spring into action. It’s like hitting the "on" switch on a computer; DNA methylation is the operating system of the body, helping it to regulate important processes such as cellular growth and repair, production of immune cells to fight disease, wound healing, and reproduction. The undermethylation of DNA is believed to be a causal factor in cancer, because it could hamper the body’s ability to repair damaged cells before they turn cancerous.

Selenium supplements may contribute to reduced HIV viral load
"The intervention resulted in no adverse events related to the study supplement," the authors write. The two groups had similar selenium levels at the beginning of the study, but after nine months of treatment, the average change in blood selenium level was greater in the treatment group. Higher blood selenium levels predicted a decreased HIV viral load, which in turn predicted increased CD4 count.

"The exact mechanism by which selenium exerts its effects on HIV-1 viral replication is not known, although the literature suggests several possibilities," the authors write. One hypothesis holds that selenium's antioxidant properties may repair damage done to immune cells by oxygen, which is produced at higher levels in the bodies of patients with HIV. However, future research is needed to confirm this relationship.

DNA methylation shown to promote development of colon tumors
The research directly demonstrated that hypermethylation switches off tumor suppressor genes—the "housekeeping" genes that keep cancer cells in check. The study, published December 1 in Genes and Development, found that hypermethylation boosted the number of intestinal tumors by 60-100 percent and significantly increased the average size of microscopic early-stage tumors.

While DNA methylation has been correlated with tumor development in numerous studies of human cancers, this is the first in vivo work demonstrating a causal connection in mammals. Better understanding of the process is a promising pathway to the prevention, diagnosis and treatment of certain cancers with minimal side effects.

Our genome changes over lifetime, Johns Hopkins experts say
"Inappropriate methylation levels can contribute to disease - too much might turn necessary genes off, too little might turn genes on at the wrong time or in the wrong cell," says Vilmundur Gudnason, MD, PhD, professor of cardiovascular genetics at the University of Iceland director of the Icelandic Heart Association's Heart Preventive Clinic and Research Institute. "Methylation levels can vary subtly from one person to the next, so the best way to get a handle on significant changes is to study the same individuals over time."

 


posted by Sepp Hasslberger on Thursday May 18 2006
updated on Tuesday December 14 2010

URL of this article:
http://www.communicationagents.com/sepp/2006/05/18/aids_retrovirus_expression_regulated_by_methylation.htm

 


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Readers' Comments


This is a wonderful article on AIDS and I am so very grateful for your publication.

Best,

Diane

Posted by: Diane Miller on May 19, 2006 07:39 PM

 


This site rocks. I LOVE it. Thank you for making the effort. We are at the cusp of a revolution my friends. People like you give me hope, for my family and for the earth. Thank you again.

Posted by: L Koskela on May 20, 2006 03:19 PM

 


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://www.curehunter.com/public/keywordSummaryD016655-HIV-Core-Protein-p24.do

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 06:41 AM

 


Cal Crilly comments on HPV and Cervical Cancer, in the light of methylation (by email):

Just in case no one noticed but the true cause of cancer from the wart virus is most likely continual nutrient deficiency in the area of infection causing genomic hypomethylation of the genes.
Just a thought anyway and this piece of the puzzle makes the cancer vaccine quite irrelevant.

"This suggests that neoplastic transformation may be suppressed by CpG methylation, while demethylation occurs as the cause of or concomitant with neoplastic progression."
CpG Methylation of Human Papillomavirus Type 16 DNA in Cervical Cancer Cell Lines and in Clinical Specimens: Genomic Hypomethylation Correlates with Carcinogenic Progression

Lower red blood cell folate enhances the HPV-16–associated risk of cervical intraepithelial neoplasia


"Conclusions. These data show that global DNA hypomethylation is a significant epigenetic event in cervical carcinogenesis and that the degree of DNA hypomethylation increases with the grade of cervical neoplasia. These data suggest that global DNA methylation may serve as a biochemical marker of cervical neoplasia."
Global DNA hypomethylation increases progressively in cervical dysplasia and carcinoma

Posted by: Cal Crilly on October 4, 2007 05:22 AM

 


Effects of Retroviruses on
Host Genome Function

http://www.annualreviews.org/doi/abs/10.1146/annurev.genet.42.110807.091501

Key Words:
ERV, LTR, transcription, recombination,methylation

Abstract:
For millions of years, retroviral infections have challenged vertebrates, occasionally leading to germline integration and inheritance as ERVs,
genetic parasites whose remnants today constitute some 7 to 8 of the human genome. Although they have had significant evolutionary
side effects, it is useful to view ERVs as fossil representatives of retroviruses extant at the time of their insertion into the germline and not as direct players in the evolutionary process itself. Expression of particular ERVs is associated with several positive physiological functions as
well as certain diseases, although their roles in human disease as etiological agents, possible contributing factors, or disease markers ?? well demonstrated in animal models ?? remain to be established. Here we discuss ERV contributions to host genome structure and function, including their ability to mediate recombination, and physiological effects on the host transcriptome resulting from their integration, expression, and other events.

Posted by: AMC on July 22, 2010 01:11 AM

 















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