An On/Off Switch for Retroviruses – Can it be that Simple?

H-E-R-V not H-I-V
An On/Off Switch for Retroviruses – Can it be that Simple?

by Liam Scheff

First, this is an area of exploration I’ve been reaching into, but am now firmly committed to, with many thanks to Cal Crilly (who I believe we are all indebted to) for leading the way. I hope you’ll jump in the pool with me. Keep your waders on and kick your feet, we’ll all learn on the way. Here goes…

Science Daily presents a new study describing an “on/off switch for retroviruses.” Did you know turning retroviruses off was that simple? Contradictions abound – here they describe retroviruses as ‘fatal,’ but intended for good; but they are generally considered normal, ubiquitous and non-toxic, except when they’re talking about their favorite cash cow, “HIV.”

“ScienceDaily (Apr. 10, 2010) — A University of British Columbia doctoral candidate has discovered a previously unknown mechanism for silencing retroviruses, segments of genetic material that can lead to fatal mutations in a cell’s DNA. The findings, published in the journal Nature, could lead to new cancer treatments that kill only tumour cells and leave healthy surrounding tissue unharmed.”

How do they intend to do this neat trick? By using an enzyme which determines how DNA is expressed. This brings us in line with Cal Crilly’s breakthrough analysis of ‘methylation,’ ‘demethylation,’ and the creation of retroviruses in AIDS, cancer and auto-immune diseases.

Methylation is a process which safeguards DNA from, or exposes it to expression of its native retroviral sequences. These comprise a large stretch of the human genome in which they live as “long terminal repeats” – LTRs – of human endogenous retroviruses – HERVs (but could also be called transposons, retrotransposons, etc. It’s a new field, and they’ll certainly be pressed to work it out as they go).

Young TurksAn aside – I’m posting many links to the Wikipedia throughout, so you can see the limits of the mainstream as they try not to give the store away, but are simultaneously forced to acknowledge that the ‘central dogma‘ of genetics has been proven wrong, almost as soon as it was laid out by Watson and Crick. Remember Watson and Crick? They said that DNA was like a library whose collection never changed, and the only thing that anybody could do was go in, make an exact copy of a few pages of a book, and leave with their loose-leaf in hand. But now all the smart boys and girls know it ain’t so. The collection changes all the time…It’s causing a major panic over in Darwin-land, too…

These long segments of human DNA are expressed when cells are starved for specific key nutrients, like selenium, glutathione and choline, or exposed to toxins, X-rays, benzene, cortisol, other carcinogens, stressors and illness, especially “auto-immune disease“; or when they are being created or rapidly dividing, such as in fetal tissue and the placenta.

In other words, human beings produce HERVs under stress and during development. These segments are usually wound tightly and guarded or locked in by chemicals – histones. Histone behavior can be changed by the addition of different chemical groups to the DNA. The star of the show in today’s research is called the ‘methyl group,’ whose activity on DNA is called ‘methylation.’

HIV is Full of HERV (and other four letter words)

HERVs are created by the ‘copying out’ of the DNA into RNA, which is then free to roam or pop out of the cell in a protein capsule and stick to the surface. What’s so special about that? These HERV proteins (or expressed transposable elements) have proven to be analogous with putative “HIV” proteins, and respond to “HIV” antigens; but not justHIV,” also “Hepatitis C,” Lupus, and other immune and auto-immune diseases and cancers. in other words, these HERVs are as much “HIV” as any of the wildly different sequences that are fished out of lymph tissue cells and called “HIV” in AIDS patients.

Some of these HERVs are “lymphotropic,” that is, they hang out in the lymph nodes and tissue – which is precisely where Luc Montagnier was looking for his “LAV” – the very ‘virus’ sample he sent to Robert Gallo. These are the two fellows credited with discovering the “AIDS virus.” Montagnier’s “LAV” stood for “Lymphadenopathy (Swollen Lymph Node) Associated Virus.” (There’s the lymph node again).

Gallo stole the sample by claiming it as his own, and introduced it to the world (at a press conference, before publishing his papers on AIDS) as “HTLV-III.” The name “HIV” was adopted later, to advertise the putative qualities he wanted it to have. But his “HTLV” was a sloppy slurry of Montagnier’s material, plus cancer cells, plus proteins, enzymes and liquids Gallo and his colleagues had squeezed out of their cadre of gay men with swollen lymph nodes.

H-I-V is really H-E-R-V

AIDS researchers have been forced to admit time and again that their “HIV” is morphologically identical to “HIV-like particles” they find in “HIV negative persons.” This is true even though their “HIV” has the bad habit of having no standard size or physical quality – it can be too small or too large, and still be “HIV” to determined true-believing AIDS researchers.

This is why AIDS patients can “suppress” or stop the production of “HIV” by taking Selenium and other pro-methylating micronutrients. Why? Because returning cells to healthy levels of methyl production is good for bringing order back to loose and disordered DNA. Methylation stops or slows the production of these transposable elements. These are mistakenly thought of as “viruses,” but “HIV” is “LAV,” which is and always was human endogenous retroviral expression in stressed and damaged cells.

And this is at least part of the reason why HIV tests are so lousy.* Humans and animals produce HERVs under stress and illness, and so “HIV tests” are really “HERV tests,” and react with proteins produced by people who are suffering from almost any illness, drug abuse, vaccination, or, of course, pregnancy – because HERVs are expressed like wildfire in the placenta. *(The other reason is because Gallo’s HIV test slurry came from so many different people, mixed with so many different chemical and biological elements, it’s really impossible to know what they’re testing for).

John p. moore of aidstruth.orgFinally, this is why “HIV” (LAV or HTLV) doesn’t kill T-Cells. This has been the central claim of the AIDS paradigm – but it was proven false from the start. Robert Gallo invented the idea of slow T-Cell depletion by a scavenging, ravaging retrovirus in order to package his product with enough fear and anxiety, covered by pseudo-scientific technobabble, so pure belief would make it stick. Gallo sold his mixed cells containing HERVs (or HTLV-III, which was both as functionless and fraudulent as his other “human lymphotropic viruses”) to Abbott Labs. But he sold them in…ready? T-Cells. His “HIV” Grows in T-Cells. It’s called an ‘eternal line’ of production, in T-Cell leukemia. It never dies. Because HERVs don’t kill T-Cells.

Do you know what does cause T-Cells to suffer? De-methylation of DNA by exposure to pharmaceuticals and toxins.

Inventing the AIDS Virus

Gallo also invented the idea that HTLV-III was a sex virus, because the men who he was studying were gay, and apparently that’s just how Robert Gallo’s mind worked – “gay=sex disease.” These were ideas that Gallo and his colleagues invented, because their reductionist paradigm allowed them to, and because they lack the personal qualities to put integrity before fame, power and profit. He, and his colleagues, including Peter Duesberg, were all searching for a way to make billions in discovering a cause and cure for cancer. Their chosen method was culturing cells and looking for ‘retroviruses,’ which are really HERVs – endogenous material expressed under stress. That’s why Rodriguez, et al (2006), admitted that “HIV” (LAV, or HTLV-III) has no significant effect, if any at all on T-Cells.

Which is why ol’ Peter Duesberg has been so adamant all these years that “HIV” isn’t the pure and single CAUSE of all the things lumped together and called AIDS. Duesberg remains enough of a reductionist to not trouble or rethink his retroviral model too much, (though I wish he would; he could kick this thing along a few yards). But he showed a long time ago that he was a genuine human being with a good soul, who would part from the company of his peers, despite their vicious and brutal attacks, when he felt, after real consideration, that they were deeply and dangerously incorrect.

In terms of character, you can ask Lindsey Nagel about the quality of Peter’s. She’s around because he bothered the world with his complaints about AIDS theory. You can’t ask Joyce Ann Hafford about Robert Gallo’s character. She, and hundreds of thousands of others, trusted the CDC and FDA, who enforce Gallo’s law, to be honest, caring ethical organizations who wouldn’t lie to the public, or sell them deadly, unneeded drugs, and for her trust, she paid with her life.

And you can bet this is why Luc Montagnier, who also has a streak of humanity in him tells people that “You can get rid of HIV in a few weeks if you have a good immune system.” Because he knows, deep down, that what they’re looking at are genetic expression and proteins that emerge under stress. Not dangerous world-killing monsters that are the root cause of all evil and turmoil. But particles and proteins that go away when measures to return health (and not destroy bodies) are enacted.

The Name Game

Back in the beginning of the play, just after Gallo stole the fame and the patent, Montagnier and the French gouvernement made a fuss, and Gallo and Montagnier were made to shake hands and share the moolah. When the cash settled, they agreed that they’d found the same thing. “HTLV-III” was Gallo’s rechristening of the various phenomena he ‘found’ by hyper-stimulating the mixed tissue of various gay men (only some of whom had “AIDS,” and only some of whom tested “HTLV-III positive”). But Gallo’s description of the expression of HTLV-III mirrors precisely the expression of HERVs.

And what are HERVs? They are bits of human genome ‘expressed’ and coated in protein and spit out of their cell, when cells are unhealthy, (or when they are developing, such as in placental cells), and are not being properly methylated. What do they do? Who knows? They may carry repair information. They may be lifeboats for genes that were being disrupted. They may be used to bind cells together – some are ‘fusogenic‘ or sticky that way.

What don’t they do? They don’t cause T-Cell depletion, that anyone can see, and they aren’t a sexually-transmitted ‘virus,’ or disease, as far as anyone can tell. In fact, they seem to be large classes of variable material, which express under such a variety of circumstances, that I’ll bet no one will be able to map all their uses for quite some time. (What makes it hard for serious researchers into HERVs to get anywhere is contending with their looney peers in the ‘poisonous sexual predator retroviral particle’ religion).

In brief, what they do is get expressed when cells are demethylated, and tucked quietly away when cells are healthy.

How Do You Methylate?

Avoid carcinogens. Don’t poison your intestines. This is most important, because your immune system starts in your intestines, with what you put into your mouth. Get enough protein of a good non-carcinogenic quality. Eat complex carbohydrates from un-refined whole grains. Eat green leafy vegetables, foods with B vitamins, and essential fatty acids. Don’t do drugs. And most of all, eat selenium, choline, vitamin C and A. In other words, follow Tine Van Der Maas’ recipe: Garlic (or Brazil nuts) (selenium), Beet (choline, vitamin A), Lemon (Vitamin C), and Olive Oil (Essential Fatty Acids for tissue repair).

Retroviruses Are Good! (Except when they’re bad).

In the Science Daily article quoted at the top, the researchers are asserting that retroviruses are dangerous-but-helpful weapons that will kill a cancer. But AIDS theory 101 states that retroviruses cause cancer!. The article notes:

“Also, for unknown reasons, cancer cells have significantly less DNA methylation than normal cells. So blocking ESET holds the promise of affecting only cancer cells, allowing retroviruses to flourish to the detriment of their hosts.”

Why do cancer cells have more retroviral expression? They give the answer, but don’t hear themselves say it: Less Methylation. Cells which are damaged by toxin or otherwise become demethylated (or hypomethylated – “hypo” meaning “beneath” or “under”). The expressed retroviruses aren’t a cause or a cure for cancer. They are a sign of damaged cells. Hypomethylation is itself indicative of cancer, and is caused by toxic exposure and major deficiency.

Their solution – to unleash the expression of retroviruses in cells, in order to destroy cancer cells (they hope!) What would an “AIDS” doctor say? Are more retrovirus particles a good idea? Will making the cells produce even more HERVs help the body to equilibrate and stop producing cancer? (I don’t think so, myself. I’d recommend the Rath technology instead – high dose Vitamin C, micronutrients, and natural protease inhibitors to occupy the cancer while the body destroys it).

More Retroviruses or Fewer?

Understanding Viral LoadWhile AIDS researchers attack cells with drugs that kill them (therefore suppressing any activity, including HERVs), cancer researchers want to increase the same material as a cure. This is good news for “AIDS” patients who can rest easy knowing their “HIV” will attack and eradicate any disease in their body…

All of this lets the observer know how disjointed genetic theory is, how locked in a medical-warfare model it remains. Researchers still want to bomb the body, instead of supplying its missing nutrients. They’re back fighting World War 1, but inside their patient’s cells and organs.

Have a look at the article below, and others like it by searching the terms and links above and in the article. And please stop and read Cal Crilly’s outstanding work in stitching this all together. The future will owe him a debt of gratitude.

Start/stop Switch’ for Retroviruses Found

ScienceDaily (Apr. 10, 2010) — A University of British Columbia doctoral candidate has discovered a previously unknown mechanism for silencing retroviruses, segments of genetic material that can lead to fatal mutations in a cell’s DNA.

The findings, published in the journal Nature, could lead to new cancer treatments that kill only tumour cells and leave healthy surrounding tissue unharmed.

Danny Leung, a 27-year-old graduate student in the laboratory of Asst. Prof. Matthew Lorincz in the Dept. of Medical Genetics, UBC Faculty of Medicine, found that a protein called ESET [an enzyme active in the methylation/histone process] is crucial to preventing the activity of endogenous retroviruses in mouse embryonic stem cells. Distant relatives of such retroviruses are more active in the cells of testicular, breast and skin cancers in humans.

If ESET can be blocked, retroviruses would become dramatically more active, thus either killing the cancer cells hosting them or flagging them as targets for the immune system.

Leung, who was co-lead author with a graduate student at Kyoto University in Japan, has devoted his studies at UBC to the growing field of epigenetics — changes to the genome that do not involve changes to the underlying genetic code. Such changes determine whether or not a gene is expressed.

The common method for silencing certain genes is DNA methylation, in which a chemical group attaches to the DNA structure. But Leung and his collaborators at UBC and Kyoto University found that the activity of ESET is far more potent than DNA methylation in silencing retroviruses in embryonic stem cells of mice. This indicates an independent parallel pathway of silencing the retroviruses.

Their research has direct bearing on cancer treatments because cancer cells are stem-like — they can differentiate into other types of cells. Also, for unknown reasons, cancer cells have significantly less DNA methylation than normal cells. So blocking ESET holds the promise of affecting only cancer cells, allowing retroviruses to flourish to the detriment of their hosts. Normal, differentiated cells, which still have DNA methylation to keep retroviruses in check, would be unaffected.

“Inhibiting ESET may affect just the cancer cells, allowing further expression of retroviruses, which in turn would kill the cancer cells,” says Leung, who is in his third year of graduate studies at UBC. His co-lead author on the paper, Toshiyuki Matsui, is a student in the lab of Yoichi Shinkai at Kyoto University.

PS – I sent all of this to Cal, and he had the following:
Allowing further expression of retroviruses, which in turn would kill the cancer cells,” will just be creating initiation of cancer in other spots.

The idea of retroviruses stopping a tumor is that one I mentioned about reversing DNA once it’s formed, as in retroviruses can dismantle DNA that cancer cells set up and replicate once a tumor has set up. (Which is why chickenpox rips your skin apart so care needs to be taken). Very similar to the idea of using herpes viruses, with someone’s tumor DNA you could extract the retroviral component and inject it into the tumor to break it down. So it is possible.

Mucking about willy nilly with any viruses/retroviruses is a bit mad, it has to be delivered right to the tumor. And diet is still vital to stop it all happening again which of course they’re not up on.

Retinoic acid and other things balances the methylation BTW. That’s why Vitamin A is so useful in cancer but I use cod liver oil as it’s not toxic, I guzzle it when I get sick, my genes need filling LOL Switching on Retinoic acid receptors stops hypermethylation which once a cancer has started is not good.

2 thoughts on “An On/Off Switch for Retroviruses – Can it be that Simple?

  1. Some surgeons have finally clicked that ERV’s are involved in cell growth while I expect the retrovirologists will take a while to get over their “plague thinking”.

    “In particular, ERVs may play crucial roles in a cascade of cellular and molecular events underlying the systemic pathologic alterations after injury and infection….”
    POTENTIAL ROLES OF ERVs AND THEIR GENE PRODUCTS IN SYSTEMIC RESPONSE TO INJURY AND INFECTION
    http://journals.lww.com/shockjournal/Fulltext/2008/08000/Endogenous_Retroviruses_in_Systemic_Response_To.2.aspx

    Which explains why you find so called HIV particles with tumours.

    Novel Family of Gynecologic Cancer Antigens Detected by Anti-HIV Antibody
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364385/

    And pregnancy…

    HIV proteins in normal human placentae.
    http://www.ncbi.nlm.nih.gov/pubmed/1930645

  2. This is some awesome material. This kind of idea has been on my mind a lot lately, and this is the first article that I’ve ever read that really makes sense of all the evidence. I have been studying the Chronic Fatigue Syndrome research lately, and they think that XMRV (Xenotropic Murine Retrovirus) is the cause of CFS. There is obviously a huge correlation between CFS and XMRV, as there is with AIDS and HIV, and Adult T-Cell Leukemia and HTLV-1. There is also a huge correlation between Multiple Sclerosis and a retrovirus called MSRV. After reading this article, it makes a lot of sense that these retroviruses are just an effect of the disease process and not the cause. Dr. Duesberg knows retroviruses better than anyone, and he definitely knows that they are rather harmless bystanders. It is absolutely mind boggling to think that the target of AIDS treatment may actually be a very important human survival mechanism.

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